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ifosfamide

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Ifosfamide is an alkylating agent chemotherapy drug used to treat a variety of cancers, including testicular cancer, ovarian cancer, and soft tissue sarcomas. It is a nitrogen mustard derivative that works by damaging the DNA of cancer cells, preventing them from dividing and growing. It is synthesized via a multi-step process involving the reaction of isophosphamide with chloroacetaldehyde and then with N,N-bis(2-chloroethyl)amine. While effective, ifosfamide has several side effects, including nausea, vomiting, and hair loss, and it can also damage the kidneys and bladder. Despite its potential toxicities, it is studied due to its effectiveness in treating certain cancers, and researchers continue to investigate ways to reduce its side effects.'

Cross-References

ID SourceID
PubMed CID3690
CHEMBL ID1024
CHEBI ID5864
SCHEMBL ID4885
MeSH IDM0010999
PubMed CID115161
MeSH IDM0010999

Synonyms (222)

Synonym
1,2-oxazaphosphorine, 3-(2-chloroethyl)-2-[(2-chloroethyl)amino]tetrahydro-, 2-oxide
2,n(sup 1)-bis(2-chloroethyl)diamido-1,3,2-oxazaphosphoridinoxy-
2h-1,2-oxazaphosphorin-2-amine, n,3-bis(2-chloroethyl)tetrahydro-, 2-oxide
wln: t6npotj am2g bo b2g
z4942 ,
z 4942
nsc-109724
3-(2-chloroethyl)-2-[(2-chloroethyl)amino]perhydro-2h-1,2-oxazaphosphorine oxide
a 4942
ifex (tn) (bristol meyers)
3-(2-chloroethyl)-2-[(2-chloroethyl)amino]tetrahydro-2h-1,2-oxazaphosphorine 2-oxide
n-(2-chloroethyl)-n'-(2-chloroethyl)-n',o-propylenephosphoric acid diamide
2,n(sup 1)-bis(2-chloroethyl)diamido-1,3,2-oxazaphosphoridinoxyd
2h-1,2-oxazaphosphorine, 3-(2-chloroethyl)-2-[(2-chloroethyl)amino]tetrahydro-, 2-oxide
n-(2-chloroethyl)-n'-(2-chloroethyl)-n',o-propylene phosphoric acid ester diamide
3-(2-chloroethyl)-2-[(2-chloroethyl)amino]perhydro-2h-1,2-oxazaphosphorineoxide
AC-2113
isocyclophosphamide
CHEMBL1024
MLS002154021
smr001233348
66849-34-1
AB00513932-07
AB00513932-08
AB00513932-06
ccris 352
1,3,2-oxazaphosphorine, 3-(2-chloroethyl)-2-((2-chloroethyl)amino)tetrahydro-, 2-oxide
n,n-bis(beta-chloroethyl)-amino-n',o-propylene-phosphoric acid ester diamide
ifosfamidum [inn-latin]
n,3-bis(2-chloroethyl)tetrahydro-2h-1,3,2-oxazaphosphorin-2-amine 2-oxide
3-(2-chloroethyl)-2-[(2-chloroethyl)amino]perhydro-2h-1,3,2-oxazaphosphorineoxide
2h-1,3,2-oxazaphosphorin-2-amine, n,3-bis(2-chloroethyl)tetrahydro-, 2-oxide
3-(2-chloroethyl)-2-((2-chloroethyl)amino)perhydro-2h-1,3,2-oxazaphosphorine oxide
ifsofamide
n-(2-chloroethyl)-n'-(2-chloroethyl)-n',o-propylenephosphoric acid ester diamide
2,3-(n,n(sup 1)-bis(2-chloroethyl)diamido)-1,3,2-oxazaphosphoridinoxyd
holoxan
2h-1,3,2-oxazaphosphorine, 3-(2-chloroethyl)-2-((2-chloroethyl)amino)tetrahydro-, 2-oxide
ifosfamida [inn-spanish]
mjf-9325
n-(2-chloraethyl)-n'-(2-chloraethyl)-n',o-propylen-phosphorsaureester-diamid [german]
iso-endoxan
einecs 223-237-3
hsdb 7023
nsc 109724
3-(2-chloroethyl)-2-[(2-chloroethyl)amino]tetrahydro-2h-1,3,2-oxazaphosphorine 2-oxide
brn 0611835
ifex
z-4942 ,
cas-3778-73-2
NCGC00016639-01
PRESTWICK2_000833
NCGC00179435-01
ifosfamid
n-(2-chloroethyl)-n-(3-(2-chloroethyl)-2-oxido-1,3,2-oxazaphosphinan-2-yl)amine
iphosphamid
n,3-bis(2-chloroethyl)-1,3,2-oxazaphosphinan-2-amine 2-oxide
holoxan 1000
isoendoxan
iphosphamide
isofosfamide
naxamide
{3-(2-chloroethyl)-2-[(2-chloroethyl)amino]perhydro-2h-1,3,} 2-oxazaphosphorine oxide
i-phosphamide
asta z 4942
{3-(2-chloroethyl)-2-[(2-
mjf 9325
cyfos
nsc109724
mitoxana
n,3-bis(2-chloroethyl)-2-oxo-1,3,2$l^{5}-oxazaphosphinan-2-amine
nci-c01638
PRESTWICK3_000833
BSPBIO_000785
BPBIO1_000865
AB00513932
C07047
ifosfamide ,
isophosphamide
3778-73-2
isosfamide
DB01181
3-(2-chloroethyl)-2-((2-chloroethyl)amino)tetrahydro-2h-1,3,2-oxazaphosphorine 2-oxide
ifex (tn)
D00343
ifosfamide (jan/usp/inn)
NCI60_000233
PRESTWICK0_000833
PRESTWICK1_000833
SPBIO_002706
iso endoxan
HMS2090M12
HMS2093N07
ifosfamidum
CHEBI:5864 ,
ifosfamida
STL058690
HMS1570H07
NCGC00179435-03
NCGC00179435-02
HMS2097H07
ifosfamide [usan:usp:inn:ban:jan]
n-(2-chloraethyl)-n'-(2-chloraethyl)-n',o-propylen-phosphorsaureester-diamid
unii-um20qqm95y
um20qqm95y ,
NCGC00256413-01
dtxsid7020760 ,
dtxcid90760
tox21_302775
NCGC00259364-01
tox21_201815
A823873
pharmakon1600-01505480
nsc759154
nsc-759154
tox21_110539
AKOS005711213
HMS2232O10
ifosfamide sterile
ifosphamide
CS-1424
FT-0603650
NCGC00179435-07
AB02316
S1302
BRD-A67097164-001-11-2
3-(2-chloroethyl)-2-[(2-chloroethyl)amino]-1,3,2lambda5-oxazaphosphinan-2-one
gtpl7201
HMS3374B08
ifosfamide [mi]
ifosfamide [usp-rs]
ifosfamide [who-dd]
ifosfamide [usan]
ifosfamide [mart.]
ifosfamide [vandf]
ifosfamide [orange book]
ifosfamide [usp monograph]
ifosfamide [ep impurity]
ifosfamide [hsdb]
ifosfamide [inn]
ifosfamide [jan]
ifosfamide [ep monograph]
isophosphamide [iarc]
CCG-213464
HY-17419
BBL028071
SCHEMBL4885
tox21_110539_1
NCGC00179435-06
n,3-bis(2-chloroethyl)tetrahydro-2h-1,3,2-oxazaphosphinan-2-amine 2-oxide #
3-(2-chloroethyl)-2-((2-chloroethyl)amino)perhydro-2h-1,3,2-oxazaphosphorineoxide
Q-101874
ifomide
ifosfamide, british pharmacopoeia (bp) reference standard
3-(2-chloroethyl)-2-((2-chloroethyl)amino)-1,3,2-oxazaphosphinane 2-oxide
AB00513932_10
AB00513932_09
bdbm189358
n,3-bis(2-chloroethyl)-2-oxo-1,3,2$l;{5}-oxazaphosphinan-2-amine
3-(2-chloroethyl)-2-[(2-chloroethyl)amino]-1,3,2$l^{5}-oxazaphosphinan-2-one
n,3-bis(2-chloroethyl)-2-oxo-1,3,2lambda5-oxazaphosphinan-2-amine
mfcd00057374
sr-05000002022
SR-05000002022-5
ifosfamide, analytical reference material
ifosfamide, united states pharmacopeia (usp) reference standard
ifosfamide, >=98%
ifosfamide, european pharmacopoeia (ep) reference standard
HMS3654B15
SR-05000002022-3
SR-05000002022-1
ifosfamide; (rs)-n,3-bis(2-chloroethyl)-1,3,2-oxazaphosphinan-2-amine 2-oxide
ifosfamid a
SBI-0206804.P001
HMS3714H07
SW197177-4
BCP06596
Q418560
n,3-bis(2-chloroethyl)tetrahydro-2h-1,3,2-oxazaphosphorin-2-amine-2-oxide
FT-0670282
isophosphamide,(s)
AS-10978
(r)-3-(2-chloroethyl)-2-((2-chloroethyl)amino)-1,3,2-oxazaphosphinane 2-oxide
intermediate of ifosfamide
3-(2-chloroethyl)-2-(2-chloroethylamino)tetrahydro-2h-1,3,2-oxaazaphosphorin 2-oxide
STARBLD0001221
BI166243
ifosfamide - bio-x
ifosfamide in bulk
(2-chloro-ethyl)-[(r)-3-(2-chloro-ethyl)-2-oxo-2lambda5-[1,3,2]oxazaphosphinan-2-yl]-amine
3-(2-chloroethyl)-2-((2-chloroethyl)amino)tetrahydro-2h-1,3,2-oxazaphosphorine-2 -oxide
ifosfamide (ep monograph)
asta z-4942
3-(2-chloroethyl)-2-((2-chloroethyl)amino)tetrahydro-2h-1,3,2-oxazaphosphorin-2-oxide
ifosfamidum (inn-latin)
2,3-(n,n(,)-bis(2-chloroethyl)diamido)-1,3,2-oxazaphosphoridinoxy
ifosfamide (ep impurity)
l01aa06
seromida
ifolem
tronoxal
n-(2-chloraethyl)-n'-(2 chloroethyl)-n'-o-propylen-phosphorsaeureester-diamid
ifo-cell
n,n-bis(beta-chloroethyl)-amino-n'-o-propylene-phosphoric acid ester diamide
ifoxan
ifosfamide (mart.)
ifosfamide (usp monograph)
ifosfamide (usan:usp:inn:ban:jan)
ifomida
ifosfamide (usp-rs)
isophosphamide (iarc)
2-oxo-n,3-bis-(2-chloroethyl) tetrahydro-2h-1,3,2-oxazaphosphorin-2-amine
nci-co1638
holoxane
ifosfamida (inn-spanish)
I0713
EN300-7476797
SY066721
lappaconitine ,
CS-3588
HY-N0383
PD100434

Research Excerpts

Overview

Ifosfamide is an alkylating agent, a synthetic analogue of cyclophosphamide, used to treat various solid cancers. It is an important chemotherapeutic agent used in the therapeutic protocols of many malignant tumors.

ExcerptReferenceRelevance
"Ifosfamide is an alkylating agent, a synthetic analogue of cyclophosphamide, used to treat various solid cancers. "( Investigation of Ifosfamide Toxicity Induces Common Upstream Regulator in Liver and Kidney.
Choi, MS; Han, HY; Kim, SK; Kim, TW; Ko, JW; Yoon, S, 2021
)
2.4
"Ifosfamide is an antitumor agent with activity against various malignancies in pediatric patients. "( Excellent Tolerability of Ifosfamide and Mesna Via Continuous Infusion in a Pediatric Patient Population.
Anderson, PM; Pierson, CE; Plutt, AA; Stanton, MP; Zahler, S; Zembillas, AS, 2022
)
2.46
"Ifosfamide is an important chemotherapeutic agent used in the therapeutic protocols of many malignant tumors. "( Ifosfamide-induced Encephalopathy With Rapid Response to Thiamine: A Pediatric Case.
Anlar, B; Aydin, B; Günbey, C; Müngen, E; Öz, S; Yaman Bajin, İ, 2022
)
3.61
"Ifosfamide (IFO) is a widely used antineoplastic drug with broad-spectrum efficacy against various types of cancer. "( Intraperitoneal pretreatment of ellagic acid and chrysin alleviate ifosfamide-induced neurotoxicity, but betanin induces death in male wistar rats.
Mohammadi, H; Salimi, A; Shabani, M; Sudi, V,
)
1.81
"Ifosfamide (IFO) is an alkylating agent administered against different types of malignancies. "( The Nephroprotective Role of Carnosine Against Ifosfamide-Induced Renal Injury and Electrolytes Imbalance is Mediated Via the Regulation of Mitochondrial Function and Alleviation of Oxidative Stress.
Farshad, O; Ghanbarinejad, V; Heidari, R; Ilkhaninasab, F; Khadijeh, M; Moezi, L; Mohammadi, HR; Negar, A; Ommati, MM; Zahra, M, 2020
)
2.26
"Ifosfamide (IFO) is an alkylating agent used to treat broad range of malignancies. "( Ifosfamide induced encephalopathy in a child with osteosarcoma.
Atay, AA; Demir, ÜF; Malbora, B; Sarbay, H; Yılmaz, G, 2021
)
3.51
"Ifosfamide is an active alkylating chemotherapeutic drug chemically related to nitrogen mustard. "( Comprehensive insight into the molecular interaction of an anticancer drug-ifosfamide with human alpha-2-macroglobulin: biophysical and
Ahsan, H; Khan, FH; Siddiqui, T; Zia, MK, 2022
)
2.39
"Ifosfamide is a widely used chemotherapeutic agent having broad-spectrum efficacy against several tumors. "( Effect of Berberis vulgaris L. root extract on ifosfamide-induced in vivo toxicity and in vitro cytotoxicity.
Abdullah, I; Ahmad, S; Ali, MS; Froeyen, M; Hussain, A; Iftikhar, A; Ilyas, S; Mirza, MU; Nazir, M; Saleem, F; Saleem, U; Tabasum, R, 2021
)
2.32
"Ifosfamide is an alkylating agent, mostly used against variety of solid tumors in pediatric oncology practice. "( Ifosfamide-related encephalopathy with severe clinical presentations in children with cancer.
Ataseven, E; Göktepe, ŞÖ; Kantar, M, 2021
)
3.51
"Ifosfamide (IFA) is a potent alkylating antitumoral agent, but its use is limited by neurological side effects. "( Possible role of CYP2B6 genetic polymorphisms in ifosfamide-induced encephalopathy: report of three cases.
Bellien, J; Duflot, T; Filhon, B; Joannidès, R; Lamoureux, F; Marie-Cardine, A; Massy-Guillemant, N; Pereira, T; Verstuyft, C, 2018
)
2.18
"Ifosfamide is a cytotoxic drug usually used in malignant sarcomas. "( [Ifosphamide nephrotoxicity].
Ensergueix, G; Karras, A, 2018
)
1.92
"Ifosfamide (IFO) is an antineoplastic drug that is commonly used to treat gynecological and breast cancers. "( Neutrophils contribute to the pathogenesis of hemorrhagic cystitis induced by ifosfamide.
Alencar, NMN; Almeida, PRC; Alves, APNN; Araújo, LCNC; Bingana, RD; Cunha, FQ; Dornelas-Filho, AF; Lima-Júnior, RCP; Melo, AT; Nobre, LMS; Nour, ML; Pereira, VBM; Pinto, FMM; Silva, CMS; Silva, PGB; Silva, RO; Souza, MHLP; Wanderley, CWS; Wong, DVT, 2018
)
2.15
"Ifosfamide is an alkylating chemotherapeutic agent used in the treatment of many malignancies. "( Hydration, methylene blue, and thiamine as a prevention regimen for ifosfamide-induced encephalopathy.
Gharaibeh, EZ; Powers, BC; Salacz, ME; Telfah, M, 2019
)
2.19
"Ifosfamide (IFOS) which is a cytotoxic alkylating agent may cause central nervous system toxicity. "( Effect of alpha lipoic acid on ifosfamide-induced central neurotoxicity in rats.
Albayrak, A; Bilen, S; Fadillioglu, E; Ginis, Z; Kurt, SN; Ozturk, G, 2014
)
2.13
"Ifosfamide is an alkylating agent useful in the treatment of a wide range of cancers including sarcomas, lymphoma, gynecologic and testicular cancers. "( Ifosfamide related encephalopathy: the need for a timely EEG evaluation.
Feyissa, AM; Tummala, S, 2014
)
3.29
"Ifosfamide is a nitrogen mustard alkylating agent used as both a first-line and a salvage chemotherapeutic agent in the treatment of testicular germ cell tumors, various sarcomas, carcinomas, and some lymphomas. "( Chronic Ifosfamide toxicity: kidney pathology and pathophysiology.
Akilesh, S; Duffield, JS; Juaire, N; Smith, KD, 2014
)
2.28
"Ifosfamide is a chloro-isophosphoramide prodrug activated by hepatic Cytochrome P450 enzymes."( Comparison of hypoxia-activated prodrug evofosfamide (TH-302) and ifosfamide in preclinical non-small cell lung cancer models.
Ahluwalia, D; Ferraro, DJ; Hart, CP; Jung, D; Liu, Q; Matteucci, MD; Sun, JD; Wang, Y, 2016
)
1.39
"Ifosfamide is an anticancer agent used largely in treatment of solid tumors. "( Antioxidant activity of simvastatin prevents ifosfamide-induced nephrotoxicity.
Ali, RM; Alkaraki, AK; Mhaidat, NM; Shotar, AM, 2016
)
2.14
"Ifosfamide is an alkylating chemotherapeutic agent that exhibits activity against a wide range of tumors. "( Prenatal effects of transplacental exposure to ifosfamide in rats.
Helal, M, 2016
)
2.13
"Ifosfamide is an alkylating agent and is considered to be one of the important drugs for the treatment of metastatic sarcoma."( Hepatitis B Reactivation After Ifosfamide Therapy for Retroperitoneal Sarcoma.
Chaudhry, R; Cheedella, NK; Chhibar, P; Wang, JC; Zhu, Z, 2016
)
1.44
"Ifosfamide (IFOS) is a bifunctional alkylator with a wide spectrum of activity in solid tumors and has an autoinductive liver metabolism through P450 cytochromes. "( An original administration of ifosfamide given once every other week: a clinical and pharmacological study.
Alexandre, J; Cacheux, W; Duffau, B; Germann, N; Goldwasser, F; Gourmel, B; Rabillon, F, 2008
)
2.08
"Ifosfamide is a DNA-alkylating agent used frequently in chemotherapy of human malignancies. "( Differential effects of ifosfamide on dendritic cell-mediated stimulation of T cell interleukin-2 production, natural killer cell cytotoxicity and interferon-gamma production.
Bleifuss, E; Hesler, Cv; Issels, RD; Kuppner, MC; Mayerhofer, C; Mocikat, R; Noessner, E, 2008
)
2.1
"Ifosfamide is a well known prodrug for cancer treatment with cytochrome P450 metabolism. "( New ifosfamide analogs designed for lower associated neurotoxicity and nephrotoxicity with modified alkylating kinetics leading to enhanced in vitro anticancer activity.
Bourget, P; Deroussent, A; Martens, T; Mercier, L; Munier, F; Paci, A; Prost, E; Re, M; Royer, J; Storme, T; Vassal, G, 2009
)
2.35
"Ifosfamide is a cornerstone of chemotherapy in bone and soft-tissue sarcoma. "( Ambulatory administration of 5-day infusion ifosfamide+mesna: a pilot study in sarcoma patients.
Alexandre, J; Anract, P; Billemont, B; Camps, S; Coriat, R; Goldwasser, F; Larousserie, F; Leconte, M; Mir, O; Ropert, S, 2010
)
2.06
"Ifosfamide is a widely used chemotherapeutic agent for the treatment of a broad spectrum of solid tumors. "( Ifosfamide-induced encephalopathy and movement disorder.
Ames, B; Chaffee, S; Kim, J; Lewis, LD; Morse, R, 2010
)
3.25
"Ifosfamide is a chemotherapeutic prodrug used in the treatment of several tumor entities, including bone and soft-tissue sarcoma. "( Palifosfamide, a bifunctional alkylator for the treatment of sarcomas.
Jung, S; Kasper, B, 2010
)
2.42
"Ifosfamide is an alkylating agent used in the treatment of several neoplasias. "( Severe ifosfamide-induced neurotoxicity: a case report.
Breña Atienza, J; Cabello Rodríguez, A; Cháfer Rudilla, M; Merino Alonso, J; Ramos Linares, S; Ríos Rull, P, 2010
)
2.26
"Ifosfamide is an alkylating agent, frequently used in the treatment of sarcoma. "( Ifosfamide nephropathy in patients with sarcoma.
Keikhaei, M; Mashhadi, MA; Sanadgol, H, 2011
)
3.25
"Ifosfamide is an alkylating agent with well-demonstrated efficacy against STS, and dose-dependent activity."( High-dose ifosfamide as second- or third-line chemotherapy in refractory bone and soft tissue sarcoma patients.
Baek, KK; Chang, MH; Han, B; Lee, J; Lee, SH; Lim, T; Park, JO, 2011
)
1.49
"Ifosfamide (IFA) is a powerful chemotherapeutic drug that is active against a variety of paediatric malignancies. "( Ifosfamide induced Fanconi syndrome.
Buttemer, S; Lau, KK; Pai, M, 2011
)
3.25
"Ifosfamide is a prodrug which is metabolized by the liver to isophosforamide mustard, an active metabolite."( Investigation of ifosfamide nephrotoxicity induced in a liver-kidney co-culture biochip.
Aninat, C; Brochot, C; Choucha-Snouber, L; Corlu, A; Grsicom, L; Guillouzo, CG; Leclerc, E; Legallais, C; Madalinski, G; Poleni, PE; Razan, F, 2013
)
1.45
"Ifosfamide is an alkylating agent used to treat different types of malignancies including lymphomas, sarcomas and germinal cell tumors. "( Ifosfamide-induced neurotoxicity reversal with continuous veno-venous hemodialysis. A case report.
Bhardwaj, H; Cherry, MA; Hopps, S; Pant, S; Srour, S, 2013
)
3.28
"Ifosfamide (IFO) is a highly effective chemotherapeutic agent for treating a variety of pediatric solid tumors. "( Protective effects of alpha lipoic acid versus N-acetylcysteine on ifosfamide-induced nephrotoxicity.
El-Desoky, KI; El-Sisi, Ael-D; El-Syaad, ME; Moussa, EA, 2015
)
2.1
"Ifosfamide is an active alkylating agent used in the first-line treatment of NSCLC."( Phase II study of docetaxel and ifosfamide combination chemotherapy in non-small-cell lung cancer patients failing previous chemotherapy with or without paclitaxel.
Chen, MC; Chen, YM; Lee, CS; Lin, WC; Perng, RP; Shih, JF; Tsai, CM, 2003
)
1.32
"Ifosfamide is a nitrogen mustard with growing clinical applications; effective modulation may lead to improved efficacy."( Selective enhancement of ifosfamide-induced toxicity in Chinese hamster ovary cells.
Dolan, ME; Gandhi, MC; Ludeman, SM; Smith, SM; Springer, JB; Wilson, LR, 2003
)
1.34
"Ifosfamide is a bifunctional alkylating agent, used as a racemic mixture by intravenous route in the treatment of various tumors. "( Pharmacology of ifosfamide.
Franceschi, L; Furlanut, M, 2003
)
2.11
"Ifosfamide is an alkylating agent with well-demonstrated efficacy against a large number of malignant diseases. "( Neurological toxicity of ifosfamide.
Giometto, B; Nicolao, P, 2003
)
2.07
"Ifosfamide is an alkylating agent that is widely used in the treatment of various neoplasms, such as sarcomas, lymphomas, pediatric malignancies, germ cell tumors, lung, breast and ovarian cancer. "( Antiblastic drug combinations with ifosfamide: an update.
Badalamenti, G; Fulfaro, F; Gebbia, N; Russo, A; Valerio, MR, 2003
)
2.04
"Ifosfamide (IFO) is an active drug in several malignancies. "( Dose finding of ifosfamide administered with a chronic two-week continuous infusion.
Bearz, A; Cartei, G; Clocchiatti, L; Mantero, J; Pastorelli, D; Pella, N; Sacco, C; Salmaso, F; Zustovich, F, 2003
)
2.11
"Ifosfamide is an old drug still considered an effective cytostatic agent in the treatment of NSCLC."( Ifosfamide in non-small cell lung cancer.
Boni, C; Zanelli, F, 2003
)
2.48
"Ifosfamide is an alkylating agent active in various tumor types including breast cancer. "( Ifosfamide in advanced/disseminated breast cancer.
La Mura, N; Lombardi, D; Sorio, R; Spazzapan, S; Tabaro, G; Veronesi, A, 2003
)
3.2
"Ifosfamide is an alkylating agent with a broad spectrum of activity in solid tumors and hematological malignancies. "( Ifosfamide in hematological malignancies of adults.
Elice, F; Rodeghiero, F, 2003
)
3.2
"Ifosfamide is a prodrug that requires bioactivation by cytochrome P450 for antitumour activity. "( CYP3A4, CYP2C9 and CYP2B6 expression and ifosfamide turnover in breast cancer tissue microsomes.
Baumann, F; Brauckhoff, M; Horn, LC; Knüpfer, H; Köhler, U; Preiss, R; Schmidt, R; Schönfelder, M, 2004
)
2.03
"Ifosfamide is an important part of chemotherapeutic regimens used to treat a variety of malignancies. "( Evaluating risk factors for the development of ifosfamide encephalopathy.
David, KA; Picus, J, 2005
)
2.03
"Ifosfamide is an alkylating agent used in the treatment of germ-cell tumors, sarcomas and lymphomas. "( [Ifosfamide induced encephalopathy: 15 observations].
Behar, C; Dufour, C; Grill, J; Hartmann, O; Motte, J; Munzer, M; Oberlin, O; Paci, A; Sabouraud, P, 2006
)
2.69
"Ifosfamide (IFO) is a widely used antitumor agent, requiring activation to isophosphoramide mustard (IPM) for DNA alkylation."( Ifosfamide: pharmacokinetic properties for central nervous system metastasis prevention.
Lokiec, F, 2006
)
2.5
"Ifosfamide (IFS) is an antineoplastic alkylating agent whose major side effect is hemorrhagic cystitis (HC). "( Amifostine and glutathione prevent ifosfamide- and acrolein-induced hemorrhagic cystitis.
Batista, CK; Brito, GA; Cunha, FQ; Leitão, BT; Mota, JM; Ribeiro, RA; Souza, MH; Souza, ML, 2007
)
2.06
"Ifosfamide is a chemotherapy agent commonly used in the treatment of several solid tumors and hematologic malignancies. "( Ifosfamide neuropsychiatric toxicity in patients with cancer.
Alici-Evcimen, Y; Breitbart, WS, 2007
)
3.23
"Ifosfamide is a chemotherapeutic agent that requires cytochrome P450 3A (CYP3A) for bioactivation and metabolism. "( Assessment of ifosfamide pharmacokinetics, toxicity, and relation to CYP3A4 activity as measured by the erythromycin breath test in patients with sarcoma.
Baker, LH; Chugh, R; Griffith, KA; Leu, KM; Taylor, JM; Thomas, DG; Wagner, T; Worden, FP; Zalupski, MM, 2007
)
2.14
"Ifosfamide is an oxazaphosphorine alkylating agent with a broad spectrum of antineoplastic activity."( Thioredoxin reductase inactivation as a pivotal mechanism of ifosfamide in cancer therapy.
Wang, X; Xu, T; Zhang, J, 2008
)
1.31
"Ifosfamide (Z 4942) is an alkylating agent with the structure of a cyclophosphamide analog. "( [Treatment of pain caused by metastases of reactivated prostatic cancer with ifosfamide].
Kawai, T; Kihara, K; Sakuramoto, T; Satomi, Y; Takeda, T, 1983
)
1.94
"Ifosfamide (IF) is an alkylating cytostatic drug with urotoxic (hemorrhagic cystitis) and nephrotoxic side effects. "( Effect of ifosfamide metabolites on sodium-dependent phosphate transport in a model of proximal tubular cells (LLC-PK1) in culture.
Brandis, M; Mohrmann, M; Pauli, A; Schönfeld, B; Walkenhorst, H,
)
1.98
"Ifosfamide (IF) is an alkylating cytostatic with urotoxic (haemorrhagic cystitis) and nephrotoxic (Fanconi syndrome) side effects. "( Dithio-bis-mercaptoethanesulphonate (DIMESNA) does not prevent cellular damage by metabolites of ifosfamide and cyclophosphamide in LLC-PK1 cells.
Ansorge, S; Brandis, M; Mohrmann, M; Schönfeld, B, 1994
)
1.95
"Ifosfamide (IF) is an alkylating cytostatic with urotoxic and tubulotoxic side effects which may result in the development of Fanconi syndrome in children. "( Ifosfamide and mesna: effects on the Na/H exchanger activity in renal epithelial cells in culture (LLC-PK1).
Brandis, M; Küpper, N; Mohrmann, M; Schönfield, B,
)
3.02
"Ifosfamide is a chiral pro-drug which is administered clinically in its racemic form. "( Pharmacokinetics of ifosfamide and its enantiomers following a single 1 h intravenous infusion of the racemate in patients with small cell lung carcinoma.
Chrystyn, H; Corlett, SA; Parker, D, 1995
)
2.06
"Ifosfamide is an active chemotherapeutic agent in the treatment of soft tissue sarcoma. "( Ifosfamide and etoposide in the treatment of advanced soft tissue sarcomas.
Baker, LH; Blair, SC; Zalupski, MM, 1994
)
3.17
"Ifosfamide is a pro-drug and requires metabolic activation to exert cytotoxic activity."( Ifosfamide metabolism and pharmacokinetics (review).
Beijnen, JH; Bult, A; Kaijser, GP; Underberg, WJ,
)
2.3
"Ifosfamide (IFF) is a nitrogen mustard with significant activity against a number of tumors. "( Efficacy and toxicity of ifosfamide stereoisomers in an in vivo rat mammary carcinoma model.
Batist, G; Granvil, CP; Wainer, IW; Wang, T, 1994
)
2.03
"Ifosfamide is a prodrug that requires biotransformation to become cytotoxic."( Ifosfamide clinical pharmacokinetics.
Wagner, T, 1994
)
2.45
"Ifosfamide is an alkylating agent which has been incorporated into frontline therapy for a number of malignant paediatric tumours. "( Ifosfamide nephrotoxicity in paediatric cancer patients.
Ashraf, MS; Brady, J; Breatnach, F; Deasy, PF; O'Meara, A, 1994
)
3.17
"Ifosfamide is a member of the oxazaphosphorine class of cytostatic drugs. "( The analysis of ifosfamide and its metabolites (review).
Beijnen, JH; Bult, A; Kaijser, GP; Korst, A; Underberg, WJ,
)
1.92
"Ifosfamide is a cyclophosphamide analogue synthesized in the 1960s with antineoplastic activity demonstrated in early broad-ranging phase I studies conducted in Germany in the 1970s. "( Ifosfamide and mesna in epithelial ovarian carcinoma.
Sutton, G, 1993
)
3.17
"Ifosfamide is an antineoplastic drug with efficacy and activity in numerous cancers. "( Ifosfamide. Patient care management.
Lynch, MP; Ruland, T, 1993
)
3.17
"Ifosfamide/VP-16 is an active combination in children with recurrent malignant solid tumors. "( Ifosfamide/etoposide combination in the treatment of recurrent malignant solid tumors of childhood. A Pediatric Oncology Group Phase II study.
Golembe, B; Holbrook, CT; Homans, AC; Jaffe, N; Kung, FH; Nitschke, R; Pratt, CB; Schwenn, M; Strother, D; Vega, RA, 1993
)
3.17
"Ifosfamide is an active agent in cisplatin-resistant cervical cancer. "( A phase II study of weekly cisplatin followed by cisplatin and ifosfamide in advanced or recurrent cervical carcinoma.
Baker, TR; Hempling, RE; Malfetano, JH; Piver, MS; Recio, FO; Rose, PG, 1993
)
1.97
"Ifosfamide is a derivative of cyclophosphamide and is used to treat malignant tumours. "( Hypophosphataemic rickets after ifosfamide treatment in children.
Sweeney, LE, 1993
)
2.01
"Ifosfamide is an oxazaphosphorine analogue of cyclophosphamide with proven activity in breast cancer but substantial urotoxicity. "( Evaluation of ifosfamide plus mesna as first-line chemotherapy in women with metastatic breast cancer.
Hartmann, LC; Ingle, JN; Krook, JE; Mailliard, JA; Wieand, HS, 1995
)
2.09
"Ifosfamide is an alkylating agent with clinical activity in the treatment of sarcomas, and data support a dose-response relationship in this disease. "( High-dose ifosfamide in the treatment of sarcomas of soft tissues and bone.
Demetri, GD, 1996
)
2.14
"Ifosfamide is an alkylating agent that has demonstrated efficacy in the treatment of several malignancies. "( Ifosfamide in the treatment of breast cancer.
Overmoyer, BA, 1996
)
3.18
"Ifosfamide is an analogue of cyclophosphamide that is active against a variety of solid tumors, including non-small cell lung cancer. "( Ifosfamide in non-small cell lung cancer.
Johnson, DH, 1996
)
3.18
"Ifosfamide is an active agent in recurrent squamous cell carcinoma of the head and neck."( A phase II study of ifosfamide in recurrent squamous cell carcinoma of the head and neck.
Benner, SE; Dimery, IW; Dunnington, JS; Hong, WK; Huber, MH; Lippman, SM; Shirinian, M, 1996
)
1.34
"Ifosfamide has proven to be an important asset in the treatment of cancer in children."( Ifosfamide in the treatment of pediatric malignancies.
Behrendt, H; de Kraker, J; Michiels, E; van den Berg, H; Voûte, PA, 1996
)
2.46
"Ifosfamide (IFX) is an agent as yet unstudied in advanced urothelial carcinoma."( Eastern Cooperative Oncology Group phase II trial of ifosfamide in the treatment of previously treated advanced urothelial carcinoma.
Bono, B; Dreicer, R; Elson, P; Knop, R; Loehrer, PJ; Richardson, RR; Witte, RS, 1997
)
1.27
"Ifosfamide is an analogue of cyclophosphamide active in the treatment of numerous tumours. "( 6-Day continuous infusion of high-dose ifosfamide with bone marrow growth factors in advanced refractory malignancies.
Alexandre, J; Brain, EC; Chaouche, M; Cvitkovic, E; Delord, JP; Errihani, H; Hardy Bessard, AC; Jasmin, C; Misset, JL; Mita, A; Soulié, P, 1997
)
2.01
"Ifosfamide is an active alkylating agent in the treatment of breast cancer, as a first-line therapy and in advanced disease. "( Ifosfamide and etoposide in previously treated patients with advanced breast cancer.
Baltali, E; Barişta, I; Benekli, M; Celik, I; Firat, D; Güler, N; Güllü, IH; Kars, A; Kiraz, S; Tekuzman, G,
)
3.02
"Ifosfamide is an effective drug in the treatment of several tumors and has known neurologic, renal, and hematologic toxicities."( Acute pancreatitis secondary to ifosfamide.
Gerson, R; Serrano, A; Sternbach, GL; Varon, J; Villalobos, A,
)
1.14
"Ifosfamide is an alkylating drug that has demonstrated activity against non-small cell lung cancer, testicular cancer, breast cancer, and soft tissue sarcoma."( Docetaxel and ifosfamide in patients with advanced solid tumors: results of a phase I study.
de Bruijn, EA; Groult, V; Locci-Tonelli, D; Planting, AS; Pronk, LC; Schellens, JH; Schrijvers, D; van Oosterom, AT; Verweij, J, 1998
)
1.38
"Ifosfamide is an active drug in the therapy of paediatric tumours such as rhabdomyosarcoma, Ewings' sarcoma, Wilms' tumour, neuroblastoma, germ cell tumours and lymphomas. "( The role of ifosfamide in paediatric cancer.
Advani, SH, 1998
)
2.12
"Ifosfamide is an oxazophosphorine widely used in the treatment of cancer in children and adults. "( Urinary proton magnetic resonance studies of early ifosfamide-induced nephrotoxicity and encephalopathy.
Foxall, PJ; Hartley, JM; Lapsley, M; Neild, GH; Nicholson, JK; Singer, JM; Souhami, RL, 1997
)
1.99
"Ifosfamide is a leading drug in soft tissue sarcoma therapy. "( Pharmacokinetics of ifosfamide administered according to three different schedules in metastatic soft tissue and bone sarcomas.
Bergnolo, P; Boglione, A; Bumma, C; Colussi, AM; Comandone, A; Dal Canton, O; Frustaci, S; Leone, L; Monteleone, M; Oliva, C, 1998
)
2.07
"Ifosfamide is an alkylating agent which has poorly understood toxic side effects such as encephalopathy. "( Ifosfamide-induced stomatocytosis and mesna-induced echinocytosis: influence on biorheological properties of blood.
Baerlocher, GM; Beer, JH; Cerny, T; Meiselman, HJ; Owen, GR; Reinhart, WH, 1999
)
3.19
"Ifosfamide is an active agent as part of combination therapy for patients with both indolent and aggressive relapsed lymphomas, and has also been used in high-dose therapy regimens followed by stem cell or bone marrow rescue."( The role of ifosfamide in the treatment of lymphomas.
Hagemeister, FB, 1999
)
1.4
"Ifosfamide is an active drug in the treatment of chemotherapy-naive patients with advanced endometrial cancer and its application in currently used (combination) regimens should be considered."( Cyclophosphamide or ifosfamide in patients with advanced and/or recurrent endometrial carcinoma: a randomized phase II study of the EORTC Gynecological Cancer Cooperative Group.
Boes, GH; Cervantes, A; Hoesel, G; Pawinski, A; Pecorelli, S; Tumolo, S; van Oosterom, AT, 1999
)
2.07
"Ifosfamide is an antineoplastic agent that requires hepatic activation to the cytotoxic active metabolite ifosforamide mustard. "( Suspected ifosfamide-induced neurotoxicity.
McVay, JI; Wood, AM, 1999
)
2.15
"Ifosfamide is an alkylating agent used in the treatment of a variety of solid tumours. "( Methylene blue in the treatment and prevention of ifosfamide-induced encephalopathy: report of 12 cases and a review of the literature.
De Vos, F; Pelgrims, J; Prové, A; Schrijvers, D; Van den Brande, J; Vermorken, JB, 2000
)
2
"Ifosfamide is an alkylating antineoplastic agent with documented activity against a variety of solid tumor types, most notably lung cancer, testicular cancer, and sarcoma. "( Ifosfamide-based drug combinations: preclinical evaluation of drug interactions and translation into the clinic.
Harstrick, A; Klaassen, U; Schleucher, N; Seeber, S; Vanhoefer, U, 2000
)
3.19
"Ifosfamide is an active drug for various tumors with elevated incidence in the elderly."( Ifosfamide in the elderly: clinical considerations for a better drug management.
Catania, C; Comandone, A; Curigliano, G; de Braud, F; De Pas, T, 2000
)
2.47
"Ifosfamide is an alkylating agent with proven efficacy in the treatment of solid tumours and malignant lymphomas. "( The role of ifosfamide in the treatment of relapsed and refractory lymphoma.
Bredenfeld, H; Diehl, V; Engert, A; Reiser, M, 2001
)
2.13
"Ifosfamide is an active drug in advanced breast cancer. "( Fourteen-day infusion of ifosfamide in the management of advanced breast cancer refractory to protracted continuous infusion of 5-fluorouracil.
Crivellari, D; Lauro, VD; Lombardi, D; Magri, MD; Paolello, C; Scuderi, C; Spazzapan, S; Veronesi, A,
)
1.88
"Ifosfamide (IF) is an alkylating cytostatic derived from nitrogen mustard. "( Inhibition of sodium-dependent transport systems in LLC-PK1 cells by metabolites of ifosfamide.
Brandis, M; Mohrmann, M; Pauli, A; Ritzer, M; Schönfeld, B; Seifert, B,
)
1.8
"Ifosfamide is a chemotherapeutic agent used for treatment of pediatric solid tumors."( Rickets--a complication of ifosfamide chemotherapy for Wilms tumor.
Boal, DK; Relf, M, 1992
)
1.3
"Ifosfamide is an effective drug for the treatment of solid tumors in children and most blastomas and sarcomas react favorably. "( Ifosfamide in pediatric oncology.
de Kraker, J; Voûte, PA, 1992
)
3.17
"Ifosfamide is an alkylating agent that has clearly demonstrated efficacy against advanced breast cancer. "( Activity of ifosfamide in breast cancer.
Hortobagyi, GN, 1992
)
2.11
"Ifosfamide is a newly available analog of cyclophosphamide in the oxazaphosphorine drug class. "( Ifosfamide vs cyclophosphamide in cancer therapy.
Weiss, RB, 1991
)
3.17
"Ifosfamide is an oxazaphosphorine alkylating agent with a broad spectrum of antineoplastic activity. "( Ifosfamide/mesna. A review of its antineoplastic activity, pharmacokinetic properties and therapeutic efficacy in cancer.
Brogden, RN; Dechant, KL; Faulds, D; Pilkington, T, 1991
)
3.17
"Ifosfamide is an active chemotherapeutic agent in a wide range of gynecologic tumors; favorable response rates have been reported in ovarian (epithelial and germ cell), uterine, and cervical neoplasms. "( Ifosfamide-induced neurotoxicity.
Curtin, JP; Gutierrez, M; Koonings, PP; Morrow, CP; Schlaerth, JB, 1991
)
3.17
"Ifosfamide is an analogue of cyclophosphamide that has been extensively investigated in sarcomas. "( The role of ifosfamide in the treatment of adult soft tissue sarcomas, Ewing's sarcoma, and osteosarcoma: a review.
Dirix, LY; Van Oosterom, AT, 1990
)
2.1
"Ifosfamide is a known nephrotoxic drug with demonstrated tubulopathies."( Lethal anuria complicating high dose ifosfamide chemotherapy in a breast cancer patient with an impaired renal function.
Paridaens, R; Piccart, M; Richard, V; Sculier, JP, 1990
)
1.27
"Ifosfamide is an important alkylating agent that should be combined with other agents in phase II and III trials."( Ifosfamide in pediatric malignant solid tumors.
Douglass, EC; Etcubanas, EL; Goren, MP; Green, AA; Hayes, FA; Horowitz, ME; Meyer, WH; Pratt, CB; Thompson, EI; Wilimas, JA, 1989
)
2.44
"Ifosfamide (IFS) is a new alkylating oxazaphosphorine related to cyclophosphamide. "( Ifosfamide cardiotoxicity in humans.
Efremidis, AP; Kandylis, K; Tsoussis, S; Vassilomanolakis, M, 1989
)
3.16

Effects

Ifosfamide (Holoxan) has an effect as a single drug on testicular carcinoma. Shows synergism with cisplatinum in mice. Has a similar spectrum of antitumor activity but has different pharmacokinetics.

Ifosfamide has been found to have antineoplastic activity in a variety of solid tumors. It has been associated with proximal renal tubular dysfunction resembling Fanconi-like syndrome and leading to rickets in young children.

ExcerptReferenceRelevance
"Ifosfamide (Holoxan) has an effect as a single drug on testicular carcinoma and shows synergism with cisplatinum in mice. "( The value of ifosfamide in the polychemotherapy of metastasized testicular cancer pretreated with chemotherapy.
Clemm, C; Hartenstein, R; Wilmanns, W, 1982
)
2.08
"Ifosfamide has a similar spectrum of antitumor activity but has different pharmacokinetics that could provide advantages in efficacy."( Ifosfamide vs cyclophosphamide in cancer therapy.
Weiss, RB, 1991
)
2.45
"Ifosfamide plus mesna have been used recently in a high-dose regimen that allows this chemotherapy to be given to outpatients with less toxicity over 14 days using a portable pump. "( Physical and chemical stability of high-dose ifosfamide and mesna for prolonged 14-day continuous infusion.
Anderson, PM; Culotta, KS; Kawedia, JD; Kramer, MA; McIntyre, CM; Myers, AL; Zhang, Y, 2014
)
2.1
"Ifosfamide has been used in neoadjuvant chemotherapy since the mid-1980s. "( Clinical efficacy of preoperative chemotherapy with or without ifosfamide in patients with osteosarcoma of the extremity: meta-analysis of randomized controlled trials.
Lai, Z; Lin, Y; Mo, Y; Su, W; Wu, F; Wu, J; Yang, Z, 2015
)
2.1
"Ifosfamide rechallenge has clinical activity in soft-tissue sarcoma and can be considered a viable option in treating metastatic disease."( Successful Ifosfamide Rechallenge in Soft-Tissue Sarcoma.
Benson, C; Constantinidou, A; Jones, RL; Judson, I; Messiou, C; Miah, A; Noujaim, J; Thway, K, 2018
)
2.31
"Ifosfamide has been shown to be associated with encephalopathy in 10-40% of patients. "( Severe post-treatment leukopenia associated with the development of encephalopathy following ifosfamide infusion.
Isola, LM; Kim, SS; Oh, WK, 2016
)
2.1
"Ifosfamide has been approved by the FDA while evofosfamide is currently in the late stage of clinical development."( Comparison of hypoxia-activated prodrug evofosfamide (TH-302) and ifosfamide in preclinical non-small cell lung cancer models.
Ahluwalia, D; Ferraro, DJ; Hart, CP; Jung, D; Liu, Q; Matteucci, MD; Sun, JD; Wang, Y, 2016
)
1.39
"Ifosfamide has shown significant activity as a single agent in head and neck squamous carcinoma."( Neoadjuvant chemotherapy with ifosfamide and cisplatin combination in advanced head and neck cancer: a retrospective analysis of 519 patients: a single institution experience.
Bakshi, AV; Deshmukh, CD; Mazumdar, AT; Mistry, RC; Pai, VR; Parikh, DM; Parikh, PM; Pathak, KA, 2003
)
1.33
"Ifosfamide (IFO) has demonstrated activity in recurrent/metastatic squamous cell head and neck carcinoma with an overall response rate of 24-26%. "( Ifosfamide in the treatment of head and neck cancer.
Airoldi, M; Bumma, C; Cortesina, G; Giordano, C; Pedani, F, 2003
)
3.2
"Ifosfamide has been studied as a single agent or in combination with other drugs in different studies."( Role of ifosfamide in cervical cancer: an overview.
Buda, A; Dell'Anna, T; Mangioni, C; Signorelli, M, 2003
)
1.47
"Ifosfamide has definite activity in nephroblastoma, where it represents the treatment of choice for children who are not cured by front-line chemotherapy, and for the adults who are diagnosed with this uncommon disease."( Ifosfamide in urologic cancer.
Boccardo, F; Guglielmini, P, 2003
)
2.48
"Ifosfamide has always had significant single-agent activity in patients with germ cell tumors. "( Ifosfamide in germ cell tumors.
Einhorn, LH, 2003
)
3.2
"Ifosfamide has been mainly used, in combination with other drugs, as a component of salvage regimens for relapsed or primarily refractory lymphoma."( Ifosfamide in hematological malignancies of adults.
Elice, F; Rodeghiero, F, 2003
)
2.48
"Ifosfamide (I) has also been approved for NSCLC treatment."( Phase I study with dose escalation of gemcitabine and cisplatin in combination with ifosfamide (GIP) in patients with non-small-cell lung carcinoma.
Billiart, I; Bourgeois, H; Chabrun, V; Chieze, S; Daban, A; Ferrand, V; Germain, T; Lemerre, D; Meurice, JC; Tourani, JM, 2004
)
1.27
"Ifosfamide has been renewed after the neurological accident in 7 of those patients."( [Ifosfamide induced encephalopathy: 15 observations].
Behar, C; Dufour, C; Grill, J; Hartmann, O; Motte, J; Munzer, M; Oberlin, O; Paci, A; Sabouraud, P, 2006
)
1.97
"Ifosfamide has antitumor activity against VAS in cats and is tolerated well by most cats. "( Results of a phase II clinical trial on the use of ifosfamide for treatment of cats with vaccine-associated sarcomas.
Chaffin, K; Khanna, C; Kristal, O; Page, RL; Rassnick, KM; Rodriguez, CO; Rosenberg, MP, 2006
)
2.03
"Ifosfamide (Holoxan) has an effect as a single drug on testicular carcinoma and shows synergism with cisplatinum in mice. "( The value of ifosfamide in the polychemotherapy of metastasized testicular cancer pretreated with chemotherapy.
Clemm, C; Hartenstein, R; Wilmanns, W, 1982
)
2.08
"Ifosfamide has been found to have antineoplastic activity in a variety of solid tumors. "( The role of ifosfamide in germ cell tumors and small cell lung cancer.
Nichols, CR, 1995
)
2.11
"Ifosfamide has single agent activity in advanced breast cancer and may potentiate the activity of doxorubicin. "( Results of chemotherapy using ifosfamide with doxorubicin in advanced breast cancer.
Cantwell, B; Gumbrell, L; Lennard, T; Lind, M; Millward, M; Robinson, A, 1994
)
2.02
"Ifosfamide has antitumor activity in previously treated ovarian epithelial tumors, squamous carcinomas of the cervix, trophoblastic disease, and untreated uterine sarcomas in Gynecologic Oncology Group (GOG) trials. "( Phase II study of ifosfamide and mesna in refractory adenocarcinoma of the endometrium. A Gynecologic Oncology Group study.
Adcock, L; Blessing, JA; Homesley, HD; McGuire, WP; Sutton, GP, 1994
)
2.07
"Ifosfamide has to be metabolized prior to expressing its cytotoxicity."( The analysis of ifosfamide and its metabolites (review).
Beijnen, JH; Bult, A; Kaijser, GP; Korst, A; Underberg, WJ,
)
1.2
"Ifosfamide has previously been shown to be active as a single agent and in combination with doxorubicin, etoposide, and teniposide in pediatric solid tumors and adult acute leukemia. "( Ifosfamide with mesna uroprotection and etoposide in recurrent, refractory acute leukemia in childhood. A Pediatric Oncology Group Study.
Bell, B; Bernstein, ML; Buchanan, GR; Devine, S; Dreyer, Z; Grier, H; Krischer, J; Kung, F; Land, V; Whitehead, VM, 1993
)
3.17
"Ifosfamide has demonstrated clinically useful antitumor activity in our hands against most sarcoma subtypes."( Single-agent ifosfamide studies in sarcomas of soft tissue and bone: the M.D. Anderson experience.
Benjamin, RS; Legha, SS; Nicaise, C; Patel, SR, 1993
)
1.38
"Ifosfamide has been associated with proximal renal tubular dysfunction resembling Fanconi-like syndrome and leading to rickets in young children. "( A prospective evaluation of ifosfamide-related nephrotoxicity in children and young adults.
Balis, FM; Blaney, S; Ho, PT; Izraeli, S; Jarosinski, P; Weaver-McClure, L; Wexler, LH; Zimmerman, K, 1995
)
2.03
"Ifosfamide has been used extensively for the treatment of patients with non-Hodgkin's lymphoma (NHL). "( Ifosfamide in the treatment of non-Hodgkin's lymphoma.
Pohlman, B, 1996
)
3.18
"Ifosfamide has been assessed in the treatment of ovarian cancer for more than two decades. "( Ifosfamide in the treatment of ovarian cancer.
Markman, M, 1996
)
3.18
"Ifosfamide has single-agent activity comparable to etoposide in very poor-prognosis, cisplatin-refractory disease."( Ifosfamide in the treatment of germ cell tumors.
Nichols, CR, 1996
)
2.46
"Ifosfamide has been used in combination with many different agents, including cisplatin and etoposide and newer drugs like vinorelbine and paclitaxel."( Ifosfamide in non-small cell lung cancer.
Johnson, DH, 1996
)
2.46
"Ifosfamide has therefore been identified as one of six new active agents in urothelial cancer, and trials of combination regimens including ifosfamide are under way."( The role of ifosfamide in the treatment of testicular and urothelial malignancies.
Roth, BJ, 1996
)
1.39
"Ifosfamide has found an established place in the treatment of these pediatric malignancies."( Ifosfamide in the treatment of pediatric malignancies.
Behrendt, H; de Kraker, J; Michiels, E; van den Berg, H; Voûte, PA, 1996
)
2.46
"Ifosfamide has shown activity in the treatment of patients who previously demonstrated clinical resistance to a platinum-cyclophosphamide combination."( Paclitaxel plus ifosfamide in advanced ovarian cancer: a multicenter phase II study.
Addamo, G; Amoroso, D; Boccardo, F; Brema, F; Bruzzone, M; Catsafados, E; Foglia, G; Granetto, C; Guarneri, D; Mammoliti, S; Martini, MC; Miglietta, L; Moraglio, L; Pastorino, G; Pedulla, F; Ragni, N,
)
1.2
"Ifosfamide has important activity in pretreated soft tissue sarcomas (STS), and recent data support a clinically significant dose-response relationship for this agent. "( Phase II study of continuous-infusion high-dose ifosfamide in advanced and/or metastatic pretreated soft tissue sarcomas.
Antimi, M; Gatti, C; Palmeri, S; Palumbo, R; Raffo, P; Toma, S; Villani, G, 1997
)
2
"Ifosfamide has been in use for several decades and is generally considered to be one of the most effective drugs for the treatment of non-small cell lung cancer (NSCLC). "( Ifosfamide and docetaxel in non-small cell lung cancer.
Büchholz, E; Drings, P; Manegold, C, 1998
)
3.19
"Ifosfamide has been combined with gemcitabine in a phase I/II study."( Combination studies with gemcitabine in the treatment of non-small-cell lung cancer.
Steward, WP, 1998
)
1.02
"Ifosfamide has been shown to possess modest activity in patients with platinum/cyclophosphamide refractory ovarian cancer. "( Phase 2 trial of single agent ifosfamide/mesna in patients with platinum/paclitaxel refractory ovarian cancer who have not previously been treated with an alkylating agent.
Belinson, J; Hurteau, J; Kennedy, A; Kulp, B; Markman, M; Peterson, G; Sutton, G; Webster, K, 1998
)
2.03
"Ifosfamide has no specific value in these approved indications."( Ifosfamide: new idications-new dose strength. Limited evidence of effectiveness.
, 1998
)
2.36
"Ifosfamide has been used in combination with several drugs including cisplatin, giving rise to multiple doublets and triplets including the ifosfamide-cisplatin-mitomycin regimen (Cullen's MIC regimen) that has been commonly used in Europe. "( Ifosfamide in non-small-cell lung cancer.
Balaña, C; Martin, C; Rosell, R, 1999
)
3.19
"Ifosfamide has been included in various drug combination protocols, usually on an empirical basis."( Ifosfamide-based drug combinations: preclinical evaluation of drug interactions and translation into the clinic.
Harstrick, A; Klaassen, U; Schleucher, N; Seeber, S; Vanhoefer, U, 2000
)
2.47
"Ifosfamide has been mainly used in therapy of lymphoma as a component of salvage regimens, but high-dose ifosfamide is also effective in the mobilization of peripheral stem cells for treatment of patients with relapsed or refractory lymphoma with regimens containing autologous stem cell transplantation."( The role of ifosfamide in the treatment of relapsed and refractory lymphoma.
Bredenfeld, H; Diehl, V; Engert, A; Reiser, M, 2001
)
1.41
"Ifosfamide has been in use as an effective antineoplastic agent for solid tumors in both children and adults since the late 1960s. "( Young age and the risk for ifosfamide-induced nephrotoxicity: a critical review of two opposing studies.
Aleksa, K; Koren, G; Woodland, C, 2001
)
2.05
"Ifosfamide has activity in refractory choriocarcinoma and, when combined with etoposide and cisplatin (VIP), may be curative."( Ifosfamide alone and in combination in the treatment of refractory malignant gestational trophoblastic disease.
Barnhill, DR; Blessing, JA; Hatch, KD; Soper, JT; Sutton, GP, 1992
)
3.17
"Ifosfamide has the broad range of clinical activity, but its ultimate role as part of initial therapy remains to be discerned."( Clinical trials with ifosfamide: the Indiana University experience.
Einhorn, LH; Loehrer, PJ; Nichols, CR; Williams, SD, 1992
)
1.32
"Ifosfamide has shown promising single-agent activity in non-small cell lung cancer (NSCLC). "( Phase II study of cisplatin, ifosfamide with mesna, and etoposide (PIE) chemotherapy for advanced non-small cell lung cancer.
Dhingra, HH; Greenberg, J; Hong, WK; Lee, JS; Shirinian, M, 1992
)
2.02
"Ifosfamide has shown promising single-agent activity in non-small cell lung cancer. "( Phase II study of cisplatin, ifosfamide, and etoposide combination for advanced non-small cell lung cancer: final report.
Dhingra, HH; Greenberg, J; Hong, WK; Lee, JS; Shirinian, M, 1992
)
2.02
"Ifosfamide/mesna has modest activity in malignant mesothelioma. "( A phase II evaluation of ifosfamide and mesna in unresectable diffuse malignant mesothelioma. A Southwest Oncology Group study.
Balcerzak, SP; Berenberg, JL; Keppen, MD; Metch, B; Militello, L; Pierce, HI; Zidar, BL, 1992
)
2.03
"Ifosfamide has documented activity in sarcoma patients who have failed treatment with doxorubicin-containing regimens."( Chemotherapy of advanced sarcomas of bone and soft tissue.
Antman, KH, 1992
)
1
"Ifosfamide has been shown to have a broad spectrum of clinical activity in various cancers."( The history of ifosfamide.
Loehrer, PJ, 1992
)
1.36
"Ifosfamide has been shown to have significant single-agent activity against non-Hodgkin's lymphoma and its use in various combinations produces response rates of 20% to 83% in patients with refractory or relapsing disease."( New perspectives in the treatment of non-Hodgkin's lymphoma.
Goss, PE, 1992
)
1
"Ifosfamide has also been used in combination regimens."( Activity of ifosfamide in breast cancer.
Hortobagyi, GN, 1992
)
1.38
"Ifosfamide has a similar spectrum of antitumor activity but has different pharmacokinetics that could provide advantages in efficacy."( Ifosfamide vs cyclophosphamide in cancer therapy.
Weiss, RB, 1991
)
2.45
"Ifosfamide has limited activity in adenocarcinoma of the oesophageal-gastric junction area."( Ifosfamide in advanced adenocarcinoma of the oesophagus or oesophageal-gastric junction area. Rotterdam Esophageal Tumor Study Group.
Kok, TC; Splinter, TA; Tilanus, HW; van der Gaast, A, 1991
)
2.45
"Ifosfamide has broad cytotoxicity against solid tumors and may prove to be an important addition to high-dose combination chemotherapy regimens."( High-dose ifosfamide with mesna uroprotection: a phase I study.
Antman, KH; Begg, CB; Eder, JP; Elias, AD; Frei, E; Shea, T, 1990
)
1.4
"Ifosfamide/mesna has activity in a wide range of gynecologic malignancies."( Early phase II Gynecologic Oncology Group experience with ifosfamide/mesna in gynecologic malignancies.
Berman, ML; Blessing, JA; Homesley, HD; Photopulos, G; Sutton, GP, 1990
)
1.24
"Ifosfamide has demonstrated significant activity as salvage therapy in patients with testicular tumors refractory to cisplatin-containing induction chemotherapy regimens. "( Ifosfamide in testicular cancer.
Loehrer, PJ, 1990
)
3.16
"Ifosfamide/mesna has activity in a wide range of gynecologic malignancies."( Gynecologic Oncology Group experience with ifosfamide.
Berman, ML; Blessing, JA; Homesley, HD; Photopulos, G; Sutton, GP, 1990
)
1.26
"Ifosfamide (IFX) has activity in a number of gynaecological malignancies and was selected for evaluation in this disease."( A phase II study of ifosfamide in endometrial cancer.
Barton, C; Blackledge, G; Buxton, EJ; Meanwell, CA; Mould, JJ, 1990
)
1.32
"Ifosfamide has definite efficacy in many malignant tumours, including breast cancer. "( Ifosfamide, methotrexate, and 5-fluorouracil: effective combination in resistant breast cancer.
el-Khodari, A; Elserafi, M; Gad-el-Mawla, N; Gafaar, R; Hamza, MR; Khaled, H; Zikri, ZK, 1990
)
3.16
"Ifosfamide has been shown to be an active agent in the treatment of several childhood cancers. "( Toxicity of high-dose ifosfamide in children.
Craft, AW; Davies, SM; Pearson, AD, 1989
)
2.03
"Ifosfamide/mesna has activity in a wide range of gynecologic malignancies."( Phase II experience with ifosfamide/mesna in gynecologic malignancies: preliminary report of Gynecologic Oncology Group studies.
Berman, ML; Blessing, JA; Homesley, HD; Photopulos, G; Sutton, GP, 1989
)
1.3
"Ifosfamide has activity in a variety of disseminated refractory solid tumors that do not traditionally respond to conventional alkylating agent therapy, specifically refractory germ cell tumors, soft tissue sarcomas, and malignant lymphomas."( Ifosfamide: a clinical review.
Einhorn, LH; Higgs, D; Nagy, C, 1989
)
2.44
"Ifosfamide has minimal activity in esophageal cancer and causes severe myelosuppression."( Phase II trial of ifosfamide in epidermoid carcinoma of the esophagus: unexpectant severe toxicity.
Eisenberger, M; Kelsen, DP; Lipperman, R; Nanus, DM, 1988
)
1.33
"Ifosfamide has definite activity against pancreatic adenocarcinoma."( Ifosfamide: an active drug in the treatment of adenocarcinoma of the pancreas.
Ansari, R; Einhorn, LH; Loehrer, PJ; Williams, SD, 1985
)
2.43

Actions

Ifosfamide and cisplatin cause urinary loss of carnitine, which is a fundamental molecule for energy production in mammalian cells.

ExcerptReferenceRelevance
"Ifosfamide can cause end-stage renal disease by a tubulotoxic effect that may be the result of a selective intracellular uptake into the proximal tubule via the human organic cation transporter 2 (OCT2)."( [End-stage renal disease after sarcoma therapy - case 3/2014].
Amann, K; Artunc, F; Bakos, G; Baumann, D; Bunz, H; Ciarimboli, G; Kluba, T; Kopp, HG; Müller, M; Schlatter, E; Steinke, I; Weyrich, P, 2014
)
1.85
"Ifosfamide and cisplatin cause urinary loss of carnitine, which is a fundamental molecule for energy production in mammalian cells. "( Potential role of levocarnitine supplementation for the treatment of chemotherapy-induced fatigue in non-anaemic cancer patients.
Baldelli, AM; Bisonni, R; Canestrari, F; Catalano, V; De Gaetano, A; Ferraro, B; Giordani, P; Graziano, F; Lai, V; Mencarini, E; Rovidati, S; Silva, R; Testa, E, 2002
)
1.76

Treatment

Ifosfamide used in the treatment of pediatric solid tumors is known to have serious adverse effects, including acute pancreatitis, a rare complication of therapy. Treatment might be a feasible approach, but it necessitates hospitalization.

ExcerptReferenceRelevance
"Ifosfamide treatment upregulated a range of proinflammatory genes."( IPSE, a urogenital parasite-derived immunomodulatory protein, ameliorates ifosfamide-induced hemorrhagic cystitis through downregulation of pro-inflammatory pathways.
Alouffi, A; Banskota, N; Falcone, FH; Hsieh, MH; Ishida, K; Jardetzky, TS; Le, L; Mbanefo, EC; Odegaard, JI; Pennington, LF; Zee, R, 2019
)
1.47
"Ifosfamide treatment increased apoptosis and caused hypoplasia of placental basal and labyrinth zones, which resulted in pathological changes in developing fetal tissue."( Prenatal effects of transplacental exposure to ifosfamide in rats.
Helal, M, 2016
)
1.41
"Ifosfamide used in the treatment of pediatric solid tumors is known to have serious adverse effects, including acute pancreatitis, a rare complication of therapy. "( Acute pancreatitis induced by ifosfamide therapy.
Agarwala, S; Bhatnagar, V; Garg, R, 2010
)
2.09
"Ifosfamide treatment significantly inhibited oxidative phosphorylation with only C-I substrates."( Ifosfamide-induced nephrotoxicity: mechanism and prevention.
Daikhin, Y; Horyn, O; Luhovyy, B; Nissim, I; Phillips, PC; Yudkoff, M, 2006
)
2.5
"Ifosfamide-treated rats had significantly lower body weight and hematocrit than sterile water-treated control rats."( Nephrotoxicity of ifosfamide in rats.
Springate, JE; Van Liew, JB,
)
1.19
"The ifosfamide treatment schedules had only minimal effects on bromisoval pharmacokinetics."( Effect of ifosfamide treatment on glutathione and glutathione conjugation activity in patients with advanced cancers.
Breimer, DD; Mulder, GJ; Mulders, TM; Ouwerkerk, J; van der Velde, EA, 1995
)
1.17
"Ifosfamide treatment might be a feasible approach, but it necessitates hospitalization. "( Chemotherapy in the treatment of recurrent glioblastoma multiforme: ifosfamide versus temozolomide.
Bamberg, M; Becker, G; Belka, C; Classen, J; Hoffmann, W; Kortmann, RD; Paulsen, F; Weinmann, M, 1999
)
1.98
"Ifosfamide/mesna treatment of 50 patients with pediatric malignant solid tumors was associated with the development of neurotoxic signs and symptoms in 11 of these individuals who received 29 courses of treatment. "( Central nervous system toxicity following the treatment of pediatric patients with ifosfamide/mesna.
Douglass, E; Etcubanas, E; Green, AA; Hayes, FA; Horowitz, ME; Igarashi, M; Meyer, WH; Pratt, CB; Thompson, E; Wilimas, J, 1986
)
1.94
"Treatment with ifosfamide chemotherapy and palliative radiation therapy was effective in reducing the growth of the tumor in the pulmonary artery and pleural lesions, indicating that this regimen may be useful for the treatment of unresectable SS in the pulmonary artery."( Intravascular synovial sarcoma of the pulmonary artery with massive pleural effusion: report of a case with a favorable response to Ifosfamide chemotherapy and palliative radiation therapy.
Atagi, S; Kawaguchi, T; Maekura, T; Matsui, H; Morimoto, M; Okuma, T; Shimizu, S, 2015
)
0.96
"treatment with ifosfamide alone or ifosfamide combined with microencapsulated CYP2B1-expressing cells."( Peritoneal cancer treatment with CYP2B1 transfected, microencapsulated cells and ifosfamide.
Hafner, M; Jesnowski, R; Keese, M; Löhr, M; Lux, A; Post, S; Prosst, R; Saller, R; Samel, S; Sturm, J, 2006
)
0.9
"treatment with ifosfamide alone or ifosfamide combined with microencapsulated CYP2B1 expressing cells."( Targeted intraabdominal chemotherapy for peritoneal carcinomatosis.
Löhr, M; Samel, S, 2007
)
0.68
"Treatment with Ifosfamide (250 mg/kg b.w.) reduced intratumoral laser Doppler flow, oxygenation and pH."( The effect of ifosfamide on tumor oxygenation at different temperatures.
Mendoza, AS; Mentzel, M; Wiedemann, G, 1994
)
0.99
"Oral treatment with ifosfamide results in dose-limiting encephalopathy. "( Comparative pharmacokinetics of oral and intravenous ifosfamide/mesna/methylene blue therapy.
Aeschlimann, C; Cerny, T; Küpfer, A; Schefer, H, 1998
)
0.87
"Treatment with ifosfamide or combination chemotherapy with vincristine, ifosfamide and peplomycin was performed in some of the 65 cases above mentioned."( [Reactivation of prostatic cancer and chemotherapy in reactivated prostatic cancer].
Ando, K; Fuse, H; Hara, S; Shimazaki, J; Zama, S, 1985
)
0.61

Toxicity

Renal proximal tubule cell injury is an important side effect of the chemotherapeutic agent ifosfamide in humans. Sequential dose intense ifosFamide, etoposide, carboplatin +/- rituximab was more toxic and no more effective than the same drugs given in a conventional fashi.

ExcerptReferenceRelevance
" The major dose-limiting toxic effect of CIA was leukopenia."( Protection against chemotherapy toxicity by IV hyperalimentation.
Bodey, GP; Copeland, EW; Dudrick, SJ; Freireich, EJ; Issell, BF; Valdivieso, M; Zaren, HA, 1978
)
0.26
"Cyclophosphamide (CP) is selectively toxic to avian and mammalian B lymphocytes, but the mechanisms of action are incompletely understood."( Cytogenetic mechanisms in the selective toxicity of cyclophosphamide analogs and metabolites towards avian embryonic B lymphocytes in vivo.
Bloom, SE; Colvin, OM; Wilmer, JL, 1992
)
0.28
"Nephrotoxicity is an important adverse effect of chemotherapy in children."( The influence of age on nephrotoxicity following chemotherapy in children.
Coulthard, MG; Craft, AW; Pearson, AD; Price, L; Skinner, R, 1992
)
0.28
" Thus, neither DSF nor DDTC impaired the antitumour effect of IFX and both diminished its adverse effects."( Drug interaction effects on antitumour drugs (VIII): prevention of ifosfamide-induced urotoxicity by disulfiram and its effect on antitumour activity and acute toxicity of alkylating agents in mice.
Ishikawa, M; Sasaki, K; Takayanagi, Y, 1991
)
0.52
"Renal dysfunction and urinary disorders are the most troublesome adverse reaction to anticancer agents such as cisplatin (CDDP) and ifosfamide (IFM)."( [New treatments for urogenital toxicity of anti-neoplastic chemotherapy].
Hirosawa, A; Niitani, H; Shibuya, M, 1990
)
0.48
" Myelosuppression occurred in all patients but was mild and reversible, with no toxic deaths."( Toxicity of high-dose ifosfamide in children.
Craft, AW; Davies, SM; Pearson, AD, 1989
)
0.59
" This selective 5HT3 antagonist is effective and safe in the control of ifosfamide-induced emesis, even in patients resistant to high-dose metoclopramide."( The efficacy and safety of GR38032F in the prophylaxis of ifosfamide-induced nausea and vomiting.
Challoner, T; Green, JA; Griggs, J; Hammond, P; Watkin, SW, 1989
)
0.75
" We observed this acute toxic effect despite the administration of sufficient mesna to prevent hemorrhagic cystitis."( Ifosfamide-induced subclinical tubular nephrotoxicity despite mesna.
Goren, MP; Horowitz, ME; Pratt, CB; Wright, RK, 1987
)
1.72
" Dose-dependent metabolism of methotrexate is unusual in that formation of the presumed toxic metabolite increases with increase in dose and is associated with a qualitative change in the pattern of drug toxicity at high compared to low doses of drug."( Dose-dependent metabolism, therapeutic effect, and toxicity of anticancer drugs in man.
Powis, G, 1983
)
0.27
" 4-OH-IF and 4-OH-CP were significantly more toxic than the parent drugs."( Toxicity of ifosfamide, cyclophosphamide and their metabolites in renal tubular cells in culture.
Ansorge, S; Brandis, M; Mohrmann, M; Schmich, U; Schönfeld, B, 1994
)
0.67
"Nephrotoxicity is a relatively common and potentially serious adverse effect of treatment with certain cytotoxic drugs (especially ifosfamide)."( Strategies to prevent nephrotoxicity of anticancer drugs.
Skinner, R, 1995
)
0.5
"2 g/m2 had a toxic death."( Cyclophosphamide dose escalation in combination with vincristine and actinomycin-D (VAC) in gross residual sarcoma. A pilot study without hematopoietic growth factor support evaluating toxicity and response.
Gehan, E; Maurer, H; Newton, WA; Ruymann, FB; Vietti, T; Wharam, M; Wiener, E, 1995
)
0.29
" No increase in the toxic side effects of IFX was demonstrated when administered with L-MTP-PE nor were delays in IFX administration due to neutropenia experienced."( Combination therapy with ifosfamide and liposome-encapsulated muramyl tripeptide: tolerability, toxicity, and immune stimulation.
Gano, JB; Jaffe, N; Jia, SF; Kleinerman, ES; Meyers, PA; Raymond, AK, 1995
)
0.59
" In the presence of known cardiovascular risk factors, the choice of a less toxic regimen is desirable and, if this is not possible, the patient should be treated with continuous monitoring of the vital parameters."( [Cardiovascular toxicity of anticancer chemotherapy: 5 cases treated in intensive care].
Sculier, JP; Sotiriou, C,
)
0.13
"Hallucinations as a symptom of central neurotoxicity are a known but poorly described side effect of ifosfamide."( Hallucinations and ifosfamide-induced neurotoxicity.
Baile, WF; Brown, R; DiMaggio, JR; Schapira, D, 1994
)
0.83
" The toxic effect appeared to be greatest in younger children and at least partly dose-dependent, although partially reversible after each course of chemotherapy."( The assessment of subclinical ifosfamide-induced renal tubular toxicity using urinary excretion of retinol-binding protein.
al Sheyyab, M; Beetham, R; Stevens, M; Worthington, D,
)
0.42
" However on multivariate analysis only the presence of bulky disease and of B symptoms were independent adverse factors for response and for survival."( EPIC: an effective low toxicity regimen for relapsing lymphoma.
Ashley, S; Catovsky, D; Cunningham, D; Gore, ME; Hickish, T; Mansi, J; Nicolson, V; Roldan, A; Smith, IE, 1993
)
0.29
" The overall incidence of adverse experiences was significantly lower in the granisetron group (60."( The antiemetic efficacy and safety of granisetron compared with metoclopramide plus dexamethasone in patients receiving fractionated chemotherapy over 5 days. The Granisetron Study Group.
, 1993
)
0.29
"With the increasing use of ifosfamide in pediatric malignancies, nephrotoxicity has emerged as a potentially serious adverse effect, which may be dose-limiting or may cause severe chronic morbidity, including glomerular impairment and/or Fanconi's syndrome."( Ifosfamide, mesna, and nephrotoxicity in children.
Craft, AW; Pearson, AD; Sharkey, IM; Skinner, R, 1993
)
2.03
" Although mesna may be capable of detoxifying the toxic metabolite(s), delivery to the renal tubule may not be sufficient to provide adequate protection of tubular glutathione from depletion by the metabolite(s), which results in a failure to prevent nephrotoxicity."( Ifosfamide, mesna, and nephrotoxicity in children.
Craft, AW; Pearson, AD; Sharkey, IM; Skinner, R, 1993
)
1.73
"A total of 64 courses of ifosfamide (IFM) treatments for sarcoma patients were evaluated for toxic effects."( [Toxic effects of ifosfamide in the treatment of bone and soft tissue sarcomas].
Ishii, T; Kitoh, M; Satoh, T; Tatezaki, S; Umeda, T, 1993
)
0.92
"Renal proximal tubule cell injury is an important side effect of the chemotherapeutic agent ifosfamide in humans."( Nephrotoxicity of ifosfamide in rats.
Springate, JE; Van Liew, JB,
)
0.69
" MIP regimen was permanently suspended in 14 patients because of toxic events."( Efficacy and toxicity of mitomycin, ifosfamide, and cisplatin (MIP) in patients with inoperable non-small cell lung cancer.
Baud, M; Bedin, A; Chouaid, C; Febvre, M; Lebeau, B; Urban, T, 1996
)
0.57
" Ifosfamide, although itself the effective antineoplastic drug useful in situations which have proved refractory to cyclophosphamide therapy, has the side-effect toxicities caused by its metabolities that pose clinically a very real problem."( Influence of mesna on urotoxic effects of selected bromosubstituted analogs of ifosfamide.
Konarski, L; Kowalski, P; Kuśnierczyk, H; Radzikowski, C, 1997
)
1.43
", this toxic effect is not accompanied by an increase in intramyocardial citrate levels."( A 13C NMR study of 2-(13)C-chloroacetaldehyde, a metabolite of ifosfamide and cyclophosphamide, in the isolated perfused rabbit heart model. Initial observations on its cardiotoxicity and cardiac metabolism.
Loqueviel, C; Malet-Martino, M; Martino, R, 1997
)
0.54
" Adverse effects on oral mucosa have been documented for several cytotoxic treatment regimens."( Oral mucosal side effects of cytotoxic chemotherapy of testicular cancer. A retrospective study.
Fosså, SD; Herlofson, BB; Norman-Pedersen, K; Redfors, M, 1997
)
0.3
" Its main adverse effects are various forms of renal tubular and glomerular damage."( Ifosfamide-induced nephrotoxicity in children: critical review of predictive risk factors.
Koren, G; Loebstein, R, 1998
)
1.74
" So we compared VAC protocol and ifosfamiide for toxic effects."( Toxicity of chemotherapeutical protocols in the treatment of uterine sarcomas (Vincristine, actinomycin D, Cyclophosphamide VAC versus ifosfamide).
Erman, O; Simşek, T; Trak, B; Uner, M; Zorlu, GC, 1998
)
0.5
"VAC protocol is more toxic for the liver, hematopoietic and peripheral neurologic system."( Toxicity of chemotherapeutical protocols in the treatment of uterine sarcomas (Vincristine, actinomycin D, Cyclophosphamide VAC versus ifosfamide).
Erman, O; Simşek, T; Trak, B; Uner, M; Zorlu, GC, 1998
)
0.5
" Its main adverse effects are various forms of renal tubular and glomerular damage."( Risk factors for long-term outcome of ifosfamide-induced nephrotoxicity in children.
Atanackovic, G; Baruchel, S; Bishai, R; Gobrial, M; Hashemi, G; Ito, S; Khattak, S; Koren, G; Loebstein, R; Wolpin, J, 1999
)
0.57
" Upon administration of ifosfamide, the P450 enzyme converts the ifosfamide into antitumorigenic toxic metabolites at the site required, thereby significantly reducing tumor burden."( Characterization of a human cell clone expressing cytochrome P450 for safe use in human somatic cell therapy.
Günzburg, WH; Karle, P; Renner, M; Renz, R; Salmons, B, 1999
)
0.61
"Renal injury is a common side effect of the chemotherapeutic agent ifosfamide."( Toxicity of ifosfamide and its metabolite chloroacetaldehyde in cultured renal tubule cells.
Chan, K; Davies, S; Lu, H; Springate, J; Taub, M, 1999
)
0.92
" Poor performance status and prior radiotherapy were risk factors for fatal adverse effects."( [Treatment of advanced testicular cancer and toxicity of chemotherapy].
Kawakita, M; Matsuda, T; Terachi, T; Yoshida, O, 1999
)
0.3
" There were no toxic deaths."( Epic as an effective, low toxicity salvage therapy for patients with poor risk lymphoma prior to beam high dose chemotherapy and peripheral blood progenitor cell transplantation.
Cavenagh, JD; Eden, AG; Hughes, A; Kelsey, SM; Lamont, A; McBride, NC; Mills, MJ; Newland, AC; Ward, MC, 1999
)
0.3
"Adjuvant ifosfamide appears to be safe and well tolerated in patients with completely resected uterine sarcoma."( Safety and efficacy of adjuvant single-agent ifosfamide in uterine sarcoma.
Belinson, JL; Kennedy, AW; Kushner, DM; Markman, M; Rybicki, LA; Webster, KD, 2000
)
0.98
" A critical question in comparing an experimental treatment to a standard is how much increase in an adverse event rate is an acceptable trade-off for achieving a targeted improvement in efficacy, or vice versa."( Treatment comparisons based on two-dimensional safety and efficacy alternatives in oncology trials.
Cheng, SC; Thall, PF, 1999
)
0.3
" The male patient was enrolled into the research programme for the evaluation of the association between deletion of the genes encoding a number of classes of glutathione S-transferases (GST) and adverse reactions to alkylating agents."( Growth retardation and osteomalacia as a result of ifosfamide nephrotoxicity in a 3-year-old boy whose genotype reveals the genes encoding glutathione S-transferases GSTM1 and GSTT1.
Bodalski, J; Zielińska, E, 2001
)
0.56
" In this study, we investigated the toxic effects of ifosfamide and cisplatin by clinical and biochemical parameters in relation to (99m)Tc-dimercaptosuccinic acid ((99m)Tc-DMSA) and Tc(99m)N, N-ethylenedicysteine (EC) renal scintigraphy."( The utility of (99m)Tc-DMSA and Tc(99m)-EC scintigraphy for early diagnosis of ifosfamide induced nephrotoxicity.
Akyuz, C; Caglar, M; Yarís, N, 2001
)
0.79
" No toxic death was reported."( Gemcitabine, Ifosfamide and Navelbine (GIN): activity and safety of a non-platinum-based triplet in advanced non-small-cell lung cancer (NSCLC).
Ardizzoni, A; Baldini, E; Boni, L; Cafferata, MA; Conte, PF; Neumaier, C; Prochilo, T; Rosso, R; Tibaldi, C, 2001
)
0.68
" Although some adverse effects (e."( Young age and the risk for ifosfamide-induced nephrotoxicity: a critical review of two opposing studies.
Aleksa, K; Koren, G; Woodland, C, 2001
)
0.61
"In large-scale pediatric chemo- and radiotherapy trials a proportion of patients as high as 10-15% is usually reported as having severe treatment related toxicity occasionally resulting in toxic death."( Fatal toxicity following radio- and chemotherapy of medulloblastoma in a child with unrecognized Nijmegen breakage syndrome.
Distel, L; Grabenbauer, G; Holter, W; Neubauer, S; Varon, R, 2003
)
0.32
"Renal injury is a common side effect of the chemotherapeutic agent ifosfamide."( Comparative toxicity of ifosfamide metabolites and protective effect of mesna and amifostine in cultured renal tubule cells.
Springate, JE; Taub, M; Zaki, EL, 2003
)
0.86
"The aim of the study was an assessment of various risk factors for nephrotoxicity of ifosfamide (IF) in children taking into account the importance of the concentrations of toxic metabolites of the drug excreted with urine and the polymorphism of genes encoding S-glutathione transferases of mi, pi, and theta classes (GSTM1, GSTP1 and GSTT1)."( [Polymorphism at the glutathione S-transferase pi locus as a risk factor for ifosfamide nephrotoxicity in children].
Bodalski, J; Zielińska, E; Zubowska, M, 2003
)
0.77
" With cyclophosphamide it shares a toxicity profile characterized by myelosuppression and urotoxicity, but ifosfamide has additionally disclosed adverse neurological effects."( Neurological toxicity of ifosfamide.
Giometto, B; Nicolao, P, 2003
)
0.84
" An objective causality assessment revealed that an adverse drug reaction was probable."( Vascular neurotoxicity following chemotherapy with cisplatin, ifosfamide, and etoposide.
Bogdahn, U; Dietrich, J; Marienhagen, J; Schalke, B; Schlachetzki, F, 2004
)
0.56
"Clinicians should be aware of the potential neurovascular adverse effects of cisplatin-based protocols."( Vascular neurotoxicity following chemotherapy with cisplatin, ifosfamide, and etoposide.
Bogdahn, U; Dietrich, J; Marienhagen, J; Schalke, B; Schlachetzki, F, 2004
)
0.56
"Cardiotoxicity is a well-known side effect of several cytotoxic drugs, especially of the anthracyclines and can lead to long term morbidity."( Cardiotoxicity of cytotoxic drugs.
Guchelaar, HJ; Richel, DJ; Schimmel, KJ; van den Brink, RB, 2004
)
0.32
" Following an uncomplicated pregnancy, a healthy child was born at full term and careful haematological and immunological monitoring has revealed no adverse effects resulting from exposure to rituximab."( Safety of rituximab therapy during the first trimester of pregnancy: a case history.
Elinder, G; Kimby, E; Sverrisdottir, A, 2004
)
0.32
" Nephrotoxicity was a major toxic event and was characterized by creatinine levels at or above three times the upper limit of normal."( High-dose ifosfamide in relapsed pediatric osteosarcoma: therapeutic effects and renal toxicity.
Berberoğlu, S; Berrak, SG; Ilhan, IE; Jaffe, N; Pearson, M, 2005
)
0.73
" This will adversely affect the health and well-being of children, especially when the developing kidney is exposed to toxic agents that may lead to acute glomerular, tubular or combined toxicity."( Cytochrome P450 3A and 2B6 in the developing kidney: implications for ifosfamide nephrotoxicity.
Aleksa, K; Gelboin, H; Ito, S; Koren, G; Krausz, K; Matsell, D, 2005
)
0.56
" The authors' multidimensional analysis model revealed that besides the total ifosfamide dose and co-administration of other toxic drugs, polymorphic locus of GSTP1 gene may be one of the factors determining a higher toxicity of the cytostatic agent."( Role of GSTM1, GSTP1, and GSTT1 gene polymorphism in ifosfamide metabolism affecting neurotoxicity and nephrotoxicity in children.
Misiura, K; Zielińska, E; Zubowska, M, 2005
)
0.81
"5 million adverse drug reaction (ADR) reports for 8620 drugs/biologics that are listed for 1191 Coding Symbols for Thesaurus of Adverse Reaction (COSTAR) terms of adverse effects."( Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
Benz, RD; Contrera, JF; Kruhlak, NL; Matthews, EJ; Weaver, JL, 2004
)
0.32
" Adverse reactions (AR) were evaluated; quality assurance of data collection reviewed."( Safety assessment of intensive induction with vincristine, ifosfamide, doxorubicin, and etoposide (VIDE) in the treatment of Ewing tumors in the EURO-E.W.I.N.G. 99 clinical trial.
Craft, A; Juergens, C; Juergens, H; Lewis, I; Michon, J; Oberlin, O; Paulussen, M; Weston, C; Whelan, J; Zoubek, A, 2006
)
0.58
"Renal injury is a common side effect of the chemotherapeutic agent ifosfamide."( Ifosfamide toxicity in cultured proximal renal tubule cells.
Springate, J; Taub, M, 2007
)
2.02
"Ifosfamide (IF) nephrotoxicity is a serious adverse effect in children undergoing chemotherapy."( The effect of N-acetylcysteine on ifosfamide-induced nephrotoxicity: in vitro studies in renal tubular cells.
Aleksa, K; Chen, N; Koren, G; Rieder, M; Woodland, C, 2007
)
2.06
"Ifosfamide nephrotoxicity is a serious adverse effect for children undergoing cancer chemotherapy."( N-Acetylcysteine prevents ifosfamide-induced nephrotoxicity in rats.
Aleksa, K; Chen, N; Koren, G; Rieder, M; Woodland, C, 2008
)
2.09
" A potential side effect is neurotoxicity, often manifesting as confusion, hallucination, or seizure."( Characterization of the occurrence of ifosfamide-induced neurotoxicity with concomitant aprepitant.
Hatfield Seung, A; Howell, JE; Nesbit, SA; Szabatura, AH, 2008
)
0.62
" In the previous five cycles of ifosfamide, carboplatin, and etoposide, the patient had no problems with the neurotoxic adverse effects associated with ifosfamide use."( Possible contribution of aprepitant to ifosfamide-induced neurotoxicity.
Jarkowski, A, 2008
)
0.9
" The toxic metabolite of IFO thought to be responsible for IFO-induced kidney damage is chloroacetaldehyde (CAA)."( Ifosfamide nephrotoxicity in children: a mechanistic base for pharmacological prevention.
Chen, N; Hanly, L; Koren, G; Rieder, M, 2009
)
1.8
" Sequential dose intense ifosfamide, etoposide, carboplatin +/- rituximab was more toxic and no more effective than the same drugs given in a conventional fashion."( Sequential high-dose ifosfamide, carboplatin and etoposide with rituximab for relapsed Hodgkin and large B-cell non-Hodgkin lymphoma: increased toxicity without improvement in progression-free survival.
Beaven, AW; Chao, N; Gabriel, DA; Garcia, RA; Gockerman, JP; Moore, DT; Rizzieri, DA; Serody, JS; Shea, TC, 2009
)
0.98
" Electrolyte abnormalities such as hypomagnesaemia and hypokalemia are commonly reported adverse effects, in addition to increased serum creatinine and uremia."( Children's toxicology from bench to bed--Drug-induced renal injury (2): Nephrotoxicity induced by cisplatin and ifosfamide in children.
Chayama, K; Fujieda, M; Hayashi, A; Matsunaga, A; Sekine, T; Tauchi, H, 2009
)
0.56
"Neurotoxicity is a clinically relevant adverse event observed with the use of ifosfamide."( Ifosfamide encephalopathy and use of methylene blue. A case report of different sequential neurotoxicity.
Garna, A; Giovanis, P; Giusto, M; Marcante, M; Nardi, K,
)
1.8
" We assumed that combined toxic effect of gemcitabine and vinorelbine resulted in serious cutaneous toxicity under pre-existing condition of diffuse ichthyosis."( [Serious cutaneous toxicity following ifosfamide, gemcitabine and vinorelbine therapy in a patient with relapsed Hodgkin lymphoma and ichthyosis].
Konífrová, E; Móciková, H; Stríteský, J, 2009
)
0.62
" Major treatment-related adverse events were grade 3 or more hematologic toxicities, which included lymphopenia corresponding to dose-limiting toxicity."( Activity and safety of combination chemotherapy with methotrexate, ifosfamide, l-asparaginase and dexamethasone (MILD) for refractory lymphoid malignancies: a pilot study.
Hosone, M; Isobe, Y; Katsuoka, Y; Komatsu, N; Oshimi, K; Shimizu, S; Sugimoto, K; Tsukune, Y; Yasuda, H, 2010
)
0.6
" An understanding of structure-activity relationships (SARs) of chemicals can make a significant contribution to the identification of potential toxic effects early in the drug development process and aid in avoiding such problems."( Developing structure-activity relationships for the prediction of hepatotoxicity.
Fisk, L; Greene, N; Naven, RT; Note, RR; Patel, ML; Pelletier, DJ, 2010
)
0.36
"A serious adverse effect that can limit the utility of ifosfamide is neurotoxicity, known as ifosfamide-induced encephalopathy (IIE)."( Evaluation of methylene blue, thiamine, and/or albumin in the prevention of ifosfamide-related neurotoxicity.
Marshall, H; McQuary, A; Richards, A, 2011
)
0.85
"In addition to hemorrhagic cystitis, Fanconi Syndrome is a serious clinical side effect during ifosfamide (IFO) therapy."( Carnitine deficiency and oxidative stress provoke cardiotoxicity in an ifosfamide-induced Fanconi Syndrome rat model.
Darweesh, AQ; Fatani, AJ; Sayed-Ahmed, MM,
)
0.58
"The adverse effects of combination chemotherapy of ifosfamide, cisplatin, and etoposide (ICE) were evaluated in the treatment of various intracranial brain tumors."( [The safety of combination chemotherapy with ifosfamide, cisplatin, and etoposide (ICE): single-institution retrospective review of 108 cases].
Kanamori, M; Kumabe, T; Saito, R; Sonoda, Y; Tominaga, T; Yamashita, Y, 2010
)
0.87
" The adverse effects were analyzed based on the the clinical or laboratory examinations."( [The safety of combination chemotherapy with ifosfamide, cisplatin, and etoposide (ICE): single-institution retrospective review of 108 cases].
Kanamori, M; Kumabe, T; Saito, R; Sonoda, Y; Tominaga, T; Yamashita, Y, 2010
)
0.62
"Common Terminology Criteria for Adverse Events ver."( [The safety of combination chemotherapy with ifosfamide, cisplatin, and etoposide (ICE): single-institution retrospective review of 108 cases].
Kanamori, M; Kumabe, T; Saito, R; Sonoda, Y; Tominaga, T; Yamashita, Y, 2010
)
0.62
"The high rate of adverse effects requires close follow up and dose reduction."( [The safety of combination chemotherapy with ifosfamide, cisplatin, and etoposide (ICE): single-institution retrospective review of 108 cases].
Kanamori, M; Kumabe, T; Saito, R; Sonoda, Y; Tominaga, T; Yamashita, Y, 2010
)
0.62
"Grade 3 toxic events were observed in 18 patients (30%) and Grade 4 events in 6 patients (10%)."( Determinants of toxicity, patterns of failure, and outcome among adult patients with soft tissue sarcomas of the extremity and superficial trunk treated with greater than conventional doses of perioperative high-dose-rate brachytherapy and external beam r
Cambeiro, M; Fernández Sanmamed, M; Gaztañaga, M; Martín-Algarra, S; Martinez-Monge, R; Pagola, M; San Julián, M; San Miguel, I; Vázquez-García, B, 2011
)
0.37
"Nephrotoxicity is an inherent adverse effect of certain anticancer drugs and may result in a variety of functional consequences that include any combination of glomerular or tubular dysfunction, hypertension and disturbance of the renal endocrine function."( Nephrotoxicity of anticancer drugs--an underestimated problem?
Kruse, V; Lameire, N; Rottey, S,
)
0.13
"The use of oxazaphosphorines (cyclophosphamide, ifosfamide) in the treatment of numerous neoplastic disorders is associated with their essential adverse effect in the form of hemorrhagic cystitis, which considerably limits the safety and efficacy of their pharmacotherapy."( Bladder urotoxicity pathophysiology induced by the oxazaphosphorine alkylating agents and its chemoprevention .
Dobrek, Ł; Thor, PJ, 2012
)
0.63
"Since all the latter test compounds, like many toxic compounds, negatively interact with cellular metabolic pathways, we also illustrate our biochemical toxicology approach in which we used not only enzymatic but also carbon 13 NMR measurements and mathematical modelling of metabolic pathways."( Use of precision-cut renal cortical slices in nephrotoxicity studies.
Baverel, G; Duplany, A; El Hage, M; Ferrier, B; Gauthier, C; Knouzy, B; Martin, G, 2013
)
0.39
"Cyclophosphamide and ifosfamide are two commonly used DNA-alkylating agents in cancer chemotherapy that undergo biotransformation to several toxic and non-toxic metabolites, including acrolein and chloroacetaldehyde (CAA)."( Acrolein and chloroacetaldehyde: an examination of the cell and cell-free biomarkers of toxicity.
Lau, V; MacAllister, SL; Martin-Brisac, N; O'Brien, PJ; Yang, K, 2013
)
0.71
" However, its use is limited due to its serious side effect on kidneys."( Protective effects of alpha lipoic acid versus N-acetylcysteine on ifosfamide-induced nephrotoxicity.
El-Desoky, KI; El-Sisi, Ael-D; El-Syaad, ME; Moussa, EA, 2015
)
0.65
" Two toxic deaths were observed."( High response rate and acceptable toxicity of a combination of rituximab, vinorelbine, ifosfamide, mitoxantrone and prednisone for the treatment of diffuse large B-cell lymphoma in first relapse: results of the R-NIMP GOELAMS study.
Alexis, M; Arakelyan, N; Banos, A; Cartron, G; Courby, S; Damotte, D; Dreyfus, F; Fontan, J; Gressin, R; Gyan, E; Lamy, T; Laribi, K; Le Gouill, S; Maisonneuve, H; Quittet, P; Schmidt-Tanguy, A; Sénécal, D; Solal-Céligny, P; Tournilhac, O, 2013
)
0.61
"Nephrotoxicity is a serious side effect associated with ifosfamide use."( N-acetylcysteine rescue protocol for nephrotoxicity in children caused by ifosfamide.
Hanly, L; Huang, SH; Koren, G; Regueira, O; Rieder, MJ; Shah, RK; Vasylyeva, TL, 2013
)
0.87
" The toxic effects of IFOS were analyzed by oxidative parameters and caspase 3 immunohistochemical examinations of brain tissue."( Effect of alpha lipoic acid on ifosfamide-induced central neurotoxicity in rats.
Albayrak, A; Bilen, S; Fadillioglu, E; Ginis, Z; Kurt, SN; Ozturk, G, 2014
)
0.69
"Since 1985, we introduced a modified combination of etoposide, ifosfamide, and cisplatin (PEI) as second-line therapy of adult male germ cell tumors with the aim to reduce toxic effect while maintaining efficacy over the original regimen."( Modified cisplatin, etoposide, and ifosfamide (PEI) salvage therapy for male germ cell tumors: long-term efficacy and safety outcomes.
Biasoni, D; Catanzaro, M; Farè, E; Giannatempo, P; Gianni, AM; Mariani, L; Milani, A; Necchi, A; Nicolai, N; Piva, L; Pizzocaro, G; Raggi, D; Salvioni, R; Stagni, S; Torelli, T, 2013
)
0.91
"2% neurotoxic effect, and no severe renal toxic effect were recorded."( Modified cisplatin, etoposide, and ifosfamide (PEI) salvage therapy for male germ cell tumors: long-term efficacy and safety outcomes.
Biasoni, D; Catanzaro, M; Farè, E; Giannatempo, P; Gianni, AM; Mariani, L; Milani, A; Necchi, A; Nicolai, N; Piva, L; Pizzocaro, G; Raggi, D; Salvioni, R; Stagni, S; Torelli, T, 2013
)
0.67
"Ifosfamide combined with other antineoplastic agents has been effective in the treatment of osteosarcoma, although adverse effects are reported in the increasing use of ifosfamide."( Effects of blood purification therapy on a patient with ifosfamide-induced neurotoxicity and acute kidney injury.
Enokida, H; Hayami, H; Komiya, S; Nagano, S; Nakagawa, M; Nishimura, H; Yokouchi, M, 2014
)
2.09
" However, childhood cancer survivors (CCS) are at great risk for developing adverse effects caused by multimodal treatment for their malignancy."( Early and late renal adverse effects after potentially nephrotoxic treatment for childhood cancer.
Blufpand, H; Bökenkamp, A; Jaspers, MW; Knijnenburg, SL; Kremer, LC; Mulder, RL; Schouten-Van Meeteren, AY; van Dulmen-den Broeder, E; Veening, MA, 2013
)
0.39
" The full-text screening of the remaining 366 articles resulted in the inclusion of 57 studies investigating the prevalence of and sometimes also risk factors for early and late renal adverse effects of treatment for childhood cancer."( Early and late renal adverse effects after potentially nephrotoxic treatment for childhood cancer.
Blufpand, H; Bökenkamp, A; Jaspers, MW; Knijnenburg, SL; Kremer, LC; Mulder, RL; Schouten-Van Meeteren, AY; van Dulmen-den Broeder, E; Veening, MA, 2013
)
0.39
"The prevalence of renal adverse events after treatment with cisplatin, carboplatin, ifosfamide, radiation therapy involving the kidney region and/or nephrectomy ranged from 0% to 84%."( Early and late renal adverse effects after potentially nephrotoxic treatment for childhood cancer.
Blufpand, H; Bökenkamp, A; Jaspers, MW; Knijnenburg, SL; Kremer, LC; Mulder, RL; Schouten-Van Meeteren, AY; van Dulmen-den Broeder, E; Veening, MA, 2013
)
0.61
" Five patients did not complete treatments because of adverse events."( AMC 048: modified CODOX-M/IVAC-rituximab is safe and effective for HIV-associated Burkitt lymphoma.
Ambinder, R; Baiocchi, R; Cesarman, E; Kaplan, L; Lee, JY; Noy, A; Ratner, L; Reid, E; Wagner-Johnston, N, 2015
)
0.42
" Those results are in agreement with literature data reporting that intracellular CAA toxic concentrations range from 35 to 320 μM, after therapeutic ifosfamide dosing."( Investigation of ifosfamide and chloroacetaldehyde renal toxicity through integration of in vitro liver-kidney microfluidic data and pharmacokinetic-system biology models.
Bois, FY; Hamon, J; Leclerc, E, 2016
)
0.97
" Risk ratios (RRs) were pooled to compare good histologic response rates and adverse event incidence."( Efficacy and safety of ifosfamide-based chemotherapy for osteosarcoma: a meta-analysis.
Cai, GP; Ding, GM; Fan, XL; Zhu, LL, 2015
)
0.73
" leopoliensis, suggesting that no stable TPs with adverse effects were formed."( Ecotoxicity and genotoxicity of cyclophosphamide, ifosfamide, their metabolites/transformation products and their mixtures.
Česen, M; Eleršek, T; Filipič, M; Heath, E; Kosjek, T; Novak, M; Žegura, B, 2016
)
0.69
" Objective The aim of this study was to determine if a rapid hydration protocol resulted in a shorter time to chemotherapy administration and during peak staffing levels without increasing adverse effects."( Evaluation of a rapid hydration protocol: Safety and effectiveness.
Hilliard, J; Meredith, S; Vaillancourt, R, 2017
)
0.46
" This single-center prospective study demonstrated that the dose-modified IVE regimen can be used as a safe treatment with high mobilizing efficacy in heavily pretreated lymphoma patients."( Dose-Modified Ifosfamide, Epirubicin, and Etoposide is a Safe and Effective Salvage Therapy with High Peripheral Blood Stem Cell Mobilization Capacity for Poorly Mobilized Hodgkin's Lymphoma and Non-Hodgkin's Lymphoma Patients.
Arima, N; Fukunaga, A; Hyuga, M; Iwasaki, M; Kishimoto, W; Maesako, Y; Nakae, Y, 2016
)
0.79
"Many adverse drug reactions are caused by the cytochrome P450 (CYP)-dependent activation of drugs into reactive metabolites."( Development of a cell viability assay to assess drug metabolite structure-toxicity relationships.
Jones, LH; Nadanaciva, S; Rana, P; Will, Y, 2016
)
0.43
"Drug-induced nephrotoxicity is one of the most frequent adverse events in pharmacotherapy."( Assessment of hepatic metabolism-dependent nephrotoxicity on an organs-on-a-chip microdevice.
Jiang, L; Li, Z; Qin, J; Shi, Y; Su, W; Tao, T; Xu, C; Zhu, Y, 2018
)
0.48
"Radiochemotherapy involving cisplatinum-based polychemotherapy is more toxic than radiotherapy in combination with temozolomide."( Concurrent radiotherapy with temozolomide vs. concurrent radiotherapy with a cisplatinum-based polychemotherapy regimen : Acute toxicity in pediatric high-grade glioma patients.
Bison, B; Bojko, S; Gielen, GH; Hoffmann, M; Kortmann, RD; Kramm, CM; Pietsch, T; Seidel, C; von Bueren, AO; Warmuth-Metz, M, 2018
)
0.48
"BACKGROUND The aim of this study was to compare nutrition-related adverse events and clinical outcomes of ifosfamide, carboplatin, and etoposide regimen (ICE therapy) and ranimustine, carboplatin, etoposide, and cyclophosphamide regimen (MCEC therapy) instituted as pretreatment for autologous peripheral blood stem cell transplantation."( Comparison of Nutrition-Related Adverse Events and Clinical Outcomes Between ICE (Ifosfamide, Carboplatin, and Etoposide) and MCEC (Ranimustine, Carboplatin, Etoposide, and Cyclophosphamide) Therapies as Pretreatment for Autologous Peripheral Blood Stem C
Aoyama, T; Arai, H; Ikeda, T; Imataki, O; Ishide, K; Katsumata, N; Kume, T; Mori, M; Shiozaki, H, 2018
)
0.92
" There is significant uncertainty as to whether using closed-system drug-transfer devices (CSTD) in addition to safe handling decreases the contamination and risk of staff exposure to infusional hazardous drugs compared to safe handling alone."( Closed-system drug-transfer devices plus safe handling of hazardous drugs versus safe handling alone for reducing exposure to infusional hazardous drugs in healthcare staff.
Best, LM; Bussières, JF; Gurusamy, KS; Korva, M; Lennan, E; Tanguay, C, 2018
)
0.48
"To assess the effects of closed-system drug-transfer of infusional hazardous drugs plus safe handling versus safe handling alone for reducing staff exposure to infusional hazardous drugs and risk of staff contamination."( Closed-system drug-transfer devices plus safe handling of hazardous drugs versus safe handling alone for reducing exposure to infusional hazardous drugs in healthcare staff.
Best, LM; Bussières, JF; Gurusamy, KS; Korva, M; Lennan, E; Tanguay, C, 2018
)
0.48
"We included comparative studies of any study design (irrespective of language, blinding, or publication status) that compared CSTD plus safe handling versus safe handling alone for infusional hazardous drugs."( Closed-system drug-transfer devices plus safe handling of hazardous drugs versus safe handling alone for reducing exposure to infusional hazardous drugs in healthcare staff.
Best, LM; Bussières, JF; Gurusamy, KS; Korva, M; Lennan, E; Tanguay, C, 2018
)
0.48
" In 21 studies, the people who used the intervention (CSTD plus safe handling) and control (safe handling alone) were pharmacists or pharmacy technicians; in the other two studies, the people who used the intervention and control were nurses, pharmacists, or pharmacy technicians."( Closed-system drug-transfer devices plus safe handling of hazardous drugs versus safe handling alone for reducing exposure to infusional hazardous drugs in healthcare staff.
Best, LM; Bussières, JF; Gurusamy, KS; Korva, M; Lennan, E; Tanguay, C, 2018
)
0.48
"There is currently no evidence to support or refute the routine use of closed-system drug transfer devices in addition to safe handling of infusional hazardous drugs, as there is no evidence of differences in exposure or financial benefits between CSTD plus safe handling versus safe handling alone (very low-quality evidence)."( Closed-system drug-transfer devices plus safe handling of hazardous drugs versus safe handling alone for reducing exposure to infusional hazardous drugs in healthcare staff.
Best, LM; Bussières, JF; Gurusamy, KS; Korva, M; Lennan, E; Tanguay, C, 2018
)
0.48
"Our study showed that the outpatient administration of interval-compressed regimen is safe and associated with acceptable adherence to this regimen."( Safety and Cost-effectiveness of Outpatient Administration of High-dose Chemotherapy in Children With Ewing Sarcoma.
Alnassan, A; Elshahoubi, A; Sultan, I, 2019
)
0.51
" Our results suggest that f-R-ICE is a safe and effective salvage therapy for r/r DLBCL and can be used for older patients and/or those with high CCI scores in outpatient clinics."( Fractionated ifosfamide, carboplatin, and etoposide with rituximab as a safe and effective treatment for relapsed/refractory diffuse large B cell lymphoma with severe comorbidities.
Imai, Y; Shiseki, M; Tanaka, J; Tanaka, N; Yoshinaga, K, 2020
)
0.93
" Common treatment-related adverse events (all grades) were diarrhoea (35."( Randomised phase 2 study comparing the efficacy and safety of the oral tyrosine kinase inhibitor nintedanib with single agent ifosfamide in patients with advanced, inoperable, metastatic soft tissue sarcoma after failure of first-line chemotherapy: EORTC-
Bovée, JVMG; Brahmi, M; Charon-Barra, C; Cousin, S; de Haan, J; De Meulemeester, L; Domènech, M; Dudzisz-Śledź, M; Estival, A; Gelderblom, H; Karavasilis, V; Litière, S; Marquina, G; Marreaud, S; Olungu, C; Schöffski, P; Steeghs, N; Toulmonde, M; Wozniak, A, 2021
)
0.83
" The primary endpoint compares and evaluates the side effect profiles of ifosfamide-treated patients in the OP/IP settings."( Transitioning ifosfamide chemotherapy regimens to the ambulatory setting: reviewing cost savings and safety profile.
Arredondo, A; Babiker, H; Banh, C; Boiles, AR; Elquza, E; Kraft, A; McBride, A; Notbohm, K; Ortega, A; Persky, D; Valsvik, K, 2022
)
1.31
" The current processes allow for safe transition of chemotherapy of chemotherapy under times of COVID."( Transitioning ifosfamide chemotherapy regimens to the ambulatory setting: reviewing cost savings and safety profile.
Arredondo, A; Babiker, H; Banh, C; Boiles, AR; Elquza, E; Kraft, A; McBride, A; Notbohm, K; Ortega, A; Persky, D; Valsvik, K, 2022
)
1.08
"Ifosfamide (IFO) is used for treating childhood solid tumors, but its use is limited by its adverse effects on kidneys."( Morin mitigates ifosfamide induced nephrotoxicity by regulation of NF-kappaB/p53 and Bcl-2 expression.
Çomaklı, S; Kandemir, FM; Küçükler, S; Özdemir, S, 2022
)
2.51
" Kidney adverse effects may include acute kidney injury (via tubular injury, tubulointerstitial nephritis, glomerular disease and thrombotic microangiopathy), long-term kidney function loss and CKD, and electrolyte disturbances."( Conventional Chemotherapy Nephrotoxicity.
Daher, A; Gupta, S; Kitchlu, A; Portales-Castillo, I, 2021
)
0.62
" Aprepitant is administered as an anti-emetic agent in chemotherapy and regarding the inhibitory effect on CYP3A4, aprepitant can increase the risk of ifosfamide adverse effects."( Aprepitant, fosaprepitant and risk of ifosfamide-induced neurotoxicity: a systematic review.
Mohammadpour, AH; Rahimi, H; Sadeghi, M; Samadi, S; Vazirian, F, 2022
)
1.19
" The treatment group received a toxic dose once daily of each investigated drug for 1 week."( Genome-wide gene expression analysis reveals molecular insights into the drug-induced toxicity of nephrotoxic agents.
Cho, YS; Kim, DH; Long, NP; Oh, JH; Park, SM; Phat, NK; Shin, JG; Thu, VTA; Yen, NTH; Yoon, S, 2022
)
0.72
" It is important to identify both the therapeutic ingredients and the toxic components to better utilize this TCM."( Assessment of in vitro cardiotoxicity of extract fractions and diterpene alkaloids from Aconitum leucostomum Worosch: A short communication.
Ji, T; Nie, J; Wang, F; Zhao, F; Zhao, J, 2017
)
0.46

Pharmacokinetics

A multicompartment pharmacokinetic model for ifosfamide has been employed using a system of first-order differential equations. Both schedules resulted in a reduction in the elimination half-life with an increased total and nonrenal clearance of ifosFamide over the 5-day period. A positive correlation was found between the eliminationhalf-life of ifOSFamide and age (r = 0.01)

ExcerptReferenceRelevance
"A multicompartment pharmacokinetic model for ifosfamide has been employed using a system of first-order differential equations, which includes a term for metabolism according to Michaelis-Menten kinetics in order to describe the distribution and elimination parameters of ifosfamide in man."( Pharmacokinetics of ifosfamide.
Allen, LM; Creaven, PJ, 1975
)
0.84
" The plasma decay of IP is biphasic with a terminal half-life of 15."( Studies on the human pharmacokinetics of isophosphamide (NSC-109724).
Allen, LM; Creaven, PJ; Nelson, RL, 1976
)
0.26
" Independent of the route of ifosfamide application on day 1, the terminal half-life on day 3 (when the drug was given by the alternative route) was decreased in 6 out of the 12 patients, thus indicating self-induction of hepatic metabolism."( Metabolism and pharmacokinetics of oral and intravenous ifosfamide.
Cerny, T; Küpfer, A; Kurowski, V; Wagner, T, 1991
)
0.82
" Pharmacokinetic data of ifosfamide and its metabolites in these cases are scanty."( Gas chromatographic determination of ifosfamide in microvolumes of urine and plasma.
Beijnen, JH; Bult, A; de Kraker, J; Kaijser, GP; Underberg, WJ; Wiese, G, 1991
)
0.86
" Similar results were found in toxicity and pharmacokinetic studies conducted in non-tumor-bearing female CBA/CaJ mice."( Efficacy, toxicity, pharmacokinetics, and in vitro metabolism of the enantiomers of ifosfamide in mice.
Houghton, PJ; Masurel, D; Wainer, IW; Young, CL, 1990
)
0.5
" The assay has been validated for routine clinical and pharmacokinetic use and has a limit of detection in plasma of 250 ng/ml of each isomer."( The determination of (-)-(S)- and (+)-(R)-ifosfamide in plasma using enantioselective gas chromatography: a validated assay for pharmacokinetic and clinical studies.
Frank, H; Stewart, CR; Wainer, IW; Young, CL, 1989
)
0.54
" Both schedules resulted in a reduction in the elimination half-life with an increased total and nonrenal clearance of ifosfamide over the 5-day period."( Comparative pharmacokinetics and alkylating activity of fractionated intravenous and oral ifosfamide in patients with bronchogenic carcinoma.
Cerny, T; Lind, MJ; Margison, JM; Thatcher, N; Wilkinson, PM, 1989
)
0.71
" The collected experience emphasizes the many individual variables encountered in clinical practice complicating the effort of correlating pharmacokinetic data with clinical results."( Pharmacokinetic studies in lung cancer patients.
Cattaneo, MT; Piazza, E; Varini, M, 1984
)
0.27
" The pharmacokinetic parameters of ifosfamide do not correlate with age, sex and weight."( Ifosfamide metabolism and pharmacokinetics (review).
Beijnen, JH; Bult, A; Kaijser, GP; Underberg, WJ,
)
1.85
" Distinct pharmacokinetic properties of mesna are responsible for the fact that in contrast to other sulphydryl compounds the uroprotective activity of mesna does not imply a loss of therapeutic efficacy."( Ifosfamide clinical pharmacokinetics.
Wagner, T, 1994
)
1.73
" As compared with the values obtained on day 1, on day 5 the terminal half-life and AUC values determined for IF were reduced by 30% (6."( Comparative pharmacokinetics of ifosfamide, 4-hydroxyifosfamide, chloroacetaldehyde, and 2- and 3-dechloroethylifosfamide in patients on fractionated intravenous ifosfamide therapy.
Kurowski, V; Wagner, T, 1993
)
0.57
"4 and 38 degrees C, the IPM solution showed a half-life of 45 min."( Preclinical pharmacokinetics and stability of isophosphoramide mustard.
Chan, KK; Muggia, F; Zheng, JJ, 1994
)
0.29
" Estimated pharmacokinetic parameters (clearance, volume of distribution, and half-life) were dependent on body size and age but not any other patient variable."( Pharmacokinetics and metabolism of ifosfamide administered as a continuous infusion in children.
Boddy, AV; Idle, JR; Pearson, AD; Price, L; Wyllie, R; Yule, SM, 1993
)
0.56
" Plasma ifosfamide concentrations were assayed by gas liquid chromatography and pharmacokinetic parameters were imputed using non-compartmental analysis."( A study of 5 day fractionated ifosfamide pharmacokinetics in consecutive treatment cycles.
Lewis, LD, 1996
)
1.02
" This study reports the results of a pharmacokinetic study of the parent drug and the two dechloroethylated metabolites in 22 patients on a 10-day continuous infusion of ifosfamide."( Pharmacokinetics of ifosfamide, 2- and 3-dechloroethylifosfamide in plasma and urine of cancer patients treated with a 10-day continuous infusion of ifosfamide.
Beijnen, JH; Bult, A; Kaijser, GP; Keizer, HJ; Underberg, WJ,
)
0.65
" IFO pharmacokinetic studies were performed on the first and third day of each course."( Phenobarbital administration does not affect high-dose ifosfamide pharmacokinetics in humans.
Lokiec, F; Santoni, J; Tubiana-Hulin, M; Weill, S, 1996
)
0.54
" These interesting data prompted us to conduct the preclinical pharmacokinetic studies in rats."( Pharmacokinetics and bioavailability of stereoisomeric analogues of ifosfamide.
Hładoń, B; Laskowska, H; Sloderbach, A, 1996
)
0.53
" Pharmacokinetic studies were performed on day 1 of the first course in 33 patients and repeated on day 14 in 13 patients (once-daily schedule only)."( Clinical effects and pharmacokinetics of the fusion protein PIXY321 in children receiving myelosuppressive chemotherapy.
Arnold, B; Furman, WL; Garrison, L; Hanna, R; Luo, X; Marina, N; Meyer, WH; Pratt, CB; Rodman, JH; Tonda, ME, 1998
)
0.3
" The pharmacokinetic studies suggest that the observed lack of hematologic benefit may be explained by low plasma concentrations resulting from increased clearance with prolonged administration."( Clinical effects and pharmacokinetics of the fusion protein PIXY321 in children receiving myelosuppressive chemotherapy.
Arnold, B; Furman, WL; Garrison, L; Hanna, R; Luo, X; Marina, N; Meyer, WH; Pratt, CB; Rodman, JH; Tonda, ME, 1998
)
0.3
" These results indicate that there is no identifiable pharmacokinetic basis for insistence on either bolus or infusional methods of IFOS administration."( The pharmacokinetics and metabolism of ifosfamide during bolus and infusional administration: a randomized cross-over study.
Brennan, C; Hartley, JM; Nicholson, PW; Singer, JM; Souhami, RL, 1998
)
0.57
" The present pharmacokinetic study investigates the potential for modulation of these alternative pathways of IF metabolism in vivo using the adult male Fischer 344 rat model."( Modulation of P450-dependent ifosfamide pharmacokinetics: a better understanding of drug activation in vivo.
Brain, EG; Drewes, P; Gustafsson, K; Waxman, DJ; Yu, LJ, 1998
)
0.59
" In this study we compare the differences in the pharmacokinetic profile between the two schedules."( Pharmacokinetics of ifosfamide administered according to three different schedules in metastatic soft tissue and bone sarcomas.
Bergnolo, P; Boglione, A; Bumma, C; Colussi, AM; Comandone, A; Dal Canton, O; Frustaci, S; Leone, L; Monteleone, M; Oliva, C, 1998
)
0.62
" The in vivo modulation of these alternative, competing pathways of P-450 metabolism was investigated in pharmacokinetic studies carried out in the rat model."( In vivo modulation of alternative pathways of P-450-catalyzed cyclophosphamide metabolism: impact on pharmacokinetics and antitumor activity.
Brain, EG; Drewes, P; Gustafsson, K; Hecht, JE; Waxman, DJ; Yu, LJ, 1999
)
0.3
" Two pharmacokinetic models were compared."( Pharmacokinetic modelling of ifosfamide administered by continuous infusion on 5 days at the dose of 6 g/m2.
Arnaud, P; Brion, F; Delepine, G; Delepine, N; Desbois, JC; Passe, P; Traoré, F; Urien, S,
)
0.42
" In 25 patients (27 cycles) extensive pharmacokinetic analyses were performed."( Saturable metabolism of continuous high-dose ifosfamide with mesna and GM-CSF: a pharmacokinetic study in advanced sarcoma patients. Swiss Group for Clinical Cancer Research (SAKK).
Boddy, AV; Brunner, J; Cerny, T; Honegger, P; Küpfer, A; Leyvraz, S; Schaad, R; Schmitz, SF; Sessa, C; von Briel, T, 1999
)
0.56
" Interpatient variability of pharmacokinetic parameters was high."( Saturable metabolism of continuous high-dose ifosfamide with mesna and GM-CSF: a pharmacokinetic study in advanced sarcoma patients. Swiss Group for Clinical Cancer Research (SAKK).
Boddy, AV; Brunner, J; Cerny, T; Honegger, P; Küpfer, A; Leyvraz, S; Schaad, R; Schmitz, SF; Sessa, C; von Briel, T, 1999
)
0.56
" More robust assay methods for the 4-hydroxy metabolites may reveal more about the clinical pharmacology of these drugs, but at present the best pharmacodynamic data indicate an inverse relationship between plasma concentration of parent drug and either toxicity or antitumour effect."( Metabolism and pharmacokinetics of oxazaphosphorines.
Boddy, AV; Yule, SM, 2000
)
0.31
" By application of the autoinduction model individual pharmacokinetic profiles of patients were described with adequate precision."( Evaluation of the autoinduction of ifosfamide metabolism by a population pharmacokinetic approach using NONMEM.
Beijnen, JH; Huitema, AD; Keizer, HJ; Kerbusch, T; Mathôt, RA; Ouwerkerk, J; Schellens, JH, 2000
)
0.58
"To determine the population pharmacokinetic (PK) parameters of doxorubicin (Dox), etoposide (Eto) and ifosfamide (Ifo) in small cell lung cancer (SCLC) patients, to assess the potential relationship between those parameters and to estimate the impact of individual morphological and biological covariates on patients' PK parameters."( Population pharmacokinetics of doxorubicin, etoposide and ifosfamide in small cell lung cancer patients: results of a multicentre study.
Ardiet, C; Boissel, JP; Court-Fortune, I; Freyer, G; Girard, P; Ligneau, B; Rebattu, P; Riou, R; Souquet, PJ; Tranchand, B; Trillet-Lenoir, V, 2000
)
0.77
" In most clinical pharmacokinetic studies, the phenomenon of autoinduction has been observed, but the mechanism is not completely understood."( Clinical pharmacokinetics and pharmacodynamics of ifosfamide and its metabolites.
Beijnen, JH; de Kraker, J; Groen, HJ; Jansen, RL; Keizer, HJ; Kerbusch, T; Schellens, JH; van Putten, JW, 2001
)
0.56
" An integrated population pharmacokinetic model was used to describe the autoinducible pharmacokinetics of ifosfamide and its four metabolites in 56 patients."( Influence of dose and infusion duration on pharmacokinetics of ifosfamide and metabolites.
Beijnen, JH; Kaijser, GP; Keizer, HJ; Kerbusch, T; Mathôt, RA; Schellens, JH, 2001
)
0.76
"The aim of this study was to develop a population pharmacokinetic model that could describe the pharmacokinetics of ifosfamide."( Population pharmacokinetics of ifosfamide and its 2- and 3-dechloroethylated and 4-hydroxylated metabolites in resistant small-cell lung cancer patients.
Beijnen, JH; Groen, HJ; Huitema, AD; Kerbusch, T; Mathĵt, RA; vanPutten, JW, 2001
)
0.81
" The population pharmacokinetic model was built in a sequential manner, starting with a covariate-free model and progressing to a covariate model with the aid of generalised additive modelling."( Population pharmacokinetics and exploratory pharmacodynamics of ifosfamide and metabolites after a 72-h continuous infusion in patients with soft tissue sarcoma.
Beijnen, JH; Keizer, HJ; Kerbusch, T; Mathĵt, RA; Ouwerkerk, J; Rodenhuis, S; Schellens, JH, 2001
)
0.55
" Autoinduction, dependent on ifosfamide levels, was characterised by an induction half-life of 11."( Population pharmacokinetics and exploratory pharmacodynamics of ifosfamide and metabolites after a 72-h continuous infusion in patients with soft tissue sarcoma.
Beijnen, JH; Keizer, HJ; Kerbusch, T; Mathĵt, RA; Ouwerkerk, J; Rodenhuis, S; Schellens, JH, 2001
)
0.84
" Following drug administration in male rats, (R)-IF exhibited a lower area under the curve value and a shorter half-life of 34."( Stereoselective pharmacokinetics of ifosfamide in male and female rats.
Chan, KK; Lu, H; Wang, JJ, 2000
)
0.58
" Since such treatment is relatively toxic, pharmacokinetic characteristics of total and ultrafiltered platinum, representing different species of platinum complexes formed, were investigated in 29 patients in relation to toxicity."( Toxicity of high-dose carboplatin: ultrafiltered and not total plasma pharmacokinetics is of clinical relevance.
Beyer, J; Jaehde, U; Kloft, C; Siegert, W, 2002
)
0.31
"A fast metabolism of TRO with a half-life of about 1 h was observed."( New insights into the clinical pharmacokinetics of trofosfamide.
Brinker, A; Brüggemann, SK; Kisro, J; Letsch, C; Wagner, T, 2002
)
0.31
" The pharmacodynamic effects of mesna on depleting plasma cysteine, a GSH precursor, were evaluated in 22 patients as part of a Phase I study."( Pharmacokinetics and pharmacodynamics of mesna-mediated plasma cysteine depletion.
Booker, BM; Creaven, P; Pendyala, L; Perez, R; Smith, PF, 2003
)
0.32
" The optimal sequence of chemotherapeutic agents was investigated by reversing the order of administration in the second cycle and by collecting a total of six pharmacokinetic blood samples per cycle from all patients during the first and second cycles."( Docetaxel-ifosfamide combination chemotherapy in patients with metastatic hormone-refractory prostate cancer: a phase I pharmacokinetic study.
Hervonen, P; Jekunen, A; Kellokumpu-Lehtinen, P; Lefebvre, P, 2003
)
0.72
" Using pharmacokinetic modeling of experimental data, we show that the median level of chloroacetaldehyde in RT cells is 80 micromol/L, ranging from 35 to 320 micromol/L."( Renal-tubule metabolism of ifosfamide to the nephrotoxic chloroacetaldehyde: pharmacokinetic modeling for estimation of intracellular levels.
Aleksa, K; Ito, S; Koren, G, 2004
)
0.62
" The authors evaluated the impact of factors such as age and prior nephrotoxic agents on MTX pharmacokinetics in children and young adults with osteosarcoma and examined whether MTX pharmacokinetic parameters were associated with outcome."( High-dose methotrexate pharmacokinetics and outcome of children and young adults with osteosarcoma.
Crews, KR; Daw, NC; Link, MP; Liu, T; Meyer, WH; Panetta, JC; Rodriguez-Galindo, C; Tan, M, 2004
)
0.32
" In patients with localized osteosarcoma, a higher mean MTX area under the curve, a higher mean peak concentration of MTX, a longer mean time above a threshold concentration (500 microM), and a lower mean MTX clearance were associated with lower probability of event-free survival (EFS)."( High-dose methotrexate pharmacokinetics and outcome of children and young adults with osteosarcoma.
Crews, KR; Daw, NC; Link, MP; Liu, T; Meyer, WH; Panetta, JC; Rodriguez-Galindo, C; Tan, M, 2004
)
0.32
" With a short apparent half-life (1."( Investigations on the pharmacokinetics of trofosfamide and its metabolites-first report of 4-hydroxy-trofosfamide kinetics in humans.
Baumann, F; Niederwieser, D; Niemeyer, U; Pönisch, W; Preiss, R; Stefanovic, D, 2004
)
0.32
" Irinotecan pharmacokinetic investigations were performed before ifosfamide (day 1), after 3 days of ifosfamide (day 3), and 9 days after the end of ifosfamide (day 12)."( Effect of fractionated ifosfamide on the pharmacokinetics of irinotecan in pediatric patients with osteosarcoma.
Crews, KR; Daw, NC; Liu, T; Rodriguez-Galindo, C; Santana, VM; Stewart, CF, 2004
)
0.87
" Fractionated dosing causes a greater degree of DNA damage, which may suggest a greater degree of efficacy, with a good correlation between pharmacokinetic and pharmacodynamic data."( Pharmacokinetics and metabolism of ifosfamide in relation to DNA damage assessed by the COMET assay in children with cancer.
Boddy, AV; Cholerton, S; Ford, D; Parry, A; Pearson, AD; Price, L; Tilby, MJ; Willits, I, 2005
)
0.61
" Samples for pharmacokinetic analysis were obtained after the MTD was reached."( Phase I trial and pharmacokinetic analysis of ifosfamide in cats with sarcomas.
Beaulieu, BB; Kristal, O; Lewis, LD; Moore, AS; Northrup, NC; Page, RL; Rassnick, KM, 2006
)
0.59
" Correlations between pharmacokinetic variables and ifosfamide-associated toxicoses were not found."( Phase I trial and pharmacokinetic analysis of ifosfamide in cats with sarcomas.
Beaulieu, BB; Kristal, O; Lewis, LD; Moore, AS; Northrup, NC; Page, RL; Rassnick, KM, 2006
)
0.84
" Bayesian designed limited pharmacokinetic data were collected from an additional 41 patients."( Assessment of ifosfamide pharmacokinetics, toxicity, and relation to CYP3A4 activity as measured by the erythromycin breath test in patients with sarcoma.
Baker, LH; Chugh, R; Griffith, KA; Leu, KM; Taylor, JM; Thomas, DG; Wagner, T; Worden, FP; Zalupski, MM, 2007
)
0.7
" ERMBT was not found to correlate with pharmacokinetic parameters of ifosfamide and metabolites or toxicity."( Assessment of ifosfamide pharmacokinetics, toxicity, and relation to CYP3A4 activity as measured by the erythromycin breath test in patients with sarcoma.
Baker, LH; Chugh, R; Griffith, KA; Leu, KM; Taylor, JM; Thomas, DG; Wagner, T; Worden, FP; Zalupski, MM, 2007
)
0.93
" The peak concentration and area under the curve (AUC) were determined for the parent compound and the metabolites 4-hydroxyifosfamide and chloracetaldehyde in eight patients who received two cycles of ICE chemotherapy (ifosfamide 5 g/m(2) day 1, carboplatin 300 mg/m(2) day 1, etoposide 100 mg/m(2) days 1-3)."( Influence of short-term use of dexamethasone on the pharmacokinetics of ifosfamide in patients.
Brüggemann, SK; Peters, SO; Pfäffle, S; Wagner, T, 2007
)
0.78
" However, this in vitro concentration of NAC needed to be compared to those used in human pharmacokinetic studies since the in vitro pharmacological effect of a compound is achieved at concentrations exceeding those used in clinical."( Prevention of ifosfamide nephrotoxicity by N-acetylcysteine: clinical pharmacokinetic considerations.
Aleksa, K; Chen, N; Koren, G; Rieder, M; Woodland, C, 2007
)
0.7
" * No differences according to time of infusion have been identified in traditional pharmacokinetic endpoints, such as area under the curve."( Population pharmacokinetics and exploratory pharmacodynamics of ifosfamide according to continuous or short infusion schedules: an n = 1 randomized study.
Brain, EG; Gutierrez, M; Lokiec, F; Rezai, K; Urien, S, 2008
)
0.58
" * Pharmacodynamic modelling (renal and haematological toxicity) allows further simulations of new schedules with favourable toxicity profiles."( Population pharmacokinetics and exploratory pharmacodynamics of ifosfamide according to continuous or short infusion schedules: an n = 1 randomized study.
Brain, EG; Gutierrez, M; Lokiec, F; Rezai, K; Urien, S, 2008
)
0.58
" The pharmacodynamic parameters included were renal toxicity and myelosuppression measured using urinary beta(2)-microglobulin (BMG) and absolute neutrophil count (ANC), respectively."( Population pharmacokinetics and exploratory pharmacodynamics of ifosfamide according to continuous or short infusion schedules: an n = 1 randomized study.
Brain, EG; Gutierrez, M; Lokiec, F; Rezai, K; Urien, S, 2008
)
0.58
" pharmacokinetic data on 670 drugs representing, to our knowledge, the largest publicly available set of human clinical pharmacokinetic data."( Trend analysis of a database of intravenous pharmacokinetic parameters in humans for 670 drug compounds.
Lombardo, F; Obach, RS; Waters, NJ, 2008
)
0.35
"To investigate the prognostic value of systemic exposure to etoposide (Area Under the concentration Curve (AUC(VP16))) on overall survival (OS) in patients with small cell lung cancer (SCLC)."( Etoposide pharmacokinetics and survival in patients with small cell lung cancer: a multicentre study.
Chabaud, S; Court-Fortune, I; Falandry, C; Fournel, C; Freyer, G; Girard, P; Ribba, B; Souquet, PJ; Tod, M; Tranchand, B; Trillet-Lenoir, V; You, B, 2008
)
0.35
" Pharmacokinetic analysis revealed a linear relation between the area under the concentration-versus-time curve (AUC) and dose."( Phase I clinical and pharmacokinetic study of the glucose-conjugated cytotoxic agent D-19575 (glufosfamide) in patients with solid tumors.
Akashi, Y; Fukuoka, M; Miyazaki, M; Nakagawa, K; Okamoto, I; Ozaki, T; Satoh, T; Shimizu, T; Tamura, K, 2010
)
0.36
" Pharmacokinetic (PK) and pharmacodynamic (PD) assessments were performed."( Decreased exposure to sunitinib due to concomitant administration of ifosfamide: results of a phase I and pharmacokinetic study on the combination of sunitinib and ifosfamide in patients with advanced solid malignancies.
den Hollander, M; Gelderblom, H; Hamberg, P; Loos, WJ; Sleijfer, S; Steeghs, N; Tascilar, M; van de Biessen, D; Verweij, J, 2010
)
0.6
" Topotecan pharmacokinetic analyses were carried out, and topoisomerase I levels and activity were measured."( Phase I Study of Topotecan, Ifosfamide, and Etoposide (TIME) with autologous stem cell transplant in refractory cancer: pharmacokinetic and pharmacodynamic correlates.
Dawson, JL; Field, TL; Fields, KK; Goldstein, SC; Kim, J; Lush, RM; Maddox, BL; Neuger, AM; Partyka, JS; Perkins, JB; Simonelli, CE; Sullivan, DM, 2011
)
0.66
" Pharmacokinetic monitoring may be a valuable tool for optimizing the use of topotecan and to avoid toxicity seen with high-systemic exposures."( Phase I Study of Topotecan, Ifosfamide, and Etoposide (TIME) with autologous stem cell transplant in refractory cancer: pharmacokinetic and pharmacodynamic correlates.
Dawson, JL; Field, TL; Fields, KK; Goldstein, SC; Kim, J; Lush, RM; Maddox, BL; Neuger, AM; Partyka, JS; Perkins, JB; Simonelli, CE; Sullivan, DM, 2011
)
0.66
" This method was applied to a comparative pharmacokinetic study of 4-OHIFO from IFO and three derivatives RXIFO in mice."( Simultaneous quantification of preactivated ifosfamide derivatives and of 4-hydroxyifosfamide by high performance liquid chromatography-tandem mass spectrometry in mouse plasma and its application to a pharmacokinetic study.
Chapuis, H; Couvreur, P; Daudigeos-Dubus, E; Deroussent, A; Desmaële, D; Durand, S; Le Dret, L; Maury, A; Paci, A; Skarbek, C, 2015
)
0.68
" A pharmacokinetic (PK) model described the production of CAA by the hepatocytes and its transport to the renal cells."( Investigation of ifosfamide and chloroacetaldehyde renal toxicity through integration of in vitro liver-kidney microfluidic data and pharmacokinetic-system biology models.
Bois, FY; Hamon, J; Leclerc, E, 2016
)
0.77
" Much attention has focussed on pharmacokinetic interactions attributable to effects on hepatic microsomal enzymes, but not on competition for the renal organic anion transport system."( The pharmacokinetics of high-dose methotrexate in people living with HIV on antiretroviral therapy.
Bendle, M; Boffito, M; Bower, M; Dalla Pria, A; Ramaswami, R, 2016
)
0.43
" MTX elimination half-life was correlated with age, renal function and antiretroviral regimen."( The pharmacokinetics of high-dose methotrexate in people living with HIV on antiretroviral therapy.
Bendle, M; Boffito, M; Bower, M; Dalla Pria, A; Ramaswami, R, 2016
)
0.43
" The median MTX elimination half-life was 21."( The pharmacokinetics of high-dose methotrexate in people living with HIV on antiretroviral therapy.
Bendle, M; Boffito, M; Bower, M; Dalla Pria, A; Ramaswami, R, 2016
)
0.43
"Although there is potential competition for active renal tubular transporters between MTX and tenofovir, no prolongation of MTX half-life was observed."( The pharmacokinetics of high-dose methotrexate in people living with HIV on antiretroviral therapy.
Bendle, M; Boffito, M; Bower, M; Dalla Pria, A; Ramaswami, R, 2016
)
0.43
"A population pharmacokinetic approach was applied to analyze data obtained in 42 patients at cycle 1 (without aprepitant) and cycle 2 (with aprepitant for 34 of them)."( Population pharmacokinetic analysis reveals no impact of aprepitant on the pharmacokinetics of ifosfamide, 2-dechloroifosfamide, and 3-dechloroifosfamide.
Allal, B; Chaltiel, L; Chatelut, E; Chevreau, C; Filleron, T; Firmin, N; Lambert, M; Mseddi, M; Toulmonde, M; Valentin, T; Yakoubi, M, 2023
)
1.13
"A previously published pharmacokinetic model including a time-dependency process well fit the data."( Population pharmacokinetic analysis reveals no impact of aprepitant on the pharmacokinetics of ifosfamide, 2-dechloroifosfamide, and 3-dechloroifosfamide.
Allal, B; Chaltiel, L; Chatelut, E; Chevreau, C; Filleron, T; Firmin, N; Lambert, M; Mseddi, M; Toulmonde, M; Valentin, T; Yakoubi, M, 2023
)
1.13
" The pharmacokinetic profile of lappaconitine was linear at relatively lower dose levels (1."( Pharmacokinetic study of lappaconitine hydrobromide in mice by LC-MS.
Gao, LY; Hao, JJ; Li, MH; Li, ZJ; Sun, L; Sun, YM; Wang, Q; Zhang, X, 2011
)
0.37
" The validated method has been applied to a pharmacokinetic study of 16-O-demethylaconitine in rats, following oral administration of aconitine."( Relative quantification of the metabolite of aconitine in rat urine by LC-ESI-MS/MS and its application to pharmacokinetics.
He, H; Yan, F, 2012
)
0.38

Compound-Compound Interactions

40 patients (92% pretreated) with deep-seated, advanced soft tissue sarcomas were treated at the University of Munich. The purpose of this study was to evaluate the pharmacokinetics, biological interactions, and toxicities of ifosfamide.

ExcerptReferenceRelevance
"Nine patients with osteosarcoma were treated by chemotherapy combined with caffeine and surgery."( Effect of chemotherapy combined with caffeine for osteosarcoma.
Baba, H; Tomita, K; Tsuchiya, H; Ueda, Y; Yasutake, H; Yokogawa, A, 1992
)
0.28
"From July 1986 to 1990, 65 patients with deep-seated, advanced sarcomas (43 soft-tissue sarcomas, 12 Ewing's sarcomas, 7 chondrosarcomas and 3 osteosarcomas) were entered in a protocol involving regional hyperthermia (RHT) combined with systemic ifosfamide and etoposide."( Improvement of local control by regional hyperthermia combined with systemic chemotherapy (ifosfamide plus etoposide) in advanced sarcomas: updated report on 65 patients.
Denzlinger, C; Gerl, A; Issels, RD; Mittermüller, J; Ortmaier, A; Sauer, H; Simon, W; Wilmanns, W, 1991
)
0.68
"Combination chemotherapy is widely employed in clinical oncology; however, there is no generally accepted model to evaluate individual tumour susceptibility to a given drug combination protocol."( In vitro studies on drug interaction of ifosfamide and ACNU in primary and metastatic human brain tumours.
Apfel, R; Behl, C; Bogdahn, U; Drenkard, D; Lutz, M, 1991
)
0.55
" In the present study, we examined the effects of disulfiram (DSF) in combination with ifosfamide (IFX)."( Drug interaction effects on antitumour drugs (VIII): prevention of ifosfamide-induced urotoxicity by disulfiram and its effect on antitumour activity and acute toxicity of alkylating agents in mice.
Ishikawa, M; Sasaki, K; Takayanagi, Y, 1991
)
0.74
"From July 1986 to July 1989, 40 patients (92% pretreated) with deep-seated, advanced soft tissue sarcomas (STS, 25 patients), Ewing's sarcomas (ES, eight patients), osteosarcomas (OS, three patients) and chondrosarcomas (ChS, four patients) were treated at the University of Munich in a protocol involving regional hyperthermia (RHT) combined with ifosfamide plus etoposide."( Ifosfamide plus etoposide combined with regional hyperthermia in patients with locally advanced sarcomas: a phase II study.
Berger, H; Boehm, E; Denecke, H; Issels, RD; Jauch, KW; Nagele, A; Peter, K; Prenninger, SW; Sauer, H; Wilmanns, W, 1990
)
1.89
"In two separate studies of patients with ovarian cancer, subjects were treated on a protocol comprising 400 mg/m2 carboplatin in combination with 1 g/m2 cyclophosphamide (group A) or 5 g/m2 ifosfamide with mesna (group B)."( Dose intensity of carboplatin in combination with cyclophosphamide or ifosfamide.
Green, JA; Smith, K, 1990
)
0.7
"The response rate and survival obtained with the second-line chemotherapeutic regimen etoposide combined with ifosfamide were analyzed in a series of 32 patients progressing or relapsing after cisplatin-based front-line treatment."( A phase II study of etoposide combined with ifosfamide as second-line therapy in cisplatin-resistant ovarian carcinomas.
Kaern, J; Tropé, C; Vergote, I; Vossli, S, 1990
)
0.75
"Thirty six patients with advanced solid tumors (24 lung: 3 oat-cell, 14 squamous, 7 adenocarcinomas, 3 soft tissue sarcomas, 6 breast carcinomas; 1 seminoma; 2 ovarian adenocarcinomas) entered a phase II study of high-dose ifosfamide (IF) administered in combination with the uroprotective agent sodium 2-mercapto-ethane-sulfonate (Mesna)."( Phase II study of ifosfamide combined with Mesna uroprotection in advanced non-small-cell lung carcinoma and other solid tumors.
Brema, F; Cinquegrana, A; Nobile, MT; Rosso, R; Santi, L, 1984
)
0.79
"The Intergroup Rhabdomyosarcoma Study (IRS) initiated an escalating-dose cyclophosphamide (Cyc) pilot without hematopoietic growth factor (HGF) support in combination with vincristine (Vcr) and actinomycin-D (Amd), known as VAC, to establish a Cyc dose with myelotoxicity comparable to an ifosfamide (Ifos), Vcr, and Amd combination regimen (VAI)."( Cyclophosphamide dose escalation in combination with vincristine and actinomycin-D (VAC) in gross residual sarcoma. A pilot study without hematopoietic growth factor support evaluating toxicity and response.
Gehan, E; Maurer, H; Newton, WA; Ruymann, FB; Vietti, T; Wharam, M; Wiener, E, 1995
)
0.47
"The purpose of this study was to evaluate the pharmacokinetics, biological interactions, and toxicities of ifosfamide and carboplatin combined with 41."( Ifosfamide and carboplatin combined with 41.8 degrees C whole-body hyperthermia in patients with refractory sarcoma and malignant teratoma.
Bucsky, P; d'Oleire, F; Eleftheriadis, S; Feddersen, S; Geisler, J; Klouche, M; Knop, E; Mentzel, M; Schmucker, P; Wiedemann, GJ, 1994
)
1.94
" The seven agents combined with CI-973 were mitomycin C, cyclophosphamide, doxorubicin, vinblastine, etoposide, ifosfamide, and methotrexate."( Chemotherapy with [SP-4-3-(R)]-[1,1-cyclobutanedicarboxylato(2-)](2- methyl-1,4-butanediamine-N,N')platinum (CI-973, NK121) in combination with standard agents against murine tumors in vivo.
Elliott, WL; Howard, CT; Leopold, WR; Roberts, BJ, 1994
)
0.5
"The tolerance for and activity of escalating targeted doses of carboplatin combined with ifosfamide and etoposide (ICE) were assessed in children with advanced germ cell tumors or other rare solid tumors for which no standard therapy exists."( Phase I study of escalating targeted doses of carboplatin combined with ifosfamide and etoposide in treatment of newly diagnosed pediatric solid tumors.
Bowman, LC; Furman, W; Jones, DP; Marina, NM; Meyer, WH; Murry, DJ; Pratt, CB; Rodman, JH; Shema, SJ, 1994
)
0.74
"The tolerance of escalating targeted doses of carboplatin combined with ifosfamide (IFOS)/etoposide (VP-16) (ICE) was assessed in children with recurrent solid tumors."( Phase I study of escalating targeted doses of carboplatin combined with ifosfamide and etoposide in children with relapsed solid tumors.
Bowman, LC; Douglass, E; Furman, W; Hudson, M; Marina, NM; Meyer, W; Rodman, J; Santana, VM; Shema, SJ; Wilimas, J, 1993
)
0.75
"5 g/m2 by intravenous drip for half an hour in 125 ml of dextrose saline for 5 days and mesna 20% of the total ifosfamide dose in 3 doses for 5 days, or in combination with cisplatin 10 mg/m2 by intravenous infusion for 5 days following the ifosfamide drip."( Phase II study of high-dose ifosfamide as a single agent and in combination with cisplatin in the treatment of advanced and/or recurrent squamous cell carcinoma of head and neck.
Mazumdar, AT; Pai, VR; Parikh, DM; Rao, RS,
)
0.64
"From November 1990 to September 1991, 23 adults with high-risk, nonmetastatic sarcomas (20 soft-tissue sarcomas and 3 chondrosarcomas) were entered in a pilot protocol (RHT-91) involving regional hyperthermia combined with systemic chemotherapy followed by surgery."( Preoperative systemic etoposide/ifosfamide/doxorubicin chemotherapy combined with regional hyperthermia in high-risk sarcoma: a pilot study.
Abdel-Rahman, S; Berger, H; Bosse, D; Issels, RD; Jauch, KW; Panzer, M; Peter, K; Sauer, H; Starck, M; Stiegler, H, 1993
)
0.57
" Ifosfamide was given at a dose of 3,750 mg/m2 on days 1 and 2 every 3 weeks in combination with 30 mg/m2 doxorubicin given each day for 2 days; additionally, mesna was given to counter the genitourinary toxicity associated with ifosfamide."( Efficacy of ifosfamide in combination with doxorubicin for the treatment of metastatic soft-tissue sarcoma. The Eastern Cooperative Oncology Group.
Blum, RH; Edmonson, J; Pelletier, L; Ryan, L, 1993
)
1.58
"The purpose of this phase I study is to determine the maximally tolerated doses of paclitaxel and carboplatin (dosed by area under the concentration-time curve) when given at specified times in combination with 6 g/m2 ifosfamide (3 g/m2 at 8 AM on days 1 and 2) with mesna and 5 microg/kg/d filgrastim (from day 4 until the absolute neutrophil count is > 10,000/microL) every 21 days for six cycles."( Phase I trial of dose-escalated paclitaxel and carboplatin in combination with ifosfamide and filgrastim: preliminary results.
Palackdharry, CS, 1996
)
0.71
"The ongoing phase I study reported here sought to determine the maximum tolerated doses of paclitaxel (Taxol; Bristol-Myers Squibb Company, Princeton, NJ) and carboplatin when given at specific times in combination with ifosfamide, mesna, and filgrastim."( Phase I trial of dose-escalated paclitaxel and carboplatin in combination with ifosfamide and filgrastim: preliminary results.
Palackdharry, CS, 1997
)
0.71
" ifosfamide (5 g/m2), carboplatin (300 mg/m2), and etoposide given with WBH, as well as, day 2 and 3 post-WBH (100 mg/m2) for adult patients with refractory sarcoma."( Ifosfamide, carboplatin and etoposide (ICE) combined with 41.8 degrees C whole body hyperthermia in patients with refractory sarcoma.
Crahé, R; Deeken, M; Eleftheriadis, S; Gutsche, S; Katschinski, DM; Mentzel, M; Robins, HI; Storer, B; Wagner, T; Weiss, C; Wiedemann, GJ, 1996
)
2.65
" Effective modulatory doses of etanidazole could not be given with acceptable toxicity using this schedule."( Dose escalation of the hypoxic cell sensitizer etanidazole combined with ifosfamide, carboplatin, etoposide, and autologous hematopoietic stem cell support.
Antman, KH; Ayash, LJ; Coleman, N; Elias, AD; Frei, E; Ibrahim, J; McCauley, M; Mills, L; Schnipper, L; Schwartz, G; Teicher, BA; Warren, D; Wheeler, C, 1998
)
0.53
"The aims of the present open, randomized, single-blind (patient), single institution, phase II study were: i) to compare the therapeutic effectiveness and toxicity of two dosages and schedules of ifosfamide (IFO) in combination with cisplatin (CDDP) mainly in the neo-adjuvant setting of patients (pts) with locally advanced (stage III-IV) head and neck squamous cell cancer (HNSCC) (primary endpoint); ii) to assess the quality of life (QL) of pts included in the study before and after treatment (secondary endpoint)."( Clinical evaluation of two dosages and schedules of ifosfamide in combination with cisplatin in neo-adjuvant chemotherapy of patients with advanced (stage III-IV) head and neck squamous cell carcinoma: a phase II randomized study.
Cadeddu, G; Curreli, L; Dessi, D; Esu, S; Ghiani, M; Lai, P; Maccio, A; Mantovani, G; Massa, D; Mulas, C; Proto, E; Succu, G; Tore, G,
)
0.57
", hypotension (which requires catecholamine support) results in unique nephrotoxicity in combination with select chemotherapeutic agents."( Whole-body hyperthermia combined with ifosfamide and carboplatin causes hypotension and nephrotoxicity.
Brauer, LP; Kriz, W; Pagel, H; Prieshof, B; Robins, HI; Schramm, U; Weiss, C; Wiedemann, GJ, 1998
)
0.57
" Ifosfamide with G-CSF in combination with doxorubicin or paclitaxel achieves effective mobilization of PBPC and anti-tumor activity with minimal toxicity."( Ifosfamide in combination with paclitaxel or doxorubicin: regimens which effectively mobilize peripheral blood progenitor cells while demonstrating anti-tumor activity in patients with metastatic breast cancer.
Brettell, M; Briggs, P; Chapple, P; Francis, P; Gardyn, J; Gates, P; Januszewicz, EH; Juneja, S; Millward, MJ; Prince, HM; Quinn, M; Richardson, G; Rischin, D; Scarlett, J; Toner, GC; Wolf, M, 1999
)
2.66
" To investigate its optimal combinations, we studied the effect of 4-hydroperoxy ifosfamide (the active form of ifosfamide) in combination with other anticancer agents against two human cancer cell lines, MG-63 (an osteosarcoma cell line) and MOLT-3 cells (a T-cell leukemia cell line)."( Effects of 4-hydroperoxy ifosfamide in combination with other anticancer agents on human cancer cell lines.
Asakura, S; Kano, Y; Suzuki, K; Takagi, T; Yazawa, Y, 1999
)
0.83
"Evaluate response, duration of response, and toxicity of paclitaxel in combination with other drugs known to be effective in non-Hodgkin's lymphoma (NHL)."( Phase II study of paclitaxel in combination with mitoxantrone and ifosfamide/mesna for patients with relapsed or refractory non-Hodgkin's lymphoma after failure to cytarabine/cisplatin combination.
Cabanillas, F; Hagemeister, FB; McLaughlin, P; Preti, A; Rodriguez, J; Rodriguez, MA; Romaguera, JE; Sarris, AH; Younes, A, 1999
)
0.54
" Ifosfamide has been included in various drug combination protocols, usually on an empirical basis."( Ifosfamide-based drug combinations: preclinical evaluation of drug interactions and translation into the clinic.
Harstrick, A; Klaassen, U; Schleucher, N; Seeber, S; Vanhoefer, U, 2000
)
2.66
"Although whole-body hyperthermia combined with specific genotoxic chemotherapy can be shown to enhance neoplastic cell killing without a concomitant rise in bone marrow toxicity, nephrotoxicity can become treatment-limiting."( Nephrotoxicity of ifosfamide, carboplatin and etoposide (ICE) alone or combined with extracorporeal or radiant-heat-induced whole-body hyperthermia.
Filejski, W; Gerke, P; Robins, HI; Steinhoff, J; Wiedemann, GJ, 2000
)
0.64
" The patient received ifosfamide (5 g/m2, day 1), carboplatin (300 mg/m2, day 1), etoposide (150 mg/m2, days 2-3) combined with WBH at 41."( [Chemotherapy in combination with whole-body hyperthermia in advanced malignant pleural mesothelioma].
Bakhshandeh, A; Bruns, I; Eberhardt, K; Wiedemann, GJ, 2000
)
0.62
" The pharmacokinetics of docetaxel are not influenced by combination with ifosfamide, regardless of the drug sequence, but ifosfamide pharmacokinetics are changed by docetaxel, depending on the sequence of administration."( Pharmacokinetics of ifosfamide are changed by combination with docetaxel: results of a phase I pharmacologic study.
Bruno, R; De Bruijn, E; Highley, M; Locci-Tonelli, D; Pronk, L; Schrijvers, D; Van Oosterom, AT; Verweij, J, 2000
)
0.86
" We report the use of a continuous high dose infusion of ïfosfamide at a dose of 9g/m(2) over 3 days in combination with etoposide and epirubicin followed by autologous stem cell transplant with either BEAM or Melphalan/VP16 conditioning in this difficult group."( High dose ifosfamide in combination with etoposide and epirubicin followed by autologous stem cell transplantation in the treatment of relapsed/refractory Hodgkin's disease: a report on toxicity and efficacy.
Angus, B; Carey, PJ; Finney, RD; Galloway, MJ; Goff, DK; Haynes, A; Jackson, GH; Lennard, AL; Leonard, RC; McQuaker, IG; Proctor, SJ; Russell, N; Taylor, PR; Windebank, K, 2000
)
0.71
" was applied in combination with high-dose methotrexate (HDMTX) and adriamycin (ADM) within a three-drug regimen."( A comparison of methods of loco-regional chemotherapy combined with systemic chemotherapy as neo-adjuvant treatment of osteosarcoma of the extremity.
Bacchini, P; Bacci, G; Bertoni, F; De Giorgi, U; Ferrari, S; Fiorentini, G; Forni, C; Longhi, A; Mercuri, M; Picci, P; Rimondini, S; Tienghi, A, 2001
)
0.31
"To find the maximum tolerated dose for ifosfamide in combination with paclitaxel and carboplatin in small-cell lung cancer patients (SCLC), who are resistant to cyclophosphamide, doxorubicin and etoposide (CDE)."( Dose-finding and pharmacological study of ifosfamide in combination with paclitaxel and carboplatin in resistant small-cell lung cancer.
Beijnen, JH; Groen, HJ; Kerbush, T; Sleijfer, DT; Smit, EF; van Putten, JW; van Rijswijk, R, 2001
)
0.84
"Different dose schedules of ifosfamide were combined with fixed doses of paclitaxel 175 mg/m2 and carboplatin AUC 6 mg/ml min."( Dose-finding and pharmacological study of ifosfamide in combination with paclitaxel and carboplatin in resistant small-cell lung cancer.
Beijnen, JH; Groen, HJ; Kerbush, T; Sleijfer, DT; Smit, EF; van Putten, JW; van Rijswijk, R, 2001
)
0.87
"The maximum tolerated dose of this combination for patients with resistant SCLC is ifosfamide 2000 mg/m2 in combination with paclitaxel 175 mg/m2 and carboplatin AUC 6 mg/ml min administered on the first day of a 21-day cycle."( Dose-finding and pharmacological study of ifosfamide in combination with paclitaxel and carboplatin in resistant small-cell lung cancer.
Beijnen, JH; Groen, HJ; Kerbush, T; Sleijfer, DT; Smit, EF; van Putten, JW; van Rijswijk, R, 2001
)
0.8
"In this phase II study, activity and safety of neoadjuvant regional hyperthermia (RHT) combined with chemotherapy was investigated in 59 patients with primary advanced or recurrent high-risk soft-tissue sarcoma (STS)."( Neoadjuvant chemotherapy combined with regional hyperthermia (RHT) for locally advanced primary or recurrent high-risk adult soft-tissue sarcomas (STS) of adults: long-term results of a phase II study.
Abdel-Rahman, S; Aydemir, U; Falk, MH; Hiddemann, W; Issels, RD; Kurze, V; Sauer, H; Wendtner, C, 2001
)
0.31
" 54 patients were prospectively treated with four cycles of etoposide, ifosfamide and doxorubicin (EIA) combined with regional hyperthermia (RHT) followed by surgery, another four cycles of EIA without RHT and external beam radiation."( Treatment of primary, recurrent or inadequately resected high-risk soft-tissue sarcomas (STS) of adults: results of a phase II pilot study (RHT-95) of neoadjuvant chemotherapy combined with regional hyperthermia.
Abdel-Rahman, S; Baumert, J; Falk, MH; Hiddemann, W; Issels, RD; Krych, M; Santl, M; Wendtner, C, 2001
)
0.54
"Alternating COPP/ABVD and rapid alternating COPP/ABV/IMEP in combination with extended-field radiotherapy are equally effective in intermediate-stage Hodgkin's lymphoma and produce excellent long-term treatment results."( Rapidly alternating COPP/ABV/IMEP is not superior to conventional alternating COPP/ABVD in combination with extended-field radiotherapy in intermediate-stage Hodgkin's lymphoma: final results of the German Hodgkin's Lymphoma Study Group Trial HD5.
Anselmo, AP; Brosteanu, O; Diehl, V; Doelken, G; Duehmke, E; Engert, A; Franklin, J; Georgii, A; Greil, R; Hasenclever, D; Herrmann, R; Josting, A; Kirchner, H; Koch, P; Koch, T; Lathan, B; Loeffler, M; Munker, R; Paulus, U; Pfistner, B; Pfreundschuh, M; Rueffer, U; Schalk, KP; Sieber, M; Tesch, H; Wolf, J, 2002
)
0.31
"To determine the efficacy of neoadjuvant chemotherapy combined with regional hyperthermia (RHT) for local tumor control and overall survival (OS) in adult patients with retroperitoneal or visceral (RP/V) high-risk soft tissue sarcomas (HR-STS)."( Response to neoadjuvant chemotherapy combined with regional hyperthermia predicts long-term survival for adult patients with retroperitoneal and visceral high-risk soft tissue sarcomas.
Abdel-Rahman, S; Baumert, J; Baur, A; Hiddemann, W; Issels, RD; Krych, M; Lindner, LH; Wendtner, CM, 2002
)
0.31
"From 1991 to 1997, 58 patients with HR-STS at RP/V sites were prospectively treated with four cycles of etoposide, ifosfamide, and doxorubicin combined with RHT followed by surgery, adjuvant chemotherapy, and radiation."( Response to neoadjuvant chemotherapy combined with regional hyperthermia predicts long-term survival for adult patients with retroperitoneal and visceral high-risk soft tissue sarcomas.
Abdel-Rahman, S; Baumert, J; Baur, A; Hiddemann, W; Issels, RD; Krych, M; Lindner, LH; Wendtner, CM, 2002
)
0.52
"Response to neoadjuvant chemotherapy combined with RHT is predictive for an improved local tumor control resulting in a long-term survival benefit for patients with HR-STS at unfavorable RP/V sites; however, the impact of RHT has to be defined in a randomized phase III trial."( Response to neoadjuvant chemotherapy combined with regional hyperthermia predicts long-term survival for adult patients with retroperitoneal and visceral high-risk soft tissue sarcomas.
Abdel-Rahman, S; Baumert, J; Baur, A; Hiddemann, W; Issels, RD; Krych, M; Lindner, LH; Wendtner, CM, 2002
)
0.31
"To observe the efficacy of navelbine combined with ifosfamide and cisplatin in the treatment of advanced breast cancer."( [Clinical observation of the efficacy of navelbine combined with ifosfamide and cisplatin in the treatment of advanced breast cancer].
Luo, RC; You, CX; Zheng, H, 2003
)
0.81
"Navelbine in combination with ifosfamide and cisplatin is effective and safe in the treatment of advanced breast cancer."( [Clinical observation of the efficacy of navelbine combined with ifosfamide and cisplatin in the treatment of advanced breast cancer].
Luo, RC; You, CX; Zheng, H, 2003
)
0.85
" The pharmacologic features of this drug enable its combination with other antiblastic agents, such as vinorelbine, gemcitabine, paclitaxel and docetaxel."( Antiblastic drug combinations with ifosfamide: an update.
Badalamenti, G; Fulfaro, F; Gebbia, N; Russo, A; Valerio, MR, 2003
)
0.6
" In this study, one cycle of chemotherapy combined the following: ifosfamide: 3 g/m2 fixed dose (24-hour intravenous infusion) combined with mesna, day 1; gemcitabine: starting dose 1,000 mg/m2/d, escalating by 250 mg/m2 increments, days 1 and 15; cisplatin: starting dose 80 mg/m2, subsequently 100 mg/m2, day 15; in cohorts of at least 3 patients."( Phase I study with dose escalation of gemcitabine and cisplatin in combination with ifosfamide (GIP) in patients with non-small-cell lung carcinoma.
Billiart, I; Bourgeois, H; Chabrun, V; Chieze, S; Daban, A; Ferrand, V; Germain, T; Lemerre, D; Meurice, JC; Tourani, JM, 2004
)
0.79
"5 g m(-2), carboplatin 100 mg m(-2) and etoposide 150 mg m(-2), days 1-4, q 28 days, G-CSF 5 microg kg(-1) starting from day 6) alone and in combination with regional hyperthermia (RHT) in soft tissue sarcoma (STS) refractory to previous standard doxorubicin-ifosfamide-based chemotherapy."( Ifosfamide, carboplatin and etoposide (ICE) as second-line regimen alone and in combination with regional hyperthermia is active in chemo-pre-treated advanced soft tissue sarcoma of adults.
Abdel-Rahman, S; Fahn, W; Fiegl, M; Issels, RD; Schlemmer, M; Wendtner, CM, 2004
)
1.95
" A median of four courses of ICE were administered with RHT on days 1 and 3 (60 min, T(max) 42 degrees C)."( Ifosfamide, carboplatin and etoposide (ICE) as second-line regimen alone and in combination with regional hyperthermia is active in chemo-pre-treated advanced soft tissue sarcoma of adults.
Abdel-Rahman, S; Fahn, W; Fiegl, M; Issels, RD; Schlemmer, M; Wendtner, CM, 2004
)
1.77
"These results suggest that ICE alone or combined with RHT shows activity as second-line therapy in doxorubicin-ifosfamide-refractory STS."( Ifosfamide, carboplatin and etoposide (ICE) as second-line regimen alone and in combination with regional hyperthermia is active in chemo-pre-treated advanced soft tissue sarcoma of adults.
Abdel-Rahman, S; Fahn, W; Fiegl, M; Issels, RD; Schlemmer, M; Wendtner, CM, 2004
)
1.98
" We therefore investigated the therapeutic efficacy of STI571, alone or combined with chemotherapy, in human SCLC cells or tumors xenografted into nude mice."( In vivo efficacy of STI571 in xenografted human small cell lung cancer alone or combined with chemotherapy.
de Cremoux, P; Decaudin, D; Fréneaux, P; Judde, JG; Livartowski, A; Nemati, F; Pouillart, P; Poupon, MF; Sastre, X; Tran-Perennou, C, 2005
)
0.33
" Hence, we decided to explore the option of neoadjuvant chemotherapy using effective agents like ifosfamide and paclitaxel in combination with cisplatin in these patients."( Two- vs three-drug combination chemotherapy in advanced or recurrent head and neck cancer: a single institution experience of 361 patients.
Bakshi, AV; D'Cruz, AK; Deshmukh, CD; Mazumdar, AT; Mistry, RC; Pai, VR; Parikh, DM; Parikh, PM; Pathak, KA, 2004
)
0.54
"Patients with progressing platinum-sensitive or resistant disease were included in 5 dose levels consisting of PLD (25 mg/m2 to 45 mg/m2, day 1) combined with a fixed IFO dose administered as a continuous infusion (1700 mg/m2/d, day 1 to 3) to define the MTD on the basis of acute toxicity during the first 2 cycles, then confirm the MTD, by the evaluation of delayed toxicity (hand-foot syndrome)."( Phase I study of pegylated liposomal doxorubicin in combination with ifosfamide in pretreated ovarian cancer patients.
Bourgeois, H; Chabrun, V; Chieze, S; Cure, H; Ferru, A; Guastalla, JP; Joly, F; Pujade-Lauraine, E; Tourani, JM, 2006
)
0.57
"To evaluate safety and pharmacokinetics and to establish the maximum tolerated dose of glufosfamide when administered in combination with gemcitabine in advanced solid tumors."( A Phase 1 dose-escalation trial of glufosfamide in combination with gemcitabine in solid tumors including pancreatic adenocarcinoma.
Chiorean, EG; Colowick, AB; Dragovich, T; Hamm, J; Jung, DT; Kroll, S; Langmuir, VK; Loehrer, PJ; Tidmarsh, GF, 2008
)
0.35
"Phase I data indicate that full dose glufosfamide (4,500 mg/m(2)) can be given safely in combination with gemcitabine."( A Phase 1 dose-escalation trial of glufosfamide in combination with gemcitabine in solid tumors including pancreatic adenocarcinoma.
Chiorean, EG; Colowick, AB; Dragovich, T; Hamm, J; Jung, DT; Kroll, S; Langmuir, VK; Loehrer, PJ; Tidmarsh, GF, 2008
)
0.35
"Cohorts of four patients with metastatic soft tissue sarcomas received up to five cycles of intravenous ifosfamide 3000 mg/m2 on days 1- 3 in combination with escalating doses of intravenous Myocet on day 1 every 3 weeks until dose limiting toxicity (DLT) in at least one patient."( Phase I study of non-pegylated liposomal doxorubicin in combination with ifosfamide in adult patients with metastatic soft tissue sarcomas.
Barbato, A; Bertuzzi, A; Di Comite, G; Lutman, RF; Mussi, C; Santoro, A; Stroppa, E, 2010
)
0.81
"To compare the radiological criteria RECIST, WHO, and tumor volume for evaluation of tumor response in patients with soft tissue sarcomas (STS) showing either good or poor pathohistological response to neoadjuvant chemotherapy combined with regional hyperthermia, and to examine the dependence of the findings on the applied thermal dose."( Comparison of radiological and pathohistological response to neoadjuvant chemotherapy combined with regional hyperthermia (RHT) and study of response dependence on the applied thermal parameters in patients with soft tissue sarcomas (STS).
Abdel-Rahman, S; Issels, RD; Lindner, LH; Reiser, MF; Santl, M; Stahl, R; Wang, T, 2009
)
0.35
"The effect of immunotherapy with interleukin-18 (IL-18) in combination with preoperative chemotherapy on the postoperative progression of pulmonary metastasis was examined using a spontaneous pulmonary metastasis model of mouse osteosarcoma."( Immunotherapy with interleukin-18 in combination with preoperative chemotherapy with ifosfamide effectively inhibits postoperative progression of pulmonary metastases in a mouse osteosarcoma model.
Futani, H; Hata, M; Kogoe, N; Nakasho, K; Ohyama, H; Okamura, H; Terada, N; Yamada, N; Yamanegi, K, 2009
)
0.58
"Paclitaxel combined with ifosfamide was effective and tolerable in anthracycline-/docetaxel-pretreated MBC."( Paclitaxel combined with ifosfamide in anthracycline- and docetaxel-pretreated metastatic breast cancer: activity independence of prior docetaxel resistance.
Chang, H; Choi, HJ; Chung, HC; Kim, JH; Kim, SI; Kim, YT; Koo, JS; Moon, YW; Park, BW; Park, S; Roh, JK; Sohn, JH, 2010
)
0.97
"To investigate the feasibility and efficacy of rituximab combined with high-dose chemotherapy supported by autologous peripheral blood stem cell transplantation (ASCT) in patients with aggressive B-cell non-Hodgkin lymphoma (NHL)."( [A prospective multicenter study of rituximab combined with high-dose chemotherapy and autologous peripheral blood stem cell transplantation for aggressive B-cell lymphoma].
Cen, XN; Chen, H; Han, MZ; Han, XH; He, XH; Huang, H; Huang, HQ; Jiang, WQ; Liu, P; Ma, J; Ren, HY; Shen, XM; Shi, YK; Wang, C; Wang, JM; Yang, S; Zhou, SY; Zhu, J, 2009
)
0.35
"We evaluated the feasibility and toxicity of bevacizumab in combination with sequential high-dose (HD) ifosfamide, carboplatin and etoposide refractory to standard chemotherapy in patients with sarcoma and germ cell cancer (GCC)."( Bevacizumab in combination with sequential high-dose chemotherapy in solid cancer, a feasibility study.
Arnold, D; Behlendorf, T; Jordan, K; Kegel, T; Mueller, LP; Schmoll, HJ; Sippel, C; Voigt, W; Wolf, HH, 2010
)
0.58
" Fifty-nine patients underwent primary surgery by wide or marginal excision and were subsequently randomized to receive radiotherapy alone or in combination with six courses of chemotherapy consisting of ifosfamide, DTIC, and doxorubicin administered in 14-day intervals supported by G-CSF on days 5-13."( Intensified adjuvant IFADIC chemotherapy in combination with radiotherapy versus radiotherapy alone for soft tissue sarcoma: long-term follow-up of a prospective randomized feasibility trial.
Abdolvahab, F; Brodowicz, T; Dominkus, M; Ebm, C; Fakhrai, N; Jantsch, M; Kauer-Dorner, D; Kostler, WJ; Pokrajac, B; Zielinski, CC, 2010
)
0.55
" The AIM regimen combined with radiation therapy may be an effective treatment option for this disease."( [Long-term remission of Langerhans cell sarcoma by AIM regimen combined with involved-field irradiation].
Fujikawa, Y; Ichikawa, N; Kirihara, T; Kobayashi, H; Nakamura, S; Sato, K; Shimizu, I; Sumi, M; Takeda, W; Uehara, T; Ueki, T; Ueno, M; Watanabe, M, 2012
)
0.38
" We performed a multi-center phase II trial investigating the safety and efficacy of ofatumumab, a monoclonal antibody against CD20, combined with ICE or DHAP second-line therapy in patients with relapsed or refractory DLBCL, grade 3b follicular lymphoma, or transformed follicular lymphoma."( Ofatumumab in combination with ICE or DHAP chemotherapy in relapsed or refractory intermediate grade B-cell lymphoma.
Czuczman, MS; Edvardsen, K; Fayad, L; Fecteau, D; Fennessy, M; Henkel, K; Jewell, RC; Joyce, R; Kharfan-Dabaja, MA; Liao, Q; Lisby, S; Lossos, IS; Matasar, MJ; Moskowitz, CH; Rodriguez, MA; Shea, TC; Singh, RP; Spitzer, G, 2013
)
0.39
" In the present analysis, we retrospectively investigated the feasibility and effectiveness of bevacizumab combined with ICE in patients with glioblastoma at second relapse during ICE treatment."( Retrospective analysis of bevacizumab in combination with ifosfamide, carboplatin, and etoposide in patients with second recurrence of glioblastoma.
Arakawa, Y; Fujimoto, K; Kikuchi, T; Kunieda, T; Miyamoto, S; Mizowaki, T; Murata, D; Takagi, Y; Takahashi, JC, 2013
)
0.63
" We conducted a dose-finding and pharmacokinetic (PK)/pharmacodynamics study of pazopanib combined with two different schedules of ifosfamide."( Pazopanib exposure decreases as a result of an ifosfamide-dependent drug-drug interaction: results of a phase I study.
Boers-Sonderen, MJ; de Bruijn, P; Eskens, FA; Hamberg, P; Sleijfer, S; Suttle, AB; van der Graaf, WT; van Herpen, CM; Verweij, J, 2014
)
0.86
"In a 3+3+3 design, patients with advanced solid tumours received escalating doses of oral pazopanib combined with ifosfamide either given 3 days continuously or given 3-h bolus infusion daily for 3 days (9 g m(-2) per cycle, every 3 weeks)."( Pazopanib exposure decreases as a result of an ifosfamide-dependent drug-drug interaction: results of a phase I study.
Boers-Sonderen, MJ; de Bruijn, P; Eskens, FA; Hamberg, P; Sleijfer, S; Suttle, AB; van der Graaf, WT; van Herpen, CM; Verweij, J, 2014
)
0.87
" Pazopanib with continuous ifosfamide infusion appeared to be safe up to 1000 mg per day, while combination with bolus infusion ifosfamide turned out to be too toxic based on a variety of adverse events."( Pazopanib exposure decreases as a result of an ifosfamide-dependent drug-drug interaction: results of a phase I study.
Boers-Sonderen, MJ; de Bruijn, P; Eskens, FA; Hamberg, P; Sleijfer, S; Suttle, AB; van der Graaf, WT; van Herpen, CM; Verweij, J, 2014
)
0.96
"Continuous as opposed to bolus infusion ifosfamide can safely be combined with pazopanib."( Pazopanib exposure decreases as a result of an ifosfamide-dependent drug-drug interaction: results of a phase I study.
Boers-Sonderen, MJ; de Bruijn, P; Eskens, FA; Hamberg, P; Sleijfer, S; Suttle, AB; van der Graaf, WT; van Herpen, CM; Verweij, J, 2014
)
0.93
"To investigate the electronic anti-nausea instrument (EANI) combined with hydrochloride palonosetron for prevention of chemotherapy-induced nausea and vomiting following highly emetogenic chemotherapy."( Phase II study on EANI combined with hydrochloride palonosetron for prevention of chemotherapy-induced nausea and vomiting following highly emetogenic chemotherapy.
Guo, JX; Huang, XE; Liu, J; Liu, YC; Wei, W; Xiao, Y, 2014
)
0.4
"Patients who received highly emetogenic chemotherapy were randomly assigned to a treatment group (60 patients) treated with EANI combined with hydrochloride palonosetron, and control group (also 60 patients) given only hydrochloride palonosetron."( Phase II study on EANI combined with hydrochloride palonosetron for prevention of chemotherapy-induced nausea and vomiting following highly emetogenic chemotherapy.
Guo, JX; Huang, XE; Liu, J; Liu, YC; Wei, W; Xiao, Y, 2014
)
0.4
"EANI combined with hydrochloride palonosetron for prevention of nausea and vomiting induced by chemotherapy could be more effective than hydrochloride palonosetron alone, and can be recommended for use in prevention and treatment of chemotherapy-induced nausea and vomiting following highly emetogenic chemotherapy."( Phase II study on EANI combined with hydrochloride palonosetron for prevention of chemotherapy-induced nausea and vomiting following highly emetogenic chemotherapy.
Guo, JX; Huang, XE; Liu, J; Liu, YC; Wei, W; Xiao, Y, 2014
)
0.4
" The aim of this retrospective study was to evaluate the activity and toxicity of bevacizumab combined with chemotherapy in the treatment of recurrence or platinum-refractory ovarian cancer."( Bevacizumab combined with chemotherapy in the treatment of recurrence or platinum-refractory ovarian cancer: a retrospective study of 37 cases.
Li, Y; Shang, YM; Yang, Y; Zheng, H, 2014
)
0.4
"Totally, 37 ovarian cancer patients with complete data who treated with bevacizumab combined with chemotherapy were reviewed from the databases of Beijing Cancer hospital and included in this retrospective study."( Bevacizumab combined with chemotherapy in the treatment of recurrence or platinum-refractory ovarian cancer: a retrospective study of 37 cases.
Li, Y; Shang, YM; Yang, Y; Zheng, H, 2014
)
0.4
" The aim of this study was to assess the efficacy and safety of ifosfamide in combination with carboplatin and etoposide (ICE) in previously untreated patients with SCLC."( Efficacy and safety of ifosfamide in combination with carboplatin and etoposide in small cell lung cancer.
Koo, DH; Lee, HS; Lee, SS; Lee, YG; Lim, SY; Nam, H; Oh, S; Song, JU, 2015
)
0.97
"To evaluate the efficacy and safety of gemcitabine combined with ifosfamide (GI regimen)in patients with recurrent or metastatic nasopharyngeal carcinoma after failure of platinum-based chemotherapy."( [Efficacy and safety evaluation of gemcitabine combined with ifosfamide in patients with advanced nasopharyngeal carcinoma after failure of platinum-based chemotherapy].
Dong, M; Gui, L; He, X; Hu, S; Jia, B; Liu, P; Qin, Y; Yang, J; Yang, S; Zhang, C; Zhou, S, 2015
)
0.9
"Based on preclinical data for the antitumour effect of zoledronate in osteosarcoma, we assessed whether zoledronate combined with chemotherapy and surgery improved event-free survival in children and adults with osteosarcoma."( Zoledronate in combination with chemotherapy and surgery to treat osteosarcoma (OS2006): a randomised, multicentre, open-label, phase 3 trial.
Blay, JY; Bompas, E; Bonnet, N; Brisse, H; Brugières, L; Chevance, A; Corradini, N; Entz-Werlé, N; Gentet, JC; Gomez-Brouchet, A; Gouin, F; Guinebretière, JM; Italiano, A; Le Deley, MC; Lervat, C; Marec-Bérard, P; Mascard, E; Pacquement, H; Penel, N; Petit, P; Piperno-Neumann, S; Rédini, F; Tabone, MD, 2016
)
0.43
" Balanced randomisation between the two groups was done centrally with online randomisation software, based on a minimisation algorithm taking into account centre, age, combined with chemotherapy regimen, and risk group (resectable primary and no metastasis vs other)."( Zoledronate in combination with chemotherapy and surgery to treat osteosarcoma (OS2006): a randomised, multicentre, open-label, phase 3 trial.
Blay, JY; Bompas, E; Bonnet, N; Brisse, H; Brugières, L; Chevance, A; Corradini, N; Entz-Werlé, N; Gentet, JC; Gomez-Brouchet, A; Gouin, F; Guinebretière, JM; Italiano, A; Le Deley, MC; Lervat, C; Marec-Bérard, P; Mascard, E; Pacquement, H; Penel, N; Petit, P; Piperno-Neumann, S; Rédini, F; Tabone, MD, 2016
)
0.43
"The aim of this study was to compare asparaginase-related toxicities in two asparaginase preparations, namely native Escherichia coli L-asparaginase (L-ASP) and pegylated asparaginase (PEG-ASP) in combination with ifosfamide, methotrexate, etoposide, and prednisolone (IMEP) in natural killer (NK)/T-cell lymphoma (NTCL)."( Comparison of Native Escherichia coli L-Asparaginase versus Pegylated Asparaginase, in Combination with Ifosfamide, Methotrexate, Etoposide, and Prednisolone, in Extranodal NK/T-Cell Lymphoma, Nasal Type.
Cho, YS; Heo, DS; Jung, SH; Keam, B; Kim, DW; Kim, HJ; Kim, IH; Kim, M; Kim, TM; Lee, JY; Lee, SH; Ock, CY, 2018
)
0.88
"This phase-I/phase-II study evaluated panobinostat in combination with ifosfamide, carboplatin, etoposide (P-ICE) in relapsed/refractory classical Hodgkin lymphoma."( Phase-I and randomized phase-II trial of panobinostat in combination with ICE (ifosfamide, carboplatin, etoposide) in relapsed or refractory classical Hodgkin lymphoma.
Claret, L; Copeland, AR; Fanale, MA; Fayad, LE; Feng, L; Fowler, N; Hagemeister, FB; Hu, B; Nastoupil, LJ; Neelapu, S; Nieto, Y; Oki, Y; Rodriguez, MA; Romaguera, J; Samaniego, F; Turturro, F; Westin, JR; Younes, A, 2018
)
0.94
" This phase II study evaluated the efficacy and safety of IFM combination with recommended current supportive therapy for recurrent SCLC in second-line and heavily treated setting."( A phase II trial of Ifosfamide combination with recommended supportive therapy for recurrent SCLC in second-line and heavily treated setting.
Fukatsu, A; Hase, T; Hasegawa, Y; Hayashi, H; Kawada, K; Kondo, M; Morise, M; Nomura, F; Sokai, A; Tanaka, I, 2018
)
0.8
" We conducted a single-center phase 1 study evaluating dose-escalated ibrutinib, in a 3-by-3 design, in combination with rituximab, ifosfamide, carboplatin, and etoposide (R-ICE) in physiologically transplant-eligible rel/ref DLBCL patients."( A phase 1 study of ibrutinib in combination with R-ICE in patients with relapsed or primary refractory DLBCL.
Courtien, AI; Devlin, SM; Drullinsky, P; Gerecitano, J; Kumar, A; Matasar, MJ; McCall, SJ; Miller, ST; Moskowitz, CH; Noy, A; Palomba, ML; Portlock, CS; Sauter, CS; Schoder, H; Straus, DJ; Younes, A; Zelenetz, AD, 2018
)
0.69
"Considering the physical condition of patient, the patient underwent surgical resection of the right lung lesion after receiving endostar combined with chemotherapy and maintained endostar alone for 47 cycles."( Endostar combined with chemotherapy in a pediatric osteosarcoma with pulmonary metastasis and malignant pleural effusion: A case report.
Dong, Y; Jiang, S; Wang, G, 2017
)
0.46
"Olaratumab (OLA), a monoclonal antibody against platelet-derived growth factor receptor alpha (PDGFRα), has recently been used against soft-tissue sarcoma (STS) combined with doxorubicin (DOX), with limited efficacy."( Olaratumab combined with doxorubicin and ifosfamide overcomes individual doxorubicin and olaratumab resistance of an undifferentiated soft-tissue sarcoma in a PDOX mouse model.
Bouvet, M; Hayashi, K; Higuchi, T; Hoffman, RM; Igarashi, K; Kimura, H; Miwa, S; Miyake, K; Oshiro, H; Razmjooei, S; Singh, SR; Sugisawa, N; Tsuchiya, H; Yamamoto, N; Zhang, Z, 2019
)
0.78
" We performed a phase I study to determine the safety and maximum tolerated dose (MTD) of selinexor when combined with high-dose dexamethasone, ifosfamide, carboplatin and etoposide (DICE) in relapsed/refractory (R/R) T-cell lymphoma (TCL) and natural-killer/T-cell lymphoma (NKTL)."( Phase I study of selinexor in combination with dexamethasone, ifosfamide, carboplatin, etoposide chemotherapy in patients with relapsed or refractory peripheral T-cell or natural-killer/T-cell lymphoma
Chan, JY; Farid, M; Lim, C; Lim, ST; Martin, P; Poon, E; Somasundaram, N; Tang, T; Tao, M; Toh, SQ; Yan, SX; Yunon, MJ, 2021
)
1.06
" We conducted a phase 1 trial to evaluate the safety of olaratumab and determine a recommended dose in combination with three different chemotherapy regimens in children."( Phase 1 trial of olaratumab monotherapy and in combination with chemotherapy in pediatric patients with relapsed/refractory solid and central nervous system tumors.
Bishop, MW; Borinstein, SC; DuBois, SG; Hingorani, P; Krystal, J; Laetsch, TW; Levy, DE; Mascarenhas, L; Mo, G; Muscal, JA; Ogawa, C; Shahir, A; Slotkin, EK; Weigel, BJ; Wright, J, 2021
)
0.62
" Romidepsin (Ro) and brentuximab vedotin (Bv), combined with ifosfamide, carboplatin, and etoposide (ICE) has not been significantly studied in PTCL."( Use of ifosfamide, carboplatin and etoposide in combination with brentuximab vedotin or romidepsin based on CD30 positivity in relapsed/refractory peripheral T-cell lymphoma.
Gentille, C; Joshi, J; Pingali, SR; Randhawa, J; Sarfraz, H; Shah, S, 2022
)
1.42
"To investigate the value of contrast-enhanced computed tomography (CECT) radiomics features in predicting the efficacy of epirubicin combined with ifosfamide in patients with pulmonary metastases from soft tissue sarcoma."( Prediction of the therapeutic efficacy of epirubicin combined with ifosfamide in patients with lung metastases from soft tissue sarcoma based on contrast-enhanced CT radiomics features.
Jiang, X; Li, M; Ma, ST; Miao, L; Wang, YM; Zhang, HH, 2022
)
1.16
"A retrospective analysis of 51 patients with pulmonary metastases from soft tissue sarcoma who received the chemotherapy regimen of epirubicin combined with ifosfamide was performed, and efficacy was evaluated by Recist1."( Prediction of the therapeutic efficacy of epirubicin combined with ifosfamide in patients with lung metastases from soft tissue sarcoma based on contrast-enhanced CT radiomics features.
Jiang, X; Li, M; Ma, ST; Miao, L; Wang, YM; Zhang, HH, 2022
)
1.15
"This prospective single-arm phase II clinical trial aimed to evaluate the efficacy and safety of pegylated liposomal doxorubicin (PLD) combined with ifosfamide (IFO) as the first-line treatment for patients with advanced or metastatic soft-tissue sarcoma (STS)."( Pegylated Liposomal Doxorubicin Combined with Ifosfamide for Treating Advanced or Metastatic Soft-tissue Sarcoma: A Prospective, Single-arm Phase II Study.
Chen, H; Chen, Y; Huang, M; Jiang, S; Liu, X; Luo, Z; Miao, J; Wang, C; Wang, H; Wang, J; Wu, X; Xia, J; Xu, Y; Yan, W; Yao, W; Yu, L; Zhang, X, 2022
)
1.18
"Patients received PLD (30 mg/m2; day 1) in combination with IFO (1."( Pegylated Liposomal Doxorubicin Combined with Ifosfamide for Treating Advanced or Metastatic Soft-tissue Sarcoma: A Prospective, Single-arm Phase II Study.
Chen, H; Chen, Y; Huang, M; Jiang, S; Liu, X; Luo, Z; Miao, J; Wang, C; Wang, H; Wang, J; Wu, X; Xia, J; Xu, Y; Yan, W; Yao, W; Yu, L; Zhang, X, 2022
)
0.98
" We conducted an investigator initiated, single-center, open-label, prospective phase 1 study evaluating the safety and efficacy of CFZ in combination with rituximab, ifosfamide, carboplatin, and etoposide (C-R-ICE) in high-dose chemotherapy with autologous stem cell transplant (HDC-ASCT) eligible patients with R/R DLBCL (NCT01959698)."( Carfilzomib combined with rituximab, ifosfamide, carboplatin, and etoposide for relapsed or refractory DLBCL.
Anampa-Guzmán, A; Block, A; Darrall, A; DeMarco, J; Ghione, P; Groman, A; Hernandez-Ilizaliturri, FJ; Hutson, A; Johnson, M; Kader, A; Kostrewa, J; Lund, I; Mavis, C; McWhite, K; Mohr, A; Nichols, J; Przespolewski, E; Sait, SJ; Sundaram, S; Thomas, R; Torka, P; Wong, J, 2023
)
1.38
" The purpose of this study was to explore the efficacy and safety of programmed cell death 1 (PD-1) blockade combined with ICE regimen (P-ICE) in the treatment of R/R DLBCL patients."( PD-1 blockade combined with ICE regimen in relapsed/refractory diffuse large B-cell lymphoma.
Bai, B; Gao, Y; He, Y; Huang, C; Huang, H; Ping, L; Shi, L; Wang, X, 2023
)
0.91
" Carfilzomib, an irreversible proteasome inhibitor, can overcome acquired rituximab-chemotherapy resistance and, when combined with R-ICE, improves outcomes in patients with R/R DLBCL."( Population Pharmacokinetics and Pharmacodynamics of Carfilzomib in Combination with Rituximab, Ifosfamide, Carboplatin, and Etoposide in Adult Patients with Relapsed/Refractory Diffuse Large B Cell Lymphoma.
Burke, SM; Ghasemi, M; Goey, AKL; Hernandez-Ilizaliturri, FJ; Lin, LH; Mager, DE; Mavis, CK; Nichols, JR; Torka, P, 2023
)
1.13
" Further research is needed to identify sources of variability in response to treatment with carfilzomib in combination with R-ICE."( Population Pharmacokinetics and Pharmacodynamics of Carfilzomib in Combination with Rituximab, Ifosfamide, Carboplatin, and Etoposide in Adult Patients with Relapsed/Refractory Diffuse Large B Cell Lymphoma.
Burke, SM; Ghasemi, M; Goey, AKL; Hernandez-Ilizaliturri, FJ; Lin, LH; Mager, DE; Mavis, CK; Nichols, JR; Torka, P, 2023
)
1.13

Bioavailability

The bioavailability of oral N,3-bis(2-chloroethyl) tetrahydro-2H-1,3,2-oxazaphosphorin-2-amine 2-oxide (ifosfamide) (500-mg gelatine capsules) was investigated in 18 patients with bronchogenic carcinoma. Recent clinical trials suggest that oral mesna has adequate bioavailability (roughly 50% by urinary thiol measurements) to prevent urotoxicity.

ExcerptReferenceRelevance
" The stability of ifosfamide and its high bioavailability have allowed its use in chronic, 7-day ambulatory IV infusions, with decreased toxicity and hospitalization."( Novel approaches with ifosfamide in small cell lung cancer.
Cerny, T; De Campos, E; Lind, M; Thatcher, N, 1992
)
0.93
" We have studied the feasibility and bioavailability of a subcutaneously (s."( Subcutaneous continuous infusion of ifosfamide and cyclophosphamide in ambulatory cancer patients: bioavailability and feasibility.
Brunner, KW; Cerny, T; Graf, A; Küpfer, A; Rohner, P; Zeugin, T, 1991
)
0.56
" Recent clinical trials suggest that oral mesna has adequate bioavailability (roughly 50% by urinary thiol measurements) to prevent urotoxicity in high-dose ifosfamide regimens."( Chemoprotectants for cancer chemotherapy.
Dorr, RT, 1991
)
0.48
" The bioavailability of ifosfamide after oral administration exceeds 95%."( Ifosfamide and mesna.
Dana, WJ; Schoenike, SE, 1990
)
2.03
" We have studied in patients with advanced cancer the feasibility and bioavailability of a subcutaneously administered isotonic and neutral (pH 7) IFO solution given continuously over 10 h for up to 5 days."( Bioavailability of subcutaneous ifosfamide and feasibility of continuous outpatient application in cancer patients.
Brunner, KW; Cerny, T; Küpfer, A; Zeugin, T, 1990
)
0.56
"The bioavailability of oral N,3-bis(2-chloroethyl) tetrahydro-2H-1,3,2-oxazaphosphorin-2-amine 2-oxide (ifosfamide) (500-mg gelatine capsules) was investigated in 18 patients with bronchogenic carcinoma."( Pharmacokinetics and bioavailability of oral ifosfamide.
Drings, P; Wagner, T, 1986
)
0.75
" There was a proportionate increase in the AUC for the 5-g oral dose, indicating 100% bioavailability at all three dose levels."( Bioavailability of ifosfamide in patients with bronchial carcinoma.
Cerny, T; Margison, JM; Thatcher, N; Wilkinson, PM, 1986
)
0.6
"The bioavailability of orally administered sodium 2-mercaptoethane sulfonate (mesna, Uromitexan drink ampoules) was tested in 18 healthy probands and in 5 tumor patients."( Bioavailability of orally administered mesna.
Breuel, HP; Burkert, H; Lücker, PW; Wetzelsberger, N, 1984
)
0.27
"Three bromine-ifosfamide analogues: racemic chlorobromofosfamide (+/-)-(R,S)-1, its levorotatory enantiomer (-)-(S)-2 and racemic bromofosfamide (+/-)-(R,S)-3 showed considerable stereoselective differences in their pharmacokinetics and bioavailability depending on the route of administration and regimen of dosage studies in rats."( Pharmacokinetic-stereoselective differentiation of some isomeric analogues of ifosfamide.
Hładoń, B; Kinas, R; Kuśnierczyk, H; Laskowska, H; Sloderbach, A; Sochacki, M,
)
0.72
" Its pharmacokinetics and bioavailability were studied in female mice following intravenous and oral administration of the dose of 50 mg/kg."( Pharmacokinetics of (-)-(S)-bromofosfamide after intravenous and oral administration in mice.
Kobylińska, K; Kobylińska, M; Sobik, B, 2001
)
0.31
" On the other hand, an increase in the bioavailability of some medicaments have been observed when these are ingested together with grapefruit."( Inhibitory effect of naringin on the micronuclei induced by ifosfamide in mouse, and evaluation of its modulatory effect on the Cyp3a subfamily.
Alvarez-González, I; Dorado, V; Espinosa-Aguirre, JJ; Madrigal-Bujaidar, E, 2001
)
0.55
" Bioavailability of TRO could not be calculated directly, because TRO is only available as an oral formulation."( New insights into the clinical pharmacokinetics of trofosfamide.
Brinker, A; Brüggemann, SK; Kisro, J; Letsch, C; Wagner, T, 2002
)
0.31
" The bioavailability is nearly 100% after oral application, and the main metabolites are 4-hydroxytrofosfamide, and 4-hydroxyifosfamide."( Hypersensitivity pneumonitis associated with the use of trofosfamide.
Hartmann, JT; Kanz, L; Kopp, HG, 2004
)
0.53
"Oral bioavailability (F) is a product of fraction absorbed (Fa), fraction escaping gut-wall elimination (Fg), and fraction escaping hepatic elimination (Fh)."( Physicochemical space for optimum oral bioavailability: contribution of human intestinal absorption and first-pass elimination.
Chang, G; El-Kattan, A; Miller, HR; Obach, RS; Rotter, C; Steyn, SJ; Troutman, MD; Varma, MV, 2010
)
0.36
" They can also block the action of enzymes or receptors used for endogenous metabolism or affect the efficacy and/or bioavailability of a coadministered drug."( Xenobiotic metabolomics: major impact on the metabolome.
Gonzalez, FJ; Idle, JR; Johnson, CH; Patterson, AD, 2012
)
0.38
" Oral bioavailability in rats was 48-73% of parenteral administration, and antitumor activity in mice was equivalent by both routes."( Anticancer activity of stabilized palifosfamide in vivo: schedule effects, oral bioavailability, and enhanced activity with docetaxel and doxorubicin.
Amedio, J; Jones, B; Komarnitsky, P; Miller, GT; Wallner, BP, 2012
)
0.65
" Our patient was subsequently enrolled on a phase 1 clinical trial of a novel, orally bioavailable bromodomain and extra terminal inhibitor, GSK525762 (NCT01587703)."( NUT midline carcinoma: an aggressive intrathoracic neoplasm.
Costello, BA; Dronca, RS; French, CA; Hilton, J; Marks, RS; Molina, JR; Nerby, CL; Parikh, SA; Peddareddigari, VG; Roden, AC; Shapiro, GI, 2013
)
0.39
"The ATP-binding cassette transporter P-glycoprotein (P-gp) is known to limit both brain penetration and oral bioavailability of many chemotherapy drugs."( A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
Ambudkar, SV; Brimacombe, KR; Chen, L; Gottesman, MM; Guha, R; Hall, MD; Klumpp-Thomas, C; Lee, OW; Lee, TD; Lusvarghi, S; Robey, RW; Shen, M; Tebase, BG, 2019
)
0.51

Dosage Studied

Ifosfamide has important activity in pretreated soft tissue sarcomas (STS) Recent data support a clinically significant dose-response relationship for this agent. A daily dosage of 50 to 60 mg/kg on 5 consecutive days produced the best results.

ExcerptRelevanceReference
" Experiments in 214 DS carcinosarcoma bearing Wistar rats have shown that BA 1, at a dosage of only about 12 percent LD50 (150 mg kg) and negligible lethality (1."( [Demonstration of tumor inhibiting properties of a strongly immunostimulating low-molecular weight substance. Comparative studies with ifosfamide on the immuno-labile DS carcinosarcoma. Stimulation of the autoimmune activity for approx. 20 days by BA 1, a
Ardenne, M; Reitnauer, PG, 1975
)
0.46
" The combination treatments with 6-thioguanine and each of six agents, especially with ACNU, showed a distinct therapeutic effect against the early L-1210 leukemia at dosage levels not producing any significant antitumor activity with each agent alone (ip-ip)."( Combination chemotherapy of 6-thioguanine with various antitumor agents against murine leukemia L-1210.
Fujimoto, S; Horikoshi, N; Hoshino, A; Inagaki, J, 1977
)
0.26
" Similarly, there was a significant improvement in response duration for the low dosage regimen."( Ifosfamide in the treatment of recurrent or disseminated lung cancer: a phase II study of two dose schedules.
Costanzi, JJ; Gagliano, R; Hokanson, JA; Loukas, D; Panettiere, FJ, 1978
)
1.7
" A daily dosage of 50 to 60 mg/kg ifosfamide on 5 consecutive days produced the best results."( Evaluation of a cooperative clinical study of the cytostatic agent ifosfamide.
Brock, N; Burkert, H; Fichtner, E; Schnitker, J, 1976
)
0.77
" A policy of no dosage reduction is feasible in patients receiving combination chemotherapy with ifosfamide given as a 24-hour intravenous (IV) infusion, which is much more convenient than the more commonly used 4- to 5-day fractionated regimen."( Novel approaches with ifosfamide in small cell lung cancer.
Cerny, T; De Campos, E; Lind, M; Thatcher, N, 1992
)
0.82
" It could be tested using alternate dosage schedules and in combination with other agents in treating this highly resistant neoplasm."( A phase II evaluation of ifosfamide and mesna in unresectable diffuse malignant mesothelioma. A Southwest Oncology Group study.
Balcerzak, SP; Berenberg, JL; Keppen, MD; Metch, B; Militello, L; Pierce, HI; Zidar, BL, 1992
)
0.59
" Additional studies are needed to determine the role of ifosfamide in well-defined patient subsets, to assess its cross-resistance with other alkylating agents, and to determine the slope of the dose-response curve in patients with breast cancer."( Activity of ifosfamide in breast cancer.
Hortobagyi, GN, 1992
)
0.91
" The predictive capability of a published nomogram is restricted by differences in dosage regimens and encephalopathic classifications."( Ifosfamide-induced neurotoxicity: a case report and review of the literature.
Eaton, VE; Miller, LJ, 1992
)
1.73
" The highest percentages were reported in studies using doses of doxorubicin of 60 mg/m2 or higher, with a suggested dose-response correlation."( Doxorubicin (or epidoxorubicin) combined with ifosfamide in the treatment of adult advanced soft tissue sarcomas.
Palumbo, R; Santi, L; Sogno, G; Toma, S; Venturino, A, 1992
)
0.54
" Myelosuppression and granulocytopenia correlated better with day 1 versus day 5 ifosfamide pharmacokinetics suggesting that the alteration of ifosfamide pharmacology with multiple dosing has a significant effect on drug activity."( Clinical pharmacokinetics of ifosfamide in combination with N-acetylcysteine.
Ayele, W; Benvenuto, JA; Legha, SS; Newman, RA; Nicaise, C; Raber, MN, 1992
)
0.8
" Both drugs show an increased therapeutic index when given as a fractionated dosage over several days."( Subcutaneous continuous infusion of ifosfamide and cyclophosphamide in ambulatory cancer patients: bioavailability and feasibility.
Brunner, KW; Cerny, T; Graf, A; Küpfer, A; Rohner, P; Zeugin, T, 1991
)
0.56
", but on oral dosing of IFO."( Dosing and side-effects of ifosfamide plus mesna.
Araujo, CE; Brade, WP; Herdrich, K; Kachel-Fischer, U, 1991
)
0.58
"Maximal dosing of cytotoxic chemotherapy drugs is often limited by the development of severe nonmyelosuppressive toxicities."( Chemoprotectants for cancer chemotherapy.
Dorr, RT, 1991
)
0.28
"The chemistry, pharmacology, pharmacokinetics, and adverse effects of ifosfamide and mesna are described separately, followed by a discussion of the adverse effects of concurrent ifosfamide and mesna, the clinical spectrum of ifosfamide, and the dosage and administration of the two drugs."( Ifosfamide and mesna.
Dana, WJ; Schoenike, SE, 1990
)
1.96
" It has an increased therapeutic index when given as a fractionated dosage over 3-5 days."( Bioavailability of subcutaneous ifosfamide and feasibility of continuous outpatient application in cancer patients.
Brunner, KW; Cerny, T; Küpfer, A; Zeugin, T, 1990
)
0.56
" The VIhP regimen for salvage therapy gives the same rate of long term survivors than the regimen with conventional cisplatin dosage (VIP) but is much more toxic and cannot be recommended."( [Salvage chemotherapy of non-seminomatous germ cell tumors. Phase II trial of a combination of etoposide, ifosfamide and high-dose cisplatin].
Azab, M; Bouleuc, C; Droz, JP; Ghosn, M; Hayat, M; Ostronoff, M; Pico, JL; Ribrag, V; Theodore, C,
)
0.34
" Treatment was repeated every 3 weeks for a maximum of six courses and no dosage reductions were allowed."( Ifosfamide, doxorubicin and etoposide in small cell lung cancer patients with poor prognosis.
Bronchud, MH; Kamthan, AG; Lind, MJ; Ranson, MR; Steward, WP; Stout, R; Thatcher, N, 1990
)
1.72
"One hundred and forty-six patients with advanced malignant disease were treated with 6 different dosage schedules of ifosfamide (IFX)."( Ifosfamide and mesna in the treatment of malignant disease mesna as urothelial protector.
Falkson, CI; Falkson, G; Falkson, HC, 1989
)
1.93
" There was statistically significant greater myelosuppression, stomatitis, and diarrhea in the very high dosage DTIC and melphalan (Regimen A) compared with the other two regimens."( High-dose, double alkylating agent chemotherapy with DTIC, melphalan, or ifosfamide and marrow rescue for metastatic malignant melanoma.
Carr, T; Chadwick, G; Craig, P; Jones, R; Lind, M; Morgenstern, G; Thatcher, D, 1989
)
0.51
" No significant dose-response relationship was demonstrated in this heterogeneous group of patients."( A dose escalation study of carboplatin and ifosfamide in advanced ovarian cancer.
Coleman, RE; Gallagher, CJ; Harper, PG; Wiltshaw, E, 1989
)
0.54
" IFN-alpha nl alone at this dosage was shown to have some cytotoxic activity."( Augmentation of cytotoxicity of chemotherapy by human alpha-interferons in human non-small cell lung cancer xenografts.
Balkwill, FR; Carmichael, J; Fergusson, RJ; Smyth, JF; Wolf, CR, 1986
)
0.27
" Mesna has been given in higher dosage (5 g/m2 over 24 h), but otherwise the schedule is as above."( Ifosfamide plus mesna with and without adriamycin in soft tissue sarcoma.
Fisher, C; Harmer, C; McKinna, A; Westbury, G; Wiltshaw, E, 1986
)
1.71
" The clinical course of this case had decided for us which route would be the most effective and would have the least side effect, also, how much of a dosage can be administered as a maximum adoptive dose of an anti-cancer agent, and what kind of a second-line chemotherapy is effective against resistant cancer cells."( [A case report of an advanced ovarian cancer (stage T4) treated with a total amount of 1815 mg of CDDP].
Hino, K; Ibaraki, T; Katou, Y; Kiyozuka, Y; Maruyama, M; Nabuchi, K; Ninomiya, Y; Noda, T; Okamura, Y; Oku, M, 1987
)
0.27
" Analysis of the results according to sex, age, dosage of ifosfamide and degree of histological differentiation of the tumour cells failed to show any influence of these factors on the therapeutic results."( Treatment of advanced malignancies with ifosfamide under protection with mesna.
Brock, N; Guan, ZZ; He, YJ; Li, GC; Li, JQ, 1988
)
0.79
"13 following systemic dosing of CP and IF, respectively."( Cerebrospinal fluid penetration of active metabolites of cyclophosphamide and ifosfamide in rhesus monkeys.
Arndt, CA; Balis, FM; Colvin, OM; McCully, CL; Poplack, DG, 1988
)
0.5
"Complete groups of animals can be economized by application of the Box-Wilson-method to experimental determination of an optimal dosage for a drug combination."( [Sequential animal experimental determination of optimal dosages for combinations of cytostatics using a reduced number of experimental animals (vepeside/ifosfamide combination)].
Arnold, W; Nowak, C; Steinhoff, G; Tanneberger, S, 1988
)
0.47
"In view of the divergent reports on the efficacy of ifosfamide in metastatic renal cell cancer, we tested this drug as monotherapy in nine patients on a dosage schedule of intravenous infusion of 40 mg/kg per day on days 1-5, repeated every 4 wk."( Ifosfamide chemotherapy of metastatic renal cell cancer.
Baki, M; Bodrogi, I; Eckhardt, S; Sinkovics, I, 1988
)
1.97
" Doxorubicin should be administered preferably as 3-weekly bolus injections at doses higher than 60 mg/m2 because of its dose-response relationship."( The treatment of soft tissue sarcomas with focus on chemotherapy: a review.
Pinedo, HM; Verweij, J, 1986
)
0.27
" Peak levels were reached within 1 h in both dosage groups."( Pharmacokinetics and bioavailability of oral ifosfamide.
Drings, P; Wagner, T, 1986
)
0.53
" Bone marrow suppression was the dose-limiting toxicity and led to dosage modification in 24 patients."( A phase II study of ifosfamide in advanced and relapsed carcinoma of the cervix.
Coleman, RE; Gallagher, C; Harper, PG; Osborne, R; Rankin, EM; Silverstone, AC; Slevin, ML; Souhami, RL; Tobias, JS; Trask, CW, 1986
)
0.59
" With future identification of effective chemotherapy, new studies may be focused upon patients with localized disease to reduce radiation dosage or the need for immediate surgical resection of all involved eyes."( The use of chemotherapy for extraocular retinoblastoma.
Crom, DB; Howarth, C; Pratt, CB, 1985
)
0.27
" Combination of vinblastine and bleomycin requires high dosage and a 5 day course of bleomycin."( [Chemotherapy of malignant testicular germ cell tumors: current state in children and adults].
Göbel, U; Weissbach, L,
)
0.13
" cytostatic antibiotic), the dosage (20% LD50 vs."( Immunosuppression by cytostatic drugs?
Duncker, D; Müller-Ruchholtz, W; Ulrichs, K; Yu, MY, 1984
)
0.27
" Therapeutic response to both drugs has been linked to plasma concentration of parent compound, and a nonlinear dose-response relationships might exist at high doses."( Dose-dependent metabolism, therapeutic effect, and toxicity of anticancer drugs in man.
Powis, G, 1983
)
0.27
"Pharmacokinetic measurements to monitor and design cytotoxic treatments in cancer patients are being used more and more in order to optimize dosage and administration schedules."( Pharmacokinetic studies in lung cancer patients.
Cattaneo, MT; Piazza, E; Varini, M, 1984
)
0.27
" It is likely that the reduced drug dosage might have contributed to the poor clinical response."( Timed sequential chemotherapy following drug-induced kinetic recruitment in refractory ovarian cancer.
Alama, A; Conte, PF; Favoni, R; Nicolin, A; Rosso, R; Trave, F, 1984
)
0.27
" Oral ifosfamide therapy was determined to be feasible, and further studies are justified to assess the pharmacokinetics of the optimum dosage and scheduling regimens."( The bioavailability of oral and intravenous ifosfamide in the treatment of bronchogenic carcinoma.
McNiel, NO; Morgan, LR, 1981
)
1
"We describe 2 cases of proximal tubular defects induced by the administration of ifosfamide at a dosage of 6 g/m2/course over 2 days in children with a diagnosis of malignant mesenchymal tumors."( Ifosfamide-induced renal tubular defect.
López Pérez, J; Melero, C; Muley, R; Torres Valdivieso, MJ; Vara, J; Vivanco, JL, 1994
)
1.96
"The activity of HDI in these pretreated ASTS patients and the apparent circumvention of SDI resistance suggest a real dose-response relationship for ifosfamide and deserve further evaluation."( High-dose ifosfamide: circumvention of resistance to standard-dose ifosfamide in advanced soft tissue sarcomas.
Antoine, E; Brain, E; Fontaine, F; Genin, J; Janin, N; Kayitalire, L; Le Cesne, A; Le Chevalier, T; Spielmann, M; Toussaint, C, 1995
)
0.89
"3 mmol/l) displaces the dose-response curve for acrolein to the left, indicating an increased toxicity of the combination of acrolein plus Dimesna."( Ifosfamide and mesna: effects on the Na/H exchanger activity in renal epithelial cells in culture (LLC-PK1).
Brandis, M; Küpper, N; Mohrmann, M; Schönfield, B,
)
1.57
" There was a suggestion of a dose-response curve with paclitaxel as all three partial responses were seen at the 250 mg/m2 dose level."( Paclitaxel and ifosfamide: a multicenter phase I study in advanced non-small cell lung cancer.
Bitran, JD; Drinkard, LC; Golomb, HM; Hoffman, PC; Krauss, SA; Masters, GA; Samuels, BL; Vokes, EE; Watson, S, 1995
)
0.64
" The dosage of paclitaxel was escalated from 75 to 225 mg/m2."( A phase I study of ifosfamide/carboplatin/etoposide/paclitaxel in advanced lung cancer.
Carey, RW; Elias, AD; Grossbard, ML; Jacobs, C; Jauss, S; Kwiatkowski, DJ; Lynch, TJ; Shulman, LN; Strauss, GM; Sugarbaker, DJ, 1995
)
0.62
" The overall response rate of 41% might be improved by increased dosage and growth factor support."( Ifosfamide, mitoxantrone and etoposide (VIM) as salvage therapy of low toxicity in non-Hodgkin's lymphoma.
Heinz, R; Hopfinger, G; Koller, E; Pittermann, E; Schneider, B, 1995
)
1.73
" The Eastern Cooperative Oncology Group is currently evaluating high-dose (200 mg/m2) and low-dose (135 mg/m2) paclitaxel in combination with cisplatin to assess dose-response effects, toxicity, and efficacy."( Single-agent paclitaxel and paclitaxel plus ifosfamide in the treatment of head and neck cancer.
Forastiere, AA; Urba, SG, 1995
)
0.55
"More effective high-dose combination regimens are needed which have broad cytotoxic activity, steep dose-response relations and non-overlapping non-hematologic toxicities (to allow administration of full doses of each agent)."( Phase I study of high-dose ifosfamide, carboplatin and etoposide with autologous hematopoietic stem cell support.
Ayash, LJ; Elias, AD; Frei, E; Gonin, R; Mazanet, R; McCauley, M; Schnipper, L; Schwartz, G; Tepler, I; Wheeler, C, 1995
)
0.59
" A dose-response relationship was not apparent with the mini-ICE regimen; however, among patients receiving maxi-ICE, a dose-response relationship was suggested in those patients responding to anthracycline-based chemotherapy."( Ifosfamide/carboplatin/etoposide chemotherapy for metastatic breast cancer with or without autologous hematopoietic stem cell transplantation: evaluation of dose-response relationships.
Elfenbein, GJ; Fields, KK; Perkins, JB, 1995
)
1.73
" Since ICE has substantial activity in a number of malignancies, but significant renal morbidity, real-time pharmacokinetic-guided dosing may reduce treatment-related toxicity."( High-dose ifosfamide, carboplatin, and etoposide pharmacokinetics: correlation of plasma drug levels with renal toxicity.
Andersen, J; Antman, K; Elias, A; Frel, E; Holden, S; Rosowsky, A; Schwartz, G; Tretyakov, O; Wheeler, C; Wright, JE, 1995
)
0.69
"A simple colorimetric method for the determination of cyclophosphamide and ifosphamide in pure and in dosage forms is suggested."( Colorimetric determination of cyclophosphamide and ifosphamide.
Amer, SM; el-Kousasy, AM; Mohamed, ZH, 1994
)
0.29
" These results compare favourably with other combined modality studies, using multiple radiotherapy fractions with cisplatin-based combinations and dosage reduction for patients staged in more anatomical detail."( Therapy for small cell lung cancer using carboplatin, ifosfamide, etoposide (without dose reduction), mid-cycle vincristine with thoracic and cranial irradiation.
Burt, P; Hicks, F; Leahy, B; Lorigan, P; Prendiville, J; Stout, R; Thatcher, N, 1994
)
0.54
"Agents with broad cytotoxic activity, steep linear log dose-response relationships, relative non-cross-resistance, and nonoverlapping nonhematologic toxicities can be combined to create new high-dose combination regimens."( High-dose ifosfamide/carboplatin/etoposide with autologous hematopoietic stem cell support: safety and future directions.
Antman, KH; Ayash, LJ; Elias, AD; Frei, E; Mazanet, R; McCauley, M; Schnipper, L; Schwartz, G; Tepler, I; Wheeler, C, 1994
)
0.69
" Since ifosfamide induced unexpectedly higher toxicity, response was corrected based on the shape of the dose-response curve for ifosfamide."( Efficacy of ifosfamide, dacarbazine, doxorubicin and cisplatin in human sarcoma xenografts.
Budach, V; Budach, W; Reipke, P; Scheulen, ME; Schmauder, B; Stuschke, M, 1994
)
1.12
" The dosage of IEP in this study caused moderate toxicity."( Ifosfamide, epirubicin and cisplatin (IEP): another active combination for small cell lung cancer (SCLC).
Jiamsriponges, K; Thongprasert, S, 1993
)
1.73
" Carboplatin dosing by the area under the curve (AUC) may minimize thrombocytopenia."( Ifosfamide, carboplatin, and etoposide plus granulocyte-macrophage colony-stimulating factor: a phase I study with apparent activity in non-small-cell lung cancer.
Comis, R; Haas, N; Kilpatrick, D; Krigel, RL; Langer, C; Padavic, K; Palackdharry, CS, 1994
)
1.73
" Moreover, a dose-response relationship was detectable: 1/6 patients without lung irradiation vs."( Lung irradiation for Ewing's sarcoma with pulmonary metastases at diagnosis: results of the CESS-studies.
Dunst, J; Jürgens, H; Paulussen, M, 1993
)
0.29
" More frequent dosing or infusion may be necessary to maintain adequate drug levels for antitumor activity when IPM is administered directly."( Preclinical pharmacokinetics and stability of isophosphoramide mustard.
Chan, KK; Muggia, F; Zheng, JJ, 1994
)
0.29
" The authors performed a dose-escalation trial of ifosfamide with a fixed dosage of etoposide, with mesna uroprotection, in children with multiply recurrent acute leukemia."( Ifosfamide with mesna uroprotection and etoposide in recurrent, refractory acute leukemia in childhood. A Pediatric Oncology Group Study.
Bell, B; Bernstein, ML; Buchanan, GR; Devine, S; Dreyer, Z; Grier, H; Krischer, J; Kung, F; Land, V; Whitehead, VM, 1993
)
1.98
" In addition it offered a simple and convenient dosing regimen and a safer side-effect profile."( The antiemetic efficacy and safety of granisetron compared with metoclopramide plus dexamethasone in patients receiving fractionated chemotherapy over 5 days. The Granisetron Study Group.
, 1993
)
0.29
" A randomized phase III study is now underway comparing this regimen with conventional-dose doxorubicin/ifosfamide to test the dose-response relationship."( Granulocyte-macrophage colony-stimulating factor allows safe escalation of dose-intensity of chemotherapy in metastatic adult soft tissue sarcomas: a study of the European Organization for Research and Treatment of Cancer Soft Tissue and Bone Sarcoma Grou
Clavel, M; Crowther, D; Kerbrat, P; Rouesse, J; Somers, R; Spooner, D; Steward, WP; Tueni, E; Tursz, T; Verweij, J, 1993
)
0.5
"A continuous 14-day infusion of ifosfamide admixed with carboplatin is feasible in an ambulatory setting with no need for adding mesna for urologic protection and full dosage administration for each agent."( Pilot study of ambulatory infusional ifosfamide admixed with carboplatin.
Anderson, NR; Bern, MM; Coco, F; Gonzalves, L; Lokich, JJ; Moore, C; Zipoli, TE, 1993
)
0.84
" The clear relationship between hematologic toxicity and carboplatin systemic exposure supports the use of targeted dosing in further trials of ICE chemotherapy."( Phase I study of escalating targeted doses of carboplatin combined with ifosfamide and etoposide in children with relapsed solid tumors.
Bowman, LC; Douglass, E; Furman, W; Hudson, M; Marina, NM; Meyer, W; Rodman, J; Santana, VM; Shema, SJ; Wilimas, J, 1993
)
0.52
" Our studies suggest a dose-response relationship for ifosfamide."( Single-agent ifosfamide studies in sarcomas of soft tissue and bone: the M.D. Anderson experience.
Benjamin, RS; Legha, SS; Nicaise, C; Patel, SR, 1993
)
0.9
" Ifosfamide dosage was not increased."( Epirubicin and ifosfamide in advanced soft tissue sarcoma: a phase II study.
Chevallier, B; Facchini, T; Fargeot, P; Leyvraz, S; Olivier, JP; Vo Van, ML, 1993
)
1.55
"Patients were assigned to dosage cohorts separately on the basis of prior exposure to the platinum alkylating agents cisplatin or carboplatin (n = 20) or the absence of such exposure (n = 9)."( A phase I study of ifosfamide with Mesna given daily for 3 consecutive days to children with malignant solid tumors.
Avery, L; Bowman, L; Douglass, EC; Marina, N; Meyer, WH; Ochs, J; Pratt, CB; Thompson, EI; Wilimas, J, 1993
)
0.61
"Myelosuppression was dose-limiting at the second dosage level (2560 mg/m2/d) for patients previously treated with platinum and at the third dosage level (3072 mg/m2/d) for those not previously treated with platinum."( A phase I study of ifosfamide with Mesna given daily for 3 consecutive days to children with malignant solid tumors.
Avery, L; Bowman, L; Douglass, EC; Marina, N; Meyer, WH; Ochs, J; Pratt, CB; Thompson, EI; Wilimas, J, 1993
)
0.61
"The patients were assigned to dosage cohorts separated on the basis of prior exposure to cisplatin (n = 10) or the absence of such exposure (n = 10)."( A phase I study of ifosfamide given on alternate days to treat children with brain tumors.
Avery, L; Douglass, EC; Heideman, R; Kellie, SJ; Kovnar, EH; Kun, L; Pratt, CB, 1993
)
0.61
" After dosing with the D-compound, the highest levels of radioactivity were found in the liver, kidneys, thymus, thyroid gland, and central nervous system, including the brain."( Pharmacokinetics and whole-body distribution of the new chemotherapeutic agent beta-D-glucosylisophosphoramide mustard and its effects on the incorporation of [methyl-3H]-thymidine in various tissues of the rat.
Bertram, B; Bollow, U; Hull, WE; Pohl, J; Port, R; Schaper, M; Stüben, J; Wiessler, M, 1996
)
0.29
"Ifosfamide is an alkylating agent with clinical activity in the treatment of sarcomas, and data support a dose-response relationship in this disease."( High-dose ifosfamide in the treatment of sarcomas of soft tissues and bone.
Demetri, GD, 1996
)
2.14
" Sequential dosing protocols, administration of high-dose chemotherapy with peripheral blood progenitor cell support, and other approaches, possibly combining current treatment options, may be necessary to further improve the long-term survival of patients with relapsed NHL."( Dose-intensive ifosfamide for the treatment of non-Hodgkin's lymphoma.
Vose, JM, 1996
)
0.65
" Unfortunately, the available data on ifosfamide use in advanced disease are derived from poorly designed studies that evaluated various patient populations and dosing schedules."( Ifosfamide in the treatment of breast cancer.
Overmoyer, BA, 1996
)
2.01
" This review summarizes dosing schedules and the incidence of hematuria in 47 clinical studies, in which oral mesna was given to at least 1,986 patients who received more than 6,475 courses of ifosfamide."( Oral administration of mesna with ifosfamide.
Goren, MP, 1996
)
0.76
" Our goal was to confirm a dose-response relationship for ifosfamide in soft tissue sarcoma."( High-dose ifosfamide in the treatment of advanced soft tissue sarcomas.
Tursz, T, 1996
)
0.94
"The addition of IFN-alpha to induction CT appears to confer a survival benefit to SCLC patients but optimal dosing schedule has yet to be defined."( Interferon alpha-2a and combined chemotherapy as first line treatment in SCLC patients: a randomized trial.
Charitopoulos, K; Dimitriadis, K; Economides, D; Maglaveras, N; Papagiannis, A; Vamvalis, C; Zarogoulidis, K; Ziogas, E, 1996
)
0.29
" For this first step a daily dosage of 300 mg/m2 of body surface resulted in only moderate leukopenia, whereas a daily dosage of 450 mg/m2 caused severe leukopenia."( Development of a canine chemotherapeutic model with ifosfamide.
Chao, EY; Donehower, RC; Frassica, FJ; Ikeda, K; Inoue, N; Tomita, K, 1996
)
0.54
" Dose-response curves for cisplatin (3-30 000 nmol) combined with non-toxic silibinin doses (7."( Silibinin protects against cisplatin-induced nephrotoxicity without compromising cisplatin or ifosfamide anti-tumour activity.
Bokemeyer, C; Dunn, T; Fels, LM; Gaedeke, J; Lentzen, H; Schmoll, HJ; Stolte, H; Voigt, W, 1996
)
0.51
" Such simultaneous administration enabled us to substantially increase the dosage intensity of both, thereby increasing the effectiveness of each drug."( Infusional chemotherapy combined with recombinant human granulocyte colony stimulating factor: advantages and limitations.
Lackman, RD; Weiss, AJ, 1997
)
0.3
" Tumour response was studied by the tumour growth (TG) time assay; namely, the TG time or the time for one-half of the treated tumours to reach 700 mm3 from the initial treatment day was determined and the dose-response curves was fitted between the TG time and IFO dose."( Thermal enhancement of the effect of ifosfamide against a spontaneous murine fibrosarcoma, FSa-II.
Kuroda, M; Reynolds, R; Urano, M,
)
0.4
" Both have a dose-response relationship."( Phase II study of a closely spaced ifosfamide--cisplatin schedule with the addition of G-CSF in advanced non-small-cell lung cancer and malignant melanoma.
de Wit, R; Planting, AS; Stoter, G; van der Burg, ME; Verweij, J, 1996
)
0.57
" Based on these findings, the author established a consecutive low-dose CDDP dosing method, which possibly could deliver a higher therapeutic index compared with the bolus-dosing method."( [Consecutive low-dose cisplatin-based chemotherapy for gynecologic malignancies].
Shimizu, Y, 1997
)
0.3
" No clinical evidence of renal failure was attributed to the high dosage of the drug in the course of assays of biochemical components of the blood, blood- and urine-beta-2-microglobulins, N-acetyl-D-hexoaminidase (NAG) level in urine, creatinine clearance and complex renoscintigraphy data."( [High-dose ifosfamide in the treatment of patients with soft tissue sarcoma].
Averinova, SG; Garin, AM; Kashkadaeva, AV; Liubimova, NV; Romanova, LF; Shiriaev, SV; Sidorova, NI; Tiuliandin, SA, 1996
)
0.68
" This combination of drugs at this dosage has tolerable toxicity, is efficient and deserves evaluation in phase III studies."( Ifosfamide and etoposide in childhood osteosarcoma. A phase II study of the French Society of Paediatric Oncology.
Avet-Loiseau, H; Berger, C; Bernard, JL; Brunat-Mentigny, M; De Lumley, L; Demaille, MC; Gentet, JC; Kalifa, C; Pacquement, H; Pein, F; Pillon, P; Sariban, E; Schmitt, C, 1997
)
1.74
" Pharmacokinetic study did not show induction mechanism at this dosage and with this type of administration."( [High dose ifosfamide at 15 g/m2/cycle: a feasibility study in 10 patients].
Baranzelli, MC; Deligny, N; Demaille, MC; Gourmel, B; N'Guyen, M; Pichon, F, 1997
)
0.69
" In parallel, patients with solid tumors or non-Hodgkin's lymphomas (n = 28) treated with etoposide (500 mg/m2), ifosfamide (1500 mg/m2) and cisplatin (150 mg/m2) and identical dosing of G-CSF were analyzed."( Blood progenitor cell (BPC) mobilization studied in multiple myeloma, solid tumor and non-Hodgkin's lymphoma patients after combination chemotherapy and G-CSF.
Engelhardt, M; Henschler, R; Lange, W; Mertelsmann, R; Waller, C; Winkler, J, 1997
)
0.51
" There is a definite positive dose-response curve, and bolus administration appears to be more active than continuous infusion."( High-dose ifosfamide in bone and soft tissue sarcomas: results of phase II and pilot studies--dose-response and schedule dependence.
Benjamin, RS; Burgess, MA; Hays, C; Papadopolous, N; Patel, SR; Plager, C; Vadhan-Raj, S, 1997
)
0.7
" Similar dose-response curves were found for both metabolites."( Ifosfamide cytotoxicity on human tumor and renal cells: role of chloroacetaldehyde in comparison to 4-hydroxyifosfamide.
Brüggemann, SK; Kisro, J; Wagner, T, 1997
)
1.74
"A preliminary co-operative study by 7 institutes was conducted to determine the optimal dosage of the combination regimen with nedaplatin, bleomycin and ifosfamide, which is used in a phase III clinical study, to investigate its efficacy as neoadjuvant chemotherapy against advanced cervical cancer of the uterus."( [Combination chemotherapy with nedaplatin, bleomycin and ifosfamide for advanced cervical cancer of the uterus--a preliminary study for phase III clinical study].
Hatae, M; Hirabayashi, K; Kanazawa, K; Noda, K; Ozaki, M; Terashima, Y; Yakushiji, M, 1997
)
0.74
" The study design and dosing schedule are discussed in this report."( Paclitaxel/carboplatin plus ifosfamide in non-small cell lung cancer.
Golomb, HM; Hoffman, PC; Masters, G; Mauer, AM; Vokes, EE; Watson, S, 1997
)
0.59
"We have treated 26 consecutive chemotherapy-naive patients with stage IIIB/IV non-small cell lung cancer with an innovative regimen based on a 1-hour infusion of paclitaxel (Taxol; Bristol-Myers Squibb Company, Princeton, NJ) 125 to 250 mg/m2, ifosfamide 3 g/m2 (with mesna), and carboplatin dosed to an area under the concentration-time curve of 5, every 21 days for a total of six cycles in responding or stabilized patients."( Paclitaxel, ifosfamide, and carboplatin for the treatment of stages IIIB and IV non-small cell lung cancer: preliminary results.
Alghisi, A; Bozzola, G; Marini, G; Meriggi, F; Mutti, S; Pascarella, A; Rizzi, A; Zaniboni, A, 1997
)
0.86
" Mesna was administered intravenously at a 20% of the ifosfamide dosage before ifosfamide and orally at 40% after 4 and 8 hours from the ifosfamide infusion."( Second line chemotherapy with ifosfamide as outpatient treatment for advanced bladder cancer.
Pensa, F; Pronzato, P; Tani, F; Vaira, F; Vanoli, M; Vigani, A, 1997
)
0.83
"Ifosfamide has important activity in pretreated soft tissue sarcomas (STS), and recent data support a clinically significant dose-response relationship for this agent."( Phase II study of continuous-infusion high-dose ifosfamide in advanced and/or metastatic pretreated soft tissue sarcomas.
Antimi, M; Gatti, C; Palmeri, S; Palumbo, R; Raffo, P; Toma, S; Villani, G, 1997
)
2
" However, studies for pediatric patients are limited, and there are no systematic data on the pharmacokinetics of PIXY321 given over prolonged periods at current dosage levels."( Clinical effects and pharmacokinetics of the fusion protein PIXY321 in children receiving myelosuppressive chemotherapy.
Arnold, B; Furman, WL; Garrison, L; Hanna, R; Luo, X; Marina, N; Meyer, WH; Pratt, CB; Rodman, JH; Tonda, ME, 1998
)
0.3
"The purpose of this study was to make evidence-based recommendations regarding the mode, dosage and schedule of delivery of concomitant mesna (sodium-2-mercaptoethanesulfonate) to protect against ifosfamide-induced uroepithelial toxicity."( Use of mesna to prevent ifosfamide-induced urotoxicity.
Moore, MJ; Siu, LL, 1998
)
0.8
"Three bromine-ifosfamide analogues: racemic chlorobromofosfamide (+/-)-(R,S)-1, its levorotatory enantiomer (-)-(S)-2 and racemic bromofosfamide (+/-)-(R,S)-3 showed considerable stereoselective differences in their pharmacokinetics and bioavailability depending on the route of administration and regimen of dosage studies in rats."( Pharmacokinetic-stereoselective differentiation of some isomeric analogues of ifosfamide.
Hładoń, B; Kinas, R; Kuśnierczyk, H; Laskowska, H; Sloderbach, A; Sochacki, M,
)
0.72
" The kinetics of the excretion were compared following short-term and continuous ifosfamide infusion at a dosage of 3 g/m2."( Excretion kinetics of ifosfamide side-chain metabolites in children on continuous and short-term infusion.
Blaschke, G; Boos, J; Hohenlöchter, B; Jürgens, H; Rossi, R; Silies, H, 1998
)
0.84
" Dosage of the two drugs was modified according to nadir white blood count after each cycle."( Phase II study of paclitaxel (Taxol) and ifosfamide (Holoxan) in inoperable non-small-cell lung cancer.
Thongprasert, S, 1998
)
0.57
" Five phase II studies have been performed using different scheduling and dosage regimens."( Combination studies with gemcitabine in the treatment of non-small-cell lung cancer.
Steward, WP, 1998
)
0.3
", doses > 10 g/m2), which supports a dose-response relationship for this drug."( Phase II trial of first-line high-dose ifosfamide in advanced soft tissue sarcomas of the adult: a study of the Spanish Group for Research on Sarcomas (GEIS)
Antón, A; Arranz, F; Bellmunt, J; Buesa, JM; Casado, A; Escudero, P; García del Muro, J; López-Pousa, A; Martín, J; Menéndez, D; Poveda, A; Valentí, V, 1998
)
0.57
"Ifosfamide and doxorubicin are the most active agents in the treatment of sarcomas and are characterized by a marked dose-response relationship."( Phase I multicenter study of combined high-dose ifosfamide and doxorubicin in the treatment of advanced sarcomas. Swiss Group for Clinical Research (SAKK).
Bacchi, M; Bressoud, A; Cerny, T; Hermann, R; Leyvraz, S; Lissoni, A; Sessa, C, 1998
)
2
"Adriamycin (ADM) and ifosfamide (IFO) are the two most active agents in the treatment of soft tissue sarcomas (STS) with a clear dose-response relationship."( High-dose ifosfamide plus adriamycin in the treatment of adult advanced soft tissue sarcomas: is it feasible?
Aapro, MS; De Braud, F; De Pas, T; Fazio, N; Goldhirsch, A; Munzone, E; Nolè, F; Orlando, L; Zampino, MG, 1998
)
1.02
" In older patients (> 60 years) the dosage of idarubicin and ifosfamide was reduced to 75% in the initial cycle."( DIZE (dexamethasone, idarubicin, and continuous infusion of ifosfamide and etoposide): an effective and well-tolerated new regimen for patients with relapsed lymphoma.
Borchmann, P; Diehl, V; Engert, A; Münch, R; Reiser, M; Schnell, R; Straub, G; Ubelacker, R; Wilhelm, M; Wörmann, B, 1998
)
0.78
" The ifosfamide dosage reached was 4-13 g/m2 per cycle, median 5 g/m2."( Pilot study of daily ifosfamide 1 g/m2 until grade III granulocytopenia as second-line chemotherapy for anthracycline-pretreated advanced soft tissue sarcoma.
Babović, N; Jelić, S; Matković, S; Milanović, N,
)
0.96
" Following 1 cycle of MAID at the standard dose, four patients were to be treated at each of five dosage levels: +25%, +45%, +65%, +85%, +100%."( Phase I-II trial of intensification of the MAID regimen with support of lenograstim (rHuG-CSF) in patients with advanced soft-tissue sarcoma (STS).
Bui, BN; Chevallier, B; Chevreau, C; Coindre, JM; Cour-Chabernaud, V; Gil, B; Krakowski, I; Maugard, C; Mihura, J, 1999
)
0.3
" Four patients were assigned to different dosage levels, and drug toxicity was evaluated for the first 2 cycles."( Phase I study of a combination of irinotecan and ifosfamide in advanced primary lung cancer.
Gohara, R; Ichiki, M; Kawayama, T; Kinoshita, M; Mitui, T; Oizumi, K; Okubo, Y; Rikimaru, T, 1999
)
0.56
"5 g/m(2)/day as 72-hour continuous infusion with mesna at the same dosage and schedule."( Treatment of advanced soft tissue sarcomas with ifosfamide and doxorubicin combination chemotherapy.
Altundağ, K; Baltali, E; Barişta, I; Celik, I; Firat, D; Güler, N; Güllü, I; Kars, A; Ozişik, Y; Tekuzman, G; Türker, A; Uner, A; Yalçin, S; Zengin, N, 2000
)
0.56
" The present retrospective analysis assessed two ways of dosing carboplatin: according to body surface area (mg/m2) or to the estimated targeted area under the concentration versus time curve (AUC)."( A comparison of methods of calculation for estimating carboplatin AUC with a retrospective pharmacokinetic-pharmacodynamic analysis in patients with advanced non-small cell lung cancer. European Lung Cancer Working Party.
Alexopoulos, CG; Berchier, MC; Bureau, G; Giner, V; Klastersky, J; Koumakis, G; Lafitte, JJ; Lecomte, J; Mommen, P; Ninane, V; Paesmans, M; Sculier, JP; Thiriaux, J; Zacharias, C, 1999
)
0.3
" The AUC of carboplatin measured in serum was lower than the target AUC; this may be related to underestimation of the glomerular filtration rate used in the dosing formula."( Sequential dose-intensive paclitaxel, ifosfamide, carboplatin, and etoposide salvage therapy for germ cell tumor patients.
Bains, M; Bajorin, DF; Bosl, GJ; Flombaum, C; Macapinlac, HA; Mariani, T; Mazumdar, M; Motzer, RJ; Reich, L; Sheinfeld, J; Tong, WP, 2000
)
0.58
" Optimal dosing of carboplatin in the high-dose setting warrants further investigation."( Sequential dose-intensive paclitaxel, ifosfamide, carboplatin, and etoposide salvage therapy for germ cell tumor patients.
Bains, M; Bajorin, DF; Bosl, GJ; Flombaum, C; Macapinlac, HA; Mariani, T; Mazumdar, M; Motzer, RJ; Reich, L; Sheinfeld, J; Tong, WP, 2000
)
0.58
" A doubling of the intensity of cyclophosphamide (or ifosfamide equivalent) dosing per cycle between IRS-III and IRS-IV is thought to be a key contributing factor for this improvement."( Benefit of intensified therapy for patients with local or regional embryonal rhabdomyosarcoma: results from the Intergroup Rhabdomyosarcoma Study IV.
Anderson, JR; Baker, KS; Breneman, JC; Crist, WM; Grier, HE; Link, MP; Maurer, HM; Qualman, SJ; Wiener, ES, 2000
)
0.56
" Our trial failed to demonstrate a significant improvement in response or survival when patients with metastatic NSCLC were treated, in addition to ifosfamide and mitomycin, by combination of moderate dosages of cisplatin and carboplatin instead of moderate dosage of cisplatin alone."( Phase III randomized trial comparing moderate-dose cisplatin to combined cisplatin and carboplatin in addition to mitomycin and ifosfamide in patients with stage IV non-small-cell lung cancer.
Alexopoulos, CG; Baumöhl, J; Berghmans, T; Florin, MC; Klastersky, J; Koumakis, G; Lafitte, JJ; Mommen, P; Ninane, V; Paesmans, M; Schmerber, J; Sculier, JP; Thiriaux, J; Zacharias, C, 2000
)
0.71
" At the same time the carboplatin dosing calculation was changed and an area under the curve (AUC) formula rather than by mg/m2 was used to calculate this."( Should high-dose chemotherapy be used to consolidate second or third line treatment in relapsing germ cell tumours?
Gallagher, CJ; Gupta, RK; Kelsey, S; Lister, TA; Newland, AC; O'Doherty, CA; Oliver, RT; Shamash, J, 2000
)
0.31
" A good performance status, lymph node metastasis alone and administration of chemotherapy at the full dosage had a significantly favorable impact on patient survival."( Combination chemotherapy with ifosfamide, 5-fluorouracil, etoposide and cisplatin for metastatic urothelial cancer.
Fukui, I; Ishiwata, D; Kim, T; Tohma, T; Tsukamoto, T; Yonese, J; Yoshida, T, 2001
)
0.6
" In patients with advanced stage soft tissue sarcomas (ASTS), a dose-response relationship has been established for doxorubicin and ifosfamide."( [High-dose chemotherapy in soft tissue sarcomas of adults].
Biron, P; Blay, JY; Ray-Coquard, I, 2001
)
0.51
" Clinical trials that include pharmacokinetic and pharmacodynamic studies may be the most efficient way to optimize the therapeutic efficacy of ifosfamide and define the dosing and scheduling."( Antiblastic drug combinations with ifosfamide: an update.
Badalamenti, G; Fulfaro, F; Gebbia, N; Russo, A; Valerio, MR, 2003
)
0.8
" This phase I trial aimed to determine the dose-limiting toxicity (DLT), maximum tolerated dose [maximum tolerated dosage (MTD)], and recommended dose (RD) of a GIP combination in patients with advanced/metastatic NSCLC."( Phase I study with dose escalation of gemcitabine and cisplatin in combination with ifosfamide (GIP) in patients with non-small-cell lung carcinoma.
Billiart, I; Bourgeois, H; Chabrun, V; Chieze, S; Daban, A; Ferrand, V; Germain, T; Lemerre, D; Meurice, JC; Tourani, JM, 2004
)
0.55
" Haematological toxicity and dosage reductions were higher with SuperMIP, which was nevertheless associated with a significantly increased absolute dose intensity."( A phase III randomised study comparing two different dose-intensity regimens as induction chemotherapy followed by thoracic irradiation in patients with advanced locoregional non-small-cell lung cancer.
Berghmans, T; Corhay, JL; Efremidis, A; Giner, V; Koumakis, G; Lafitte, JJ; Lecomte, J; Lothaire, P; Mommen, P; Ninane, V; Paesmans, M; Richez, M; Sculier, JP; Thiriaux, J; Van Houtte, P; Wackenier, P, 2004
)
0.32
" This observation suggests a strategy of individualized dosing adapted to hematotoxicity."( Low acute hematological toxicity during chemotherapy predicts reduced disease control in advanced Hodgkin's disease.
Brosteanu, O; Diehl, V; Hasenclever, D; Loeffler, M, 2004
)
0.32
" As cytostatics for hyperthermic peritoneal perfusion, we have used Mitomycin in a dosage of 18 mg/m2 plus Melphalan in a dosage of 25 mg/m2."( Cytoreductive surgery plus intraperitoneal hyperthermic perfusion is an effective treatment for metastasized malignant mixed mesodermal tumours (MMMT)--report of six cases.
Müller, H; Nakchbandi, V, 2004
)
0.32
" Partial responses were documented in three patients with ovarian cancer dosed below the MTD."( Phase I and pharmacokinetic study of the combination of topotecan and ifosfamide administered intravenously every 3 weeks.
Ambaum, B; Beijnen, JH; Groenewegen, G; Herben, VM; Jansen, S; Kerbusch, T; Mathôt, RA; Rosing, H; Schellens, JH; Swart, M; ten Bokkel Huinink, WW; Voest, EE, 2004
)
0.56
"The profile of mesna excretion after intravenous and oral dosing in these children was similar to that in reported studies of ifosfamide-treated adults."( Urine mesna excretion after intravenous and oral dosing in ifosfamide-treated children.
Bush, DA; Epelman, S; Goren, MP, 2004
)
0.77
" Ifosfamide was dosed either as a continuous infusion or as fractionated doses over 2 or 3 days."( Pharmacokinetics and metabolism of ifosfamide in relation to DNA damage assessed by the COMET assay in children with cancer.
Boddy, AV; Cholerton, S; Ford, D; Parry, A; Pearson, AD; Price, L; Tilby, MJ; Willits, I, 2005
)
1.52
"Data presented suggest that dosing of dactinomycin based on surface area is not optimal, either in younger patients in whom the risk of toxicity is greater, or in older patients where doses are capped."( Pharmacokinetics of dactinomycin in a pediatric patient population: a United Kingdom Children's Cancer Study Group Study.
Beane, C; Boddy, AV; Brennan, B; Chisholm, JC; Cole, M; Elsworth, AM; Errington, J; Glaser, A; Hale, J; Hemsworth, S; Howe, K; Jenner, G; McDowell, H; Nicholson, J; Parry, A; Pearson, AD; Pinkerton, R; Pritchard-Jones, K; Veal, GJ; Waters, F; Wright, Y, 2005
)
0.33
" The results however, did not show expected treatment efficacy and we raise the idea of paclitaxel dosage relevance in TIP."( Paclitaxel plus ifosfamide and cisplatin in second-line treatment of germ cell tumors: a phase II study.
Hlavatá, Z; Koza, I; Mardiak, J; Mego, M; Obertová, J; Recková, M; Sálek, T; Sycová-Milá, Z, 2005
)
0.67
" After an initial bolus of 1 g/m(2) of mesna, mesna was applied at a dosage of 5 g/m(2) concomitantly with ifosfamide followed by additional dosages of 200 mg 3 times at 4-hour intervals after termination of the ifosfamide infusion."( Ifosfamide/mesna as salvage therapy in platinum pretreated ovarian cancer patients--long-term results of a phase II study.
Baur, M; Dittrich, C; Fazeny-Doerner, B; Hudec, M; Salzer, H; Sevelda, P, 2006
)
1.99
"The starting dosage of ifosfamide was 400 mg/m(2) of body surface area, IV, and dosages were increased by 50 to 100 mg/m(2) in cohorts of 3 cats."( Phase I trial and pharmacokinetic analysis of ifosfamide in cats with sarcomas.
Beaulieu, BB; Kristal, O; Lewis, LD; Moore, AS; Northrup, NC; Page, RL; Rassnick, KM, 2006
)
0.9
"The dosage of ifosfamide recommended to treat tumor-bearing cats is 900 mg/m(2) every 3 weeks."( Phase I trial and pharmacokinetic analysis of ifosfamide in cats with sarcomas.
Beaulieu, BB; Kristal, O; Lewis, LD; Moore, AS; Northrup, NC; Page, RL; Rassnick, KM, 2006
)
0.95
" The purpose of the study was to determine the optimal dosage and the maximal tolerated dose (MTD) of a specified schedule of gemcitabine and ifosfamide."( Dose-finding study of fixed dose gemcitabine and escalating doses of ifosfamide given on days 1 and 8 in patients with advanced non-small cell lung cancer.
Aschroft, L; Baka, S; Blackhall, F; Buchholz, E; Lorigan, P; Manegold, C; Nagel, S; Schott-von-Römer, K; Thatcher, N, 2006
)
0.77
" In conclusion, this seems to be a feasible combination in patients with advanced soft tissue sarcomas, allowing ifosfamide to be given in a dosage similar to that used when given alone."( Phase 1 European Organisation for Research and Treatment of Cancer study determining safety of pegylated liposomal doxorubicin (Caelyx) in combination with ifosfamide in previously untreated adult patients with advanced or metastatic soft tissue sarcomas.
Blay, J; Christensen, TB; Daugaard, S; Hermans, C; Judson, I; Marreaud, S; Nielsen, OS; Pink, D; Reichardt, P; van Glabbeke, M, 2006
)
0.74
" Mesna was applied at a dosage of 20% of ifosfamide 3 times at 4-hour intervals after termination of the ifosfamide infusion."( [Efficacy of chemotherapy regimen using ifosphamide and carboplatin on recurrent or refractory neuroblastoma].
Ling, JY; Sun, XF; Wang, ZH; Xia, Y; Zhen, ZJ, 2006
)
0.6
" There was no compelling evidence for increased toxicity of doxorubicin when given at 100% versus 50% dosing (full dose: 20 mg/m(2) day x 3), but the number of patients analyzed was small."( Renal failure does not preclude cure in children receiving chemotherapy for Wilms tumor: a report from the National Wilms Tumor Study Group.
Breslow, NE; Feusner, JH; Green, DM; Norkool, PA; Ritchey, ML; Takashima, JR, 2008
)
0.35
"The data suggest that, in the setting of renal failure, reduction of dosing is not necessary for the three main agents used for treatment of newly diagnosed Wilms tumor, and cure is not precluded."( Renal failure does not preclude cure in children receiving chemotherapy for Wilms tumor: a report from the National Wilms Tumor Study Group.
Breslow, NE; Feusner, JH; Green, DM; Norkool, PA; Ritchey, ML; Takashima, JR, 2008
)
0.35
" These data may aid the design of studies to clarify optimal dosing and leukapheresis with pegfilgrastim."( A phase 2 pilot study of pegfilgrastim and filgrastim for mobilizing peripheral blood progenitor cells in patients with non-Hodgkin's lymphoma receiving chemotherapy.
Baker, N; Barker, P; Boogaerts, M; Canizo, CD; Johnsen, HE; Mesters, R; Russell, N; Schmitz, N; Schubert, J; Skacel, T, 2008
)
0.35
" This study aimed to determine the recommended dosage of nedaplatin plus ifosfamide chemoradiotherapy for advanced squamous cell carcinoma (SCC) of the uterine cervix."( Phase I study of chemoradiation with nedaplatin and ifosfamide in patients with advanced squamous cell carcinoma of the uterine cervix.
Hiramatsu, Y; Hongo, A; Kanazawa, S; Kodama, J; Moriya, S; Nakamura, K; Seki, N; Takemoto, M,
)
0.61
" Carboplatin dosage was based on glomerular filtration rate (GFR) to achieve targeted systemic exposure (6mg/ml min)."( Renal function after ifosfamide, carboplatin and etoposide (ICE) chemotherapy, nephrectomy and radiotherapy in children with Wilms tumour.
Daw, NC; Gregornik, D; Jenkins, JJ; Jones, DP; Kun, LE; Marina, N; McPherson, V; Rodman, J; Wilimas, J; Wu, J, 2009
)
0.67
" Grade 3/4 creatinine increase occurred in 6 patients on glufosfamide, including 4 with dosing errors."( A randomised Phase III trial of glufosfamide compared with best supportive care in metastatic pancreatic adenocarcinoma previously treated with gemcitabine.
Bodoky, G; Ciuleanu, TE; Garin, AM; Kroll, S; Langmuir, VK; Pavlovsky, AV; Tidmarsh, GT, 2009
)
0.35
" A novel five-drug combination of etoposide, vincristine, dactinomycin, ifosfamide, and doxorubicin (EVAIA) was evaluated for high-risk patients, but cumulative chemotherapy dosage and treatment duration were reduced for the remaining individuals as compared with that of the previous trial CWS-86."( Cooperative trial CWS-91 for localized soft tissue sarcoma in children, adolescents, and young adults.
Bielack, SS; Brecht, I; Dantonello, TM; Dickerhoff, R; Gadner, H; Greiner, J; Greulich, M; Harms, D; Herbst, M; Int-Veen, C; Juergens, H; Kirsch, S; Klingebiel, T; Koscielniak, E; Leuschner, I; Marky, I; Scheel-Walter, HG; Schmelzle, R; Schmidt, BF; Treuner, J, 2009
)
0.59
" Alternative dosing of glufosfamide plus gemcitabine should be explored."( A phase 2 trial of glufosfamide in combination with gemcitabine in chemotherapy-naive pancreatic adenocarcinoma.
Barrios, CH; Chiorean, EG; Dragovich, T; Gorini, CF; Hamm, J; Jung, DT; Kroll, S; Langmuir, VK; Loehrer, PJ; Tidmarsh, GT, 2010
)
0.36
" All 21 patients with DI required daily change in dosage and schedule of DDAVP."( Challenges in management of patients with intracranial germ cell tumor and diabetes insipidus treated with cisplatin and/or ifosfamide based chemotherapy.
Afzal, S; Bartels, U; Bouffet, E; Huang, A; Stephens, D; Tabori, U; Wherrett, D, 2010
)
0.57
"Ifosfamide is currently used to treat pediatric sarcomas and increasing its dosage may be associated with a better response rate."( Prolonged 14-day continuous infusion of high-dose ifosfamide with an external portable pump: feasibility and efficacy in refractory pediatric sarcoma.
Casanova, M; Cefalo, G; Favini, F; Ferrari, A; Luksch, R; Massimino, M; Meazza, C; Podda, M, 2010
)
2.06
" Primary therapies were divided into four groups: radiotherapy alone, moderately dosed COPP/ABVD-like chemotherapies for intermediate and advanced stages and BEACOPP escalated."( Impact of first- and second-line treatment for Hodgkin's lymphoma on the incidence of AML/MDS and NHL--experience of the German Hodgkin's Lymphoma Study Group analyzed by a parametric model of carcinogenesis.
Diehl, V; Engert, A; Franklin, J; Hasenclever, D; Josting, A; Loeffler, M; Scholz, M, 2011
)
0.37
" The whole kidney of an animal dosed with imatinib was measured at 35 μm spatial resolution."( Mass spectrometry imaging with high resolution in mass and space (HR(2) MSI) for reliable investigation of drug compound distributions on the cellular level.
Guenther, S; Römpp, A; Spengler, B; Takats, Z, 2011
)
0.37
" We proposed a systematic classification scheme using FDA-approved drug labeling to assess the DILI potential of drugs, which yielded a benchmark dataset with 287 drugs representing a wide range of therapeutic categories and daily dosage amounts."( FDA-approved drug labeling for the study of drug-induced liver injury.
Chen, M; Fang, H; Liu, Z; Shi, Q; Tong, W; Vijay, V, 2011
)
0.37
" No significant dose-response relationship was found in terms of LRC."( Sequential or concomitant chemotherapy in limited stage small-cell lung cancer.
Anchisi, S; Bieri, S; Elhfidh, M; Khanfir, K; Matzinger, O; Mirimanoff, RO; Ozsahin, M; Zouhair, A, 2011
)
0.37
" Once MTD was defined, we expanded this dosing cohort to include patients with high-risk lymphoma due to activity seen during dose escalation."( Phase I Study of Topotecan, Ifosfamide, and Etoposide (TIME) with autologous stem cell transplant in refractory cancer: pharmacokinetic and pharmacodynamic correlates.
Dawson, JL; Field, TL; Fields, KK; Goldstein, SC; Kim, J; Lush, RM; Maddox, BL; Neuger, AM; Partyka, JS; Perkins, JB; Simonelli, CE; Sullivan, DM, 2011
)
0.66
" It could therefore be used as an important platform for better prediction of drug dosing and schedule towards personalized medicine."( Towards personalized medicine with a three-dimensional micro-scale perfusion-based two-chamber tissue model system.
Barker, J; Foltz, G; Honkakoski, P; Küblbeck, J; Li, W; Lin, B; Ma, L; Zhang, J; Zhou, C, 2012
)
0.38
"Patients aged 18 or older with histologically confirmed, locally advanced or metastatic STS were treated with 1 cycle of AI followed by AI with eltrombopag starting at Cycle 2, using 2 different dosing schedules."( Results of a phase I dose escalation study of eltrombopag in patients with advanced soft tissue sarcoma receiving doxorubicin and ifosfamide.
Chawla, SP; Hendifar, A; Kamel, YM; Messam, CA; Patwardhan, R; Staddon, A, 2013
)
0.59
" Available data suggest a potential pre- and post-chemotherapy dosing scheme for eltrombopag when administered with AI chemotherapy, and support further investigation of eltrombopag treatment in patients with chemotherapy-induced thrombocytopenia."( Results of a phase I dose escalation study of eltrombopag in patients with advanced soft tissue sarcoma receiving doxorubicin and ifosfamide.
Chawla, SP; Hendifar, A; Kamel, YM; Messam, CA; Patwardhan, R; Staddon, A, 2013
)
0.59
"No significant dose-response effect of adjuvant RT was demonstrated."( Patterns of local recurrence and dose fractionation of adjuvant radiation therapy in 462 patients with soft tissue sarcoma of extremity and trunk wall.
Bauer, HC; Bruland, OS; Eide, GE; Engellau, J; Engström, K; Jebsen, NL; Monge, OR; Muren, LP; Trovik, CS, 2013
)
0.39
" However, the impact of dosage and dosage intensity (DI) of chemotherapeutic agents on patients with high-grade osteosarcoma is largely unknown."( Analysis of chemotherapy dosage and dosage intensity and survival outcomes of high-grade osteosarcoma patients younger than 40 years.
Li, B; Li, H; Li, Y; Sun, L; Ye, Z; Zhang, J, 2014
)
0.4
" Sufficient data were presented to calculate the planned total dosage and DI for doxorubicin, cisplatin, ifosfamide, and methotrexate."( Analysis of chemotherapy dosage and dosage intensity and survival outcomes of high-grade osteosarcoma patients younger than 40 years.
Li, B; Li, H; Li, Y; Sun, L; Ye, Z; Zhang, J, 2014
)
0.62
"We observed a correlation of higher planned methotrexate total dosage and DI with better treatment outcomes in osteosarcoma patients."( Analysis of chemotherapy dosage and dosage intensity and survival outcomes of high-grade osteosarcoma patients younger than 40 years.
Li, B; Li, H; Li, Y; Sun, L; Ye, Z; Zhang, J, 2014
)
0.4
" It is therefore necessary to investigate ketamine locally and systematically with various dosing schedules in order to reduce the bladder damage secondary to oxazaphosphorine-alkylating agents and these results may widen the spectrum of ketamine."( Protective effect of ketamine against hemorrhagic cystitis in rats receiving ifosfamide.
Onag, A; Ozguven, AA; Taneli, F; Ulman, C; Vatansever, S; Yılmaz, O,
)
0.36
"" The regimen included an intensification of ifosfamide dosing from 1,800 mg/m(2) /day × 5 days per cycle to 2,800 mg/m(2) /day × 5 days per cycle."( Ifosfamide dose-intensification for patients with metastatic Ewing sarcoma.
Chou, AJ; Goodbody, CM; Magnan, H; Pratilas, CA; Riedel, E; Wexler, LH, 2015
)
2.12
"In our experience, continuous-infusion ifosfamide and doxorubicin combination therapy at this dosage and schedule was found to be well tolerated and moderate effective, which could be considered as salvage therapy for patients with recurrent or refractory osteosarcoma."( Continuous-infusion ifosfamide and doxorubicin combination as second-line chemotherapy for recurrent or refractory osteosarcoma patients in China: a retrospective study.
He, AN; Huang, YJ; Min, DL; Shen, Z; Sun, YJ; Yao, Y, 2015
)
1.01
" The novel dosing strategy for cyclophosphamide described herein is readily translatable to standard clinical regimens, represents a potentially significant advance in addressing the drug delivery challenge, and may have broad applicability for nanomedicines."( Cyclophosphamide-Mediated Tumor Priming for Enhanced Delivery and Antitumor Activity of HER2-Targeted Liposomal Doxorubicin (MM-302).
De Souza, R; Dumont, N; Espelin, CW; Gaddy, DF; Geretti, E; Hendriks, BS; Jaffray, DA; Lee, H; Leonard, SC; Moyo, V; Nielsen, UB; Wickham, TJ; Zheng, J, 2015
)
0.42
" Reluctance to use aggressive local control measures and suboptimal chemotherapy dosing are significant contributory factors."( Rhabdomyosarcoma of the orbit in a four months old infant in Zimbabwe: A case report.
Chitsike, I; Kuona, P; Masanganise, R; Sibanda, D,
)
0.13
" Patients with encephalopathy and patients without encephalopathy were compared on age, Eastern Cooperative Oncology Group (ECOG) performance status (PS), baseline serum creatinine (SCr) level, albumin level, white blood cell count, liver function, brain metastasis, and dosage of ifosfamide."( Risk factors of ifosfamide-related encephalopathy in adult patients with cancer: A retrospective analysis.
Chen, WH; Dong, YH; Lo, Y; Shen, LJ; Wu, FL, 2016
)
0.96
" In contrast to previous studies, ifosfamide dosage and brain metastasis are not significant contributing factors."( Risk factors of ifosfamide-related encephalopathy in adult patients with cancer: A retrospective analysis.
Chen, WH; Dong, YH; Lo, Y; Shen, LJ; Wu, FL, 2016
)
1.06
"The extrapolation of the Calvert formula has utility in calculating the CBDCA dosage for DeVIC ± R therapy, and therapeutic efficacy was increased by maintaining the AUC of CBDCA at ≥4."( Evaluation of a method for calculating carboplatin dosage in DeVIC ± R therapy (combination therapy of dexamethasone, etoposide, ifosfamide and carboplatin with or without rituximab) as a salvage therapy in patients with relapsed or refractory non-Hodgkin
Ando, M; Ando, Y; Emi, N; Hayashi, T; Inaguma, Y; Ito, K; Okamoto, A; Okamoto, M; Tomono, A; Tsuge, M; Yamada, S, 2016
)
0.64
" The ifosfamide dosage was reduced to two-thirds of the original protocol."( Dose-Modified Ifosfamide, Epirubicin, and Etoposide is a Safe and Effective Salvage Therapy with High Peripheral Blood Stem Cell Mobilization Capacity for Poorly Mobilized Hodgkin's Lymphoma and Non-Hodgkin's Lymphoma Patients.
Arima, N; Fukunaga, A; Hyuga, M; Iwasaki, M; Kishimoto, W; Maesako, Y; Nakae, Y, 2016
)
1.31
" Increased hydration and dosage of mesna are administered to patients who develop IFO-induced HC; they also receive 24-h continuous infusion of mesna in subsequent treatment cycles."( A retrospective study of treatment and prophylaxis of ifosfamide-induced hemorrhagic cystitis in pediatric and adolescent and young adult (AYA) patients with solid tumors.
Kumamoto, T; Makino, Y; Ogawa, C; Saito, Y; Tamai, I; Terakado, H, 2016
)
0.68
"The incidence of IFO-induced HC may be associated with the dosage of IFO."( A retrospective study of treatment and prophylaxis of ifosfamide-induced hemorrhagic cystitis in pediatric and adolescent and young adult (AYA) patients with solid tumors.
Kumamoto, T; Makino, Y; Ogawa, C; Saito, Y; Tamai, I; Terakado, H, 2016
)
0.68
"5 mg/day dosage of olanzapine is sufficient to prevent from CINV in Japanese patients receiving continuous five-day chemotherapy."( Feasibility of olanzapine, multi acting receptor targeted antipsychotic agent, for the prevention of emesis caused by continuous cisplatin- or ifosfamide-based chemotherapy.
Akagi, T; Bun, S; Fujiwara, Y; Hayashi, Y; Makino, Y; Noguchi, E; Shimizu, C; Shimoi, T; Shimomura, A; Tamura, K; Yonemori, K; Yunokawa, M, 2018
)
0.68
" However, there is still limited data on the adherence of physicians to dosing recommendations for these drugs in cancer patients with renal impairment."( Dose adjustment of cisplatin, etoposide, and ifosfamide according to kidney function: a retrospective analysis and implications for medication safety.
Beckmann, MW; Dörje, F; Fromm, MF; Grafe, C; Hein, A; Mackensen, A; Semrau, S, 2018
)
0.74
" In this study, we adjusted the dosage of the triplet regimen and introduced carboplatin in cisplatin-intolerable patients."( Response to Combination Chemotherapy With Paclitaxel/Ifosfamide/Platinum Versus Paclitaxel/Platinum for Patients With Metastatic, Recurrent, or Persistent Carcinoma of the Uterine Cervix: A Retrospective Analysis.
Bae, DS; Choi, CH; Choi, HJ; Kim, BG; Kim, TJ; Lee, JW; Lee, YY; Paik, ES, 2018
)
0.73
"Vincristine, doxorubicin, and cyclophosphamide (VDC) alternating with ifosfamide and etoposide (IE) administered every 2 weeks demonstrated a superior event-free survival compared with 3-week dosing in a landmark pediatric trial and is now standard of care for younger patients."( Feasibility of Treating Adults with Ewing or Ewing-Like Sarcoma with Interval-Compressed Vincristine, Doxorubicin, and Cyclophosphamide Alternating with Ifosfamide and Etoposide.
Bassale, S; Davis, LE; Lim, JY; Lu, E; Ryan, CW, 2020
)
0.99
"Etoposide dosing is based on body surface area."( Pharmacokinetic and Pharmacogenetic Study of Etoposide in High-Dose Protocol (TI-CE) for Advanced Germ Cell Tumors.
Bay, JO; Chatelut, E; Chevreau, C; Delmas, C; Delva, R; Filleron, T; Fléchon, A; Gravis, G; Gross-Goupil, M; Lafont, T; Lotz, JP; Marsili, S; Massart, C; Moeung, S; Thomas, F, 2020
)
0.56
"The present study suggests that neither a priori dose individualization nor dose adaptation using TDM is required validating body surface area dosing of etoposide in the TI-CE protocol."( Pharmacokinetic and Pharmacogenetic Study of Etoposide in High-Dose Protocol (TI-CE) for Advanced Germ Cell Tumors.
Bay, JO; Chatelut, E; Chevreau, C; Delmas, C; Delva, R; Filleron, T; Fléchon, A; Gravis, G; Gross-Goupil, M; Lafont, T; Lotz, JP; Marsili, S; Massart, C; Moeung, S; Thomas, F, 2020
)
0.56
" Dosing was modified for elderly patients."( Ofatumumab with iphosphamide, etoposide and cytarabine for patients with transplantation-ineligible relapsed and refractory diffuse large B-cell lymphoma.
Borawska, A; Chełstowska, M; Dąbrowska-Iwanicka, A; Domańska-Czyż, K; Druzd-Sitek, A; Giebel, S; Knopińska-Posłuszny, W; Konecki, R; Kumiega, B; Lange, A; Malenda, A; Michalski, W; Mordak-Domagała, M; Najda, J; Osowiecki, M; Ostrowska, B; Paszkiewicz-Kozik, E; Pluta, A; Popławska, L; Romejko-Jarosińska, J; Rymkiewicz, G; Świerkowska, M; Szpila, T; Szymański, M; Targoński, Ł; Taszner, M; Walewski, J; Zaucha, JM, 2022
)
0.72
"this study suggests that chemotherapy drug and its cumulative dosage has the most influence on kidney and urinary tract related complications."( Chemotherapy induced kidney and urinary tract related complications: A study in the Department of Pediatric Oncology and Hematology.
Kiaunytė, S; Kiudelienė, R; Maškė, R; Rutkauskienė, G, 2022
)
0.72
" Concerns about excessive toxicity-as many are infants and/or undergo nephrectomy-have resulted in decreased chemotherapy dosing and omission of the nephrotoxic drug ifosfamide in collaborative group studies."( Tolerability of ifosfamide-containing regimen in patients with high-risk renal and INI-1-deficient tumors.
Benedetti, DJ; Kao, PC; Ma, C; Marcus, KJ; Mullen, EA; Wong, CI, 2023
)
1.45
" Changes in the ratio of lappaconitine to its metabolites in rat urine with time after dosing led to a proposal for one of the probable metabolic pathways of lappaconitine in the rat."( Separation and characterization of the metabolic products of lappaconitine in rat urine by high-performance liquid chromatography.
Chang, JP; Hsieh, YY; Jiang, JR; Li, JH; Shu, HL; Wang, HC; Xie, FM, 1990
)
0.28
[information is derived through text-mining from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Roles (5)

RoleDescription
antineoplastic agentA substance that inhibits or prevents the proliferation of neoplasms.
immunosuppressive agentAn agent that suppresses immune function by one of several mechanisms of action. Classical cytotoxic immunosuppressants act by inhibiting DNA synthesis. Others may act through activation of T-cells or by inhibiting the activation of helper cells. In addition, an immunosuppressive agent is a role played by a compound which is exhibited by a capability to diminish the extent and/or voracity of an immune response.
alkylating agentHighly reactive chemical that introduces alkyl radicals into biologically active molecules and thereby prevents their proper functioning. It could be used as an antineoplastic agent, but it might be very toxic, with carcinogenic, mutagenic, teratogenic, and immunosuppressant actions. It could also be used as a component of poison gases.
environmental contaminantAny minor or unwanted substance introduced into the environment that can have undesired effects.
xenobioticA xenobiotic (Greek, xenos "foreign"; bios "life") is a compound that is foreign to a living organism. Principal xenobiotics include: drugs, carcinogens and various compounds that have been introduced into the environment by artificial means.
[role information is derived from Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Drug Classes (1)

ClassDescription
ifosfamidesCompounds containing an ifosfamide skeleton.
[compound class information is derived from Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Pathways (2)

PathwayProteinsCompounds
Ifosfamide Action Pathway821
Ifosfamide Metabolism Pathway821

Protein Targets (16)

Potency Measurements

ProteinTaxonomyMeasurementAverage (µ)Min (ref.)Avg (ref.)Max (ref.)Bioassay(s)
Chain A, Beta-lactamaseEscherichia coli K-12Potency11.22020.044717.8581100.0000AID485294
GALC proteinHomo sapiens (human)Potency0.707928.183828.183828.1838AID1159614
GLI family zinc finger 3Homo sapiens (human)Potency27.27830.000714.592883.7951AID1259369
AR proteinHomo sapiens (human)Potency13.72370.000221.22318,912.5098AID1259247; AID1259381
EWS/FLI fusion proteinHomo sapiens (human)Potency22.83190.001310.157742.8575AID1259252; AID1259253; AID1259255; AID1259256
retinoid X nuclear receptor alphaHomo sapiens (human)Potency30.86160.000817.505159.3239AID1159527
pregnane X nuclear receptorHomo sapiens (human)Potency54.42730.005428.02631,258.9301AID1346982
estrogen nuclear receptor alphaHomo sapiens (human)Potency46.56600.000229.305416,493.5996AID743069; AID743075; AID743079
chromobox protein homolog 1Homo sapiens (human)Potency79.43280.006026.168889.1251AID540317
thyroid hormone receptor beta isoform 2Rattus norvegicus (Norway rat)Potency61.13060.000323.4451159.6830AID743066
lamin isoform A-delta10Homo sapiens (human)Potency0.05620.891312.067628.1838AID1487
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Inhibition Measurements

ProteinTaxonomyMeasurementAverageMin (ref.)Avg (ref.)Max (ref.)Bioassay(s)
ATP-binding cassette sub-family C member 3Homo sapiens (human)IC50 (µMol)133.00000.63154.45319.3000AID1473740
Multidrug resistance-associated protein 4Homo sapiens (human)IC50 (µMol)133.00000.20005.677410.0000AID1473741
Bile salt export pumpHomo sapiens (human)IC50 (µMol)133.00000.11007.190310.0000AID1473738
Serum paraoxonase/arylesterase 1Homo sapiens (human)Ki8,973.00009.00009.00009.0000AID1801808
Canalicular multispecific organic anion transporter 1Homo sapiens (human)IC50 (µMol)133.00002.41006.343310.0000AID1473739
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Biological Processes (49)

Processvia Protein(s)Taxonomy
xenobiotic metabolic processATP-binding cassette sub-family C member 3Homo sapiens (human)
xenobiotic transmembrane transportATP-binding cassette sub-family C member 3Homo sapiens (human)
bile acid and bile salt transportATP-binding cassette sub-family C member 3Homo sapiens (human)
glucuronoside transportATP-binding cassette sub-family C member 3Homo sapiens (human)
xenobiotic transportATP-binding cassette sub-family C member 3Homo sapiens (human)
transmembrane transportATP-binding cassette sub-family C member 3Homo sapiens (human)
leukotriene transportATP-binding cassette sub-family C member 3Homo sapiens (human)
monoatomic anion transmembrane transportATP-binding cassette sub-family C member 3Homo sapiens (human)
transport across blood-brain barrierATP-binding cassette sub-family C member 3Homo sapiens (human)
prostaglandin secretionMultidrug resistance-associated protein 4Homo sapiens (human)
cilium assemblyMultidrug resistance-associated protein 4Homo sapiens (human)
platelet degranulationMultidrug resistance-associated protein 4Homo sapiens (human)
xenobiotic metabolic processMultidrug resistance-associated protein 4Homo sapiens (human)
xenobiotic transmembrane transportMultidrug resistance-associated protein 4Homo sapiens (human)
bile acid and bile salt transportMultidrug resistance-associated protein 4Homo sapiens (human)
prostaglandin transportMultidrug resistance-associated protein 4Homo sapiens (human)
urate transportMultidrug resistance-associated protein 4Homo sapiens (human)
glutathione transmembrane transportMultidrug resistance-associated protein 4Homo sapiens (human)
transmembrane transportMultidrug resistance-associated protein 4Homo sapiens (human)
cAMP transportMultidrug resistance-associated protein 4Homo sapiens (human)
leukotriene transportMultidrug resistance-associated protein 4Homo sapiens (human)
monoatomic anion transmembrane transportMultidrug resistance-associated protein 4Homo sapiens (human)
export across plasma membraneMultidrug resistance-associated protein 4Homo sapiens (human)
transport across blood-brain barrierMultidrug resistance-associated protein 4Homo sapiens (human)
guanine nucleotide transmembrane transportMultidrug resistance-associated protein 4Homo sapiens (human)
fatty acid metabolic processBile salt export pumpHomo sapiens (human)
bile acid biosynthetic processBile salt export pumpHomo sapiens (human)
xenobiotic metabolic processBile salt export pumpHomo sapiens (human)
xenobiotic transmembrane transportBile salt export pumpHomo sapiens (human)
response to oxidative stressBile salt export pumpHomo sapiens (human)
bile acid metabolic processBile salt export pumpHomo sapiens (human)
response to organic cyclic compoundBile salt export pumpHomo sapiens (human)
bile acid and bile salt transportBile salt export pumpHomo sapiens (human)
canalicular bile acid transportBile salt export pumpHomo sapiens (human)
protein ubiquitinationBile salt export pumpHomo sapiens (human)
regulation of fatty acid beta-oxidationBile salt export pumpHomo sapiens (human)
carbohydrate transmembrane transportBile salt export pumpHomo sapiens (human)
bile acid signaling pathwayBile salt export pumpHomo sapiens (human)
cholesterol homeostasisBile salt export pumpHomo sapiens (human)
response to estrogenBile salt export pumpHomo sapiens (human)
response to ethanolBile salt export pumpHomo sapiens (human)
xenobiotic export from cellBile salt export pumpHomo sapiens (human)
lipid homeostasisBile salt export pumpHomo sapiens (human)
phospholipid homeostasisBile salt export pumpHomo sapiens (human)
positive regulation of bile acid secretionBile salt export pumpHomo sapiens (human)
regulation of bile acid metabolic processBile salt export pumpHomo sapiens (human)
transmembrane transportBile salt export pumpHomo sapiens (human)
negative regulation of plasma lipoprotein oxidationSerum paraoxonase/arylesterase 1Homo sapiens (human)
cholesterol metabolic processSerum paraoxonase/arylesterase 1Homo sapiens (human)
response to toxic substanceSerum paraoxonase/arylesterase 1Homo sapiens (human)
positive regulation of cholesterol effluxSerum paraoxonase/arylesterase 1Homo sapiens (human)
carboxylic acid catabolic processSerum paraoxonase/arylesterase 1Homo sapiens (human)
organophosphate catabolic processSerum paraoxonase/arylesterase 1Homo sapiens (human)
phosphatidylcholine metabolic processSerum paraoxonase/arylesterase 1Homo sapiens (human)
lactone catabolic processSerum paraoxonase/arylesterase 1Homo sapiens (human)
xenobiotic metabolic processCanalicular multispecific organic anion transporter 1Homo sapiens (human)
xenobiotic transmembrane transportCanalicular multispecific organic anion transporter 1Homo sapiens (human)
negative regulation of gene expressionCanalicular multispecific organic anion transporter 1Homo sapiens (human)
bile acid and bile salt transportCanalicular multispecific organic anion transporter 1Homo sapiens (human)
bilirubin transportCanalicular multispecific organic anion transporter 1Homo sapiens (human)
heme catabolic processCanalicular multispecific organic anion transporter 1Homo sapiens (human)
xenobiotic export from cellCanalicular multispecific organic anion transporter 1Homo sapiens (human)
transmembrane transportCanalicular multispecific organic anion transporter 1Homo sapiens (human)
transepithelial transportCanalicular multispecific organic anion transporter 1Homo sapiens (human)
leukotriene transportCanalicular multispecific organic anion transporter 1Homo sapiens (human)
monoatomic anion transmembrane transportCanalicular multispecific organic anion transporter 1Homo sapiens (human)
transport across blood-brain barrierCanalicular multispecific organic anion transporter 1Homo sapiens (human)
xenobiotic transport across blood-brain barrierCanalicular multispecific organic anion transporter 1Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Molecular Functions (30)

Processvia Protein(s)Taxonomy
ATP bindingATP-binding cassette sub-family C member 3Homo sapiens (human)
ABC-type xenobiotic transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
glucuronoside transmembrane transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
ABC-type glutathione S-conjugate transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
ABC-type bile acid transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
ATP hydrolysis activityATP-binding cassette sub-family C member 3Homo sapiens (human)
ATPase-coupled transmembrane transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
xenobiotic transmembrane transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
ATPase-coupled inorganic anion transmembrane transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
icosanoid transmembrane transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
ABC-type transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
guanine nucleotide transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
protein bindingMultidrug resistance-associated protein 4Homo sapiens (human)
ATP bindingMultidrug resistance-associated protein 4Homo sapiens (human)
ABC-type xenobiotic transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
prostaglandin transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
urate transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
purine nucleotide transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
ABC-type glutathione S-conjugate transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
ABC-type bile acid transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
efflux transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
15-hydroxyprostaglandin dehydrogenase (NAD+) activityMultidrug resistance-associated protein 4Homo sapiens (human)
ATP hydrolysis activityMultidrug resistance-associated protein 4Homo sapiens (human)
glutathione transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
ATPase-coupled transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
xenobiotic transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
ATPase-coupled inorganic anion transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
ABC-type transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
protein bindingBile salt export pumpHomo sapiens (human)
ATP bindingBile salt export pumpHomo sapiens (human)
ABC-type xenobiotic transporter activityBile salt export pumpHomo sapiens (human)
bile acid transmembrane transporter activityBile salt export pumpHomo sapiens (human)
canalicular bile acid transmembrane transporter activityBile salt export pumpHomo sapiens (human)
carbohydrate transmembrane transporter activityBile salt export pumpHomo sapiens (human)
ABC-type bile acid transporter activityBile salt export pumpHomo sapiens (human)
ATP hydrolysis activityBile salt export pumpHomo sapiens (human)
aryldialkylphosphatase activitySerum paraoxonase/arylesterase 1Homo sapiens (human)
arylesterase activitySerum paraoxonase/arylesterase 1Homo sapiens (human)
calcium ion bindingSerum paraoxonase/arylesterase 1Homo sapiens (human)
phospholipid bindingSerum paraoxonase/arylesterase 1Homo sapiens (human)
protein homodimerization activitySerum paraoxonase/arylesterase 1Homo sapiens (human)
acyl-L-homoserine-lactone lactonohydrolase activitySerum paraoxonase/arylesterase 1Homo sapiens (human)
protein bindingCanalicular multispecific organic anion transporter 1Homo sapiens (human)
ATP bindingCanalicular multispecific organic anion transporter 1Homo sapiens (human)
organic anion transmembrane transporter activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
ABC-type xenobiotic transporter activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
bilirubin transmembrane transporter activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
ABC-type glutathione S-conjugate transporter activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
ATP hydrolysis activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
ATPase-coupled transmembrane transporter activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
xenobiotic transmembrane transporter activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
ATPase-coupled inorganic anion transmembrane transporter activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
ABC-type transporter activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Ceullar Components (23)

Processvia Protein(s)Taxonomy
plasma membraneATP-binding cassette sub-family C member 3Homo sapiens (human)
basal plasma membraneATP-binding cassette sub-family C member 3Homo sapiens (human)
basolateral plasma membraneATP-binding cassette sub-family C member 3Homo sapiens (human)
membraneATP-binding cassette sub-family C member 3Homo sapiens (human)
nucleolusMultidrug resistance-associated protein 4Homo sapiens (human)
Golgi apparatusMultidrug resistance-associated protein 4Homo sapiens (human)
plasma membraneMultidrug resistance-associated protein 4Homo sapiens (human)
membraneMultidrug resistance-associated protein 4Homo sapiens (human)
basolateral plasma membraneMultidrug resistance-associated protein 4Homo sapiens (human)
apical plasma membraneMultidrug resistance-associated protein 4Homo sapiens (human)
platelet dense granule membraneMultidrug resistance-associated protein 4Homo sapiens (human)
external side of apical plasma membraneMultidrug resistance-associated protein 4Homo sapiens (human)
plasma membraneMultidrug resistance-associated protein 4Homo sapiens (human)
basolateral plasma membraneBile salt export pumpHomo sapiens (human)
Golgi membraneBile salt export pumpHomo sapiens (human)
endosomeBile salt export pumpHomo sapiens (human)
plasma membraneBile salt export pumpHomo sapiens (human)
cell surfaceBile salt export pumpHomo sapiens (human)
apical plasma membraneBile salt export pumpHomo sapiens (human)
intercellular canaliculusBile salt export pumpHomo sapiens (human)
intracellular canaliculusBile salt export pumpHomo sapiens (human)
recycling endosomeBile salt export pumpHomo sapiens (human)
recycling endosome membraneBile salt export pumpHomo sapiens (human)
extracellular exosomeBile salt export pumpHomo sapiens (human)
membraneBile salt export pumpHomo sapiens (human)
extracellular regionSerum paraoxonase/arylesterase 1Homo sapiens (human)
extracellular spaceSerum paraoxonase/arylesterase 1Homo sapiens (human)
endoplasmic reticulum membraneSerum paraoxonase/arylesterase 1Homo sapiens (human)
extracellular exosomeSerum paraoxonase/arylesterase 1Homo sapiens (human)
blood microparticleSerum paraoxonase/arylesterase 1Homo sapiens (human)
high-density lipoprotein particleSerum paraoxonase/arylesterase 1Homo sapiens (human)
spherical high-density lipoprotein particleSerum paraoxonase/arylesterase 1Homo sapiens (human)
extracellular spaceSerum paraoxonase/arylesterase 1Homo sapiens (human)
plasma membraneCanalicular multispecific organic anion transporter 1Homo sapiens (human)
cell surfaceCanalicular multispecific organic anion transporter 1Homo sapiens (human)
apical plasma membraneCanalicular multispecific organic anion transporter 1Homo sapiens (human)
intercellular canaliculusCanalicular multispecific organic anion transporter 1Homo sapiens (human)
apical plasma membraneCanalicular multispecific organic anion transporter 1Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Bioassays (211)

Assay IDTitleYearJournalArticle
AID504749qHTS profiling for inhibitors of Plasmodium falciparum proliferation2011Science (New York, N.Y.), Aug-05, Volume: 333, Issue:6043
Chemical genomic profiling for antimalarial therapies, response signatures, and molecular targets.
AID588499High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, MLPCN compound set2010Current protocols in cytometry, Oct, Volume: Chapter 13Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588499High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, MLPCN compound set2006Cytometry. Part A : the journal of the International Society for Analytical Cytology, May, Volume: 69, Issue:5
Microsphere-based protease assays and screening application for lethal factor and factor Xa.
AID588499High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, MLPCN compound set2010Assay and drug development technologies, Feb, Volume: 8, Issue:1
High-throughput multiplex flow cytometry screening for botulinum neurotoxin type a light chain protease inhibitors.
AID588497High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, MLPCN compound set2010Current protocols in cytometry, Oct, Volume: Chapter 13Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588497High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, MLPCN compound set2006Cytometry. Part A : the journal of the International Society for Analytical Cytology, May, Volume: 69, Issue:5
Microsphere-based protease assays and screening application for lethal factor and factor Xa.
AID588497High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, MLPCN compound set2010Assay and drug development technologies, Feb, Volume: 8, Issue:1
High-throughput multiplex flow cytometry screening for botulinum neurotoxin type a light chain protease inhibitors.
AID1745845Primary qHTS for Inhibitors of ATXN expression
AID651635Viability Counterscreen for Primary qHTS for Inhibitors of ATXN expression
AID588501High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, MLPCN compound set2010Current protocols in cytometry, Oct, Volume: Chapter 13Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588501High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, MLPCN compound set2006Cytometry. Part A : the journal of the International Society for Analytical Cytology, May, Volume: 69, Issue:5
Microsphere-based protease assays and screening application for lethal factor and factor Xa.
AID588501High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, MLPCN compound set2010Assay and drug development technologies, Feb, Volume: 8, Issue:1
High-throughput multiplex flow cytometry screening for botulinum neurotoxin type a light chain protease inhibitors.
AID504812Inverse Agonists of the Thyroid Stimulating Hormone Receptor: HTS campaign2010Endocrinology, Jul, Volume: 151, Issue:7
A small molecule inverse agonist for the human thyroid-stimulating hormone receptor.
AID504810Antagonists of the Thyroid Stimulating Hormone Receptor: HTS campaign2010Endocrinology, Jul, Volume: 151, Issue:7
A small molecule inverse agonist for the human thyroid-stimulating hormone receptor.
AID1347114qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for DAOY cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347090qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for DAOY cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347129qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for SK-N-SH cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347109qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for NB1643 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347121qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for control Hh wild type fibroblast cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347125qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for Rh18 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347096qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for U-2 OS cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347083qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lassa (LASV) Arenavirus: Viability assay - alamar blue signal for LASV Primary Screen2020Antiviral research, 01, Volume: 173A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347099qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for NB1643 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347101qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for BT-12 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347107qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh30 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347092qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for A673 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347104qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for RD cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347102qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh18 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1296008Cytotoxic Profiling of Annotated Libraries Using Quantitative High-Throughput Screening2020SLAS discovery : advancing life sciences R & D, 01, Volume: 25, Issue:1
Cytotoxic Profiling of Annotated and Diverse Chemical Libraries Using Quantitative High-Throughput Screening.
AID1347127qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for Saos-2 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347091qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SJ-GBM2 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347082qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lassa (LASV) Arenavirus: LASV Primary Screen - GLuc reporter signal2020Antiviral research, 01, Volume: 173A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347424RapidFire Mass Spectrometry qHTS Assay for Modulators of WT P53-Induced Phosphatase 1 (WIP1)2019The Journal of biological chemistry, 11-15, Volume: 294, Issue:46
Physiologically relevant orthogonal assays for the discovery of small-molecule modulators of WIP1 phosphatase in high-throughput screens.
AID1347124qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for RD cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347111qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for SK-N-MC cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347119qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for MG 63 (6-TG R) cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347126qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for Rh30 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347086qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lymphocytic Choriomeningitis Arenaviruses (LCMV): LCMV Primary Screen - GLuc reporter signal2020Antiviral research, 01, Volume: 173A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1508630Primary qHTS for small molecule stabilizers of the endoplasmic reticulum resident proteome: Secreted ER Calcium Modulated Protein (SERCaMP) assay2021Cell reports, 04-27, Volume: 35, Issue:4
A target-agnostic screen identifies approved drugs to stabilize the endoplasmic reticulum-resident proteome.
AID1347115qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for NB-EBc1 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347094qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for BT-37 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347097qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Saos-2 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347407qHTS to identify inhibitors of the type 1 interferon - major histocompatibility complex class I in skeletal muscle: primary screen against the NCATS Pharmaceutical Collection2020ACS chemical biology, 07-17, Volume: 15, Issue:7
High-Throughput Screening to Identify Inhibitors of the Type I Interferon-Major Histocompatibility Complex Class I Pathway in Skeletal Muscle.
AID1347093qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SK-N-MC cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347154Primary screen GU AMC qHTS for Zika virus inhibitors2020Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49
Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1347123qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for Rh41 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347095qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for NB-EBc1 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347116qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for SJ-GBM2 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347098qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SK-N-SH cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347118qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for TC32 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347106qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for control Hh wild type fibroblast cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347122qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for U-2 OS cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347089qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for TC32 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347128qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for OHS-50 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347103qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for OHS-50 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347110qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for A673 cells)2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347113qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for LAN-5 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347100qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for LAN-5 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347117qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for BT-37 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347108qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh41 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347425Rhodamine-PBP qHTS Assay for Modulators of WT P53-Induced Phosphatase 1 (WIP1)2019The Journal of biological chemistry, 11-15, Volume: 294, Issue:46
Physiologically relevant orthogonal assays for the discovery of small-molecule modulators of WIP1 phosphatase in high-throughput screens.
AID1347105qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for MG 63 (6-TG R) cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347112qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for BT-12 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347411qHTS to identify inhibitors of the type 1 interferon - major histocompatibility complex class I in skeletal muscle: primary screen against the NCATS Mechanism Interrogation Plate v5.0 (MIPE) Libary2020ACS chemical biology, 07-17, Volume: 15, Issue:7
High-Throughput Screening to Identify Inhibitors of the Type I Interferon-Major Histocompatibility Complex Class I Pathway in Skeletal Muscle.
AID1132157Antileukemic activity against mouse L1210 cells allografted in BDF1 mouse assessed as increase in life span at 70 mg/kg, ip administered 24 hrs relative to control1978Journal of medicinal chemistry, Feb, Volume: 21, Issue:2
Synthesis and antitumor activity of preactivated isophosphamide analogues bearing modified alkylating functionalities.
AID1132161Antileukemic activity against mouse L1210 cells allografted in iv dosed BDF1 mouse assessed as survival over 60 days administered 24 hrs1978Journal of medicinal chemistry, Feb, Volume: 21, Issue:2
Synthesis and antitumor activity of preactivated isophosphamide analogues bearing modified alkylating functionalities.
AID444053Renal clearance in human2010Journal of medicinal chemistry, Feb-11, Volume: 53, Issue:3
Physicochemical space for optimum oral bioavailability: contribution of human intestinal absorption and first-pass elimination.
AID1132160Antileukemic activity against mouse L1210 cells allografted in BDF1 mouse assessed as increase in life span at 530 mg/kg, ip administered 24 hrs relative to control1978Journal of medicinal chemistry, Feb, Volume: 21, Issue:2
Synthesis and antitumor activity of preactivated isophosphamide analogues bearing modified alkylating functionalities.
AID120481Number of survivors on the toxicity day (day = 15) at a dose of 100x1 mg/kg1986Journal of medicinal chemistry, May, Volume: 29, Issue:5
Synthesis and antitumor activity of cyclophosphamide analogues. 4. Preparation, kinetic studies, and anticancer screening of "phenylketophosphamide" and similar compounds related to the cyclophosphamide metabolite aldophosphamide.
AID425652Total body clearance in human2009Journal of medicinal chemistry, Aug-13, Volume: 52, Issue:15
Physicochemical determinants of human renal clearance.
AID1474167Liver toxicity in human assessed as induction of drug-induced liver injury by measuring verified drug-induced liver injury concern status2016Drug discovery today, Apr, Volume: 21, Issue:4
DILIrank: the largest reference drug list ranked by the risk for developing drug-induced liver injury in humans.
AID477295Octanol-water partition coefficient, log P of the compound2010European journal of medicinal chemistry, Apr, Volume: 45, Issue:4
QSPR modeling of octanol/water partition coefficient of antineoplastic agents by balance of correlations.
AID588213Literature-mined compound from Fourches et al multi-species drug-induced liver injury (DILI) dataset, effect in non-rodents2010Chemical research in toxicology, Jan, Volume: 23, Issue:1
Cheminformatics analysis of assertions mined from literature that describe drug-induced liver injury in different species.
AID1132146Antileukemic activity against mouse L1210 cells allografted in BDF1 mouse assessed as mean survival time at 70 mg/kg, ip administered 24 hrs (Rvb 4.6 +/- 0.16 days)1978Journal of medicinal chemistry, Feb, Volume: 21, Issue:2
Synthesis and antitumor activity of preactivated isophosphamide analogues bearing modified alkylating functionalities.
AID588215FDA HLAED, alkaline phosphatase increase2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID588219FDA HLAED, gamma-glutamyl transferase (GGT) increase2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID588216FDA HLAED, serum glutamic oxaloacetic transaminase (SGOT) increase2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID1473740Inhibition of human MRP3 overexpressed in Sf9 insect cell membrane vesicles assessed as uptake of [3H]-estradiol-17beta-D-glucuronide in presence of ATP and GSH measured after 10 mins by membrane vesicle transport assay2013Toxicological sciences : an official journal of the Society of Toxicology, Nov, Volume: 136, Issue:1
A multifactorial approach to hepatobiliary transporter assessment enables improved therapeutic compound development.
AID7617Portion of holoxan excreted in the form of the metabolite from 1300 mL of urine on day 8 was determined in embryonal rhabdomyosarcoma patients treated with ifosfamide1983Journal of medicinal chemistry, May, Volume: 26, Issue:5
Stereospecific synthesis of chiral metabolites of ifosfamide and their determination in the urine.
AID1132163Antileukemic activity against mouse L1210 cells allografted in po dosed BDF1 mouse assessed as survival over 60 days administered 24 hrs1978Journal of medicinal chemistry, Feb, Volume: 21, Issue:2
Synthesis and antitumor activity of preactivated isophosphamide analogues bearing modified alkylating functionalities.
AID1079933Acute liver toxicity defined via clinical observations and clear clinical-chemistry results: serum ALT or AST activity > 6 N or serum alkaline phosphatases activity > 1.7 N. This category includes cytolytic, choleostatic and mixed liver toxicity. Value is
AID588217FDA HLAED, serum glutamic pyruvic transaminase (SGPT) increase2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID540212Mean residence time in human after iv administration2008Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 36, Issue:7
Trend analysis of a database of intravenous pharmacokinetic parameters in humans for 670 drug compounds.
AID130318Percentage increase in life span of L1210 leukemia implanted mice at a dose of 600 mg/kg1988Journal of medicinal chemistry, Jan, Volume: 31, Issue:1
Synthesis and antitumor activity of analogues of ifosfamide modified in the N-(2-chloroethyl) group.
AID1132169Ratio of Cmax to Cmin for antileukemic activity against mouse L1210 cells allografted in po dosed BDF1 mouse assessed as survival over 60 days1978Journal of medicinal chemistry, Feb, Volume: 21, Issue:2
Synthesis and antitumor activity of preactivated isophosphamide analogues bearing modified alkylating functionalities.
AID1079938Chronic liver disease either proven histopathologically, or through a chonic elevation of serum amino-transferase activity after 6 months. Value is number of references indexed. [column 'CHRON' in source]
AID588218FDA HLAED, lactate dehydrogenase (LDH) increase2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID135972Number of mice that survived on day 60 at a dose of 600 mg/kg; 9/181988Journal of medicinal chemistry, Jan, Volume: 31, Issue:1
Synthesis and antitumor activity of analogues of ifosfamide modified in the N-(2-chloroethyl) group.
AID1079940Granulomatous liver disease, proven histopathologically. Value is number of references indexed. [column 'GRAN' in source]
AID588209Literature-mined public compounds from Greene et al multi-species hepatotoxicity modelling dataset2010Chemical research in toxicology, Jul-19, Volume: 23, Issue:7
Developing structure-activity relationships for the prediction of hepatotoxicity.
AID588214FDA HLAED, liver enzyme composite activity2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID135962Number of mice that survived on day 60 at a dose of 300 mg/kg; 17/301988Journal of medicinal chemistry, Jan, Volume: 31, Issue:1
Synthesis and antitumor activity of analogues of ifosfamide modified in the N-(2-chloroethyl) group.
AID1079946Presence of at least one case with successful reintroduction. [column 'REINT' in source]
AID7776Percent ratio of the enantiomeric form (-)S extracted from the urine of alveolar rhabdomyosarcoma patients was determined1983Journal of medicinal chemistry, May, Volume: 26, Issue:5
Stereospecific synthesis of chiral metabolites of ifosfamide and their determination in the urine.
AID130314Percentage increase in life span of L1210 leukemia implanted mice at a dose of 300 mg/kg1988Journal of medicinal chemistry, Jan, Volume: 31, Issue:1
Synthesis and antitumor activity of analogues of ifosfamide modified in the N-(2-chloroethyl) group.
AID7616Portion of holoxan excreted in the form of the metabolite from 1300 mL of urine on day 6 was determined in embryonal rhabdomyosarcoma patients treated with ifosfamide1983Journal of medicinal chemistry, May, Volume: 26, Issue:5
Stereospecific synthesis of chiral metabolites of ifosfamide and their determination in the urine.
AID1473738Inhibition of human BSEP overexpressed in Sf9 cell membrane vesicles assessed as uptake of [3H]-taurocholate in presence of ATP measured after 15 to 20 mins by membrane vesicle transport assay2013Toxicological sciences : an official journal of the Society of Toxicology, Nov, Volume: 136, Issue:1
A multifactorial approach to hepatobiliary transporter assessment enables improved therapeutic compound development.
AID115147Maximum tolerated dose against L1210 leukemia in mice2002Bioorganic & medicinal chemistry letters, Feb-11, Volume: 12, Issue:3
Studies on the side-chain hydroxylation of ifosfamide and its bromo analogue.
AID540209Volume of distribution at steady state in human after iv administration2008Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 36, Issue:7
Trend analysis of a database of intravenous pharmacokinetic parameters in humans for 670 drug compounds.
AID130307Percentage increase in life span of L1210 leukemia implanted mice at a dose of 120 mg/kg1988Journal of medicinal chemistry, Jan, Volume: 31, Issue:1
Synthesis and antitumor activity of analogues of ifosfamide modified in the N-(2-chloroethyl) group.
AID7772Portion of holoxan excreted in the form of the metabolite from 1700 mL of urine on day 5 was determined in embryonal rhabdomyosarcoma patients treated with ifosfamide1983Journal of medicinal chemistry, May, Volume: 26, Issue:5
Stereospecific synthesis of chiral metabolites of ifosfamide and their determination in the urine.
AID1079936Choleostatic liver toxicity, either proven histopathologically or where the ratio of maximal ALT or AST activity above normal to that of Alkaline Phosphatase is < 2 (see ACUTE). Value is number of references indexed. [column 'CHOLE' in source]
AID130311Percentage increase in life span of L1210 leukemia implanted mice at a dose of 200 mg/kg1988Journal of medicinal chemistry, Jan, Volume: 31, Issue:1
Synthesis and antitumor activity of analogues of ifosfamide modified in the N-(2-chloroethyl) group.
AID625284Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatic failure2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID625282Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for cirrhosis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1079937Severe hepatitis, defined as possibly life-threatening liver failure or through clinical observations. Value is number of references indexed. [column 'MASS' in source]
AID1197742Stimulation of human OATP1B1-mediated [3H]estrone 3-sulfate at 100 uM after 5 mins relative to control2015European journal of medicinal chemistry, Mar-06, Volume: 92Interaction of human organic anion transporter polypeptides 1B1 and 1B3 with antineoplastic compounds.
AID7773Portion of holoxan excreted in the form of the metabolite from 2310 mL of urine on day 4 was determined in embryonal rhabdomyosarcoma patients treated with ifosfamide1983Journal of medicinal chemistry, May, Volume: 26, Issue:5
Stereospecific synthesis of chiral metabolites of ifosfamide and their determination in the urine.
AID227699Virtual screen for compounds with anticonvulsant activity2003Bioorganic & medicinal chemistry letters, Aug-18, Volume: 13, Issue:16
Topological virtual screening: a way to find new anticonvulsant drugs from chemical diversity.
AID625277FDA Liver Toxicity Knowledge Base Benchmark Dataset (LTKB-BD) drugs of less concern for DILI2011Drug discovery today, Aug, Volume: 16, Issue:15-16
FDA-approved drug labeling for the study of drug-induced liver injury.
AID444058Volume of distribution at steady state in human2010Journal of medicinal chemistry, Feb-11, Volume: 53, Issue:3
Physicochemical space for optimum oral bioavailability: contribution of human intestinal absorption and first-pass elimination.
AID444055Fraction absorbed in human2010Journal of medicinal chemistry, Feb-11, Volume: 53, Issue:3
Physicochemical space for optimum oral bioavailability: contribution of human intestinal absorption and first-pass elimination.
AID444051Total clearance in human2010Journal of medicinal chemistry, Feb-11, Volume: 53, Issue:3
Physicochemical space for optimum oral bioavailability: contribution of human intestinal absorption and first-pass elimination.
AID588212Literature-mined compound from Fourches et al multi-species drug-induced liver injury (DILI) dataset, effect in rodents2010Chemical research in toxicology, Jan, Volume: 23, Issue:1
Cheminformatics analysis of assertions mined from literature that describe drug-induced liver injury in different species.
AID444052Hepatic clearance in human2010Journal of medicinal chemistry, Feb-11, Volume: 53, Issue:3
Physicochemical space for optimum oral bioavailability: contribution of human intestinal absorption and first-pass elimination.
AID540211Fraction unbound in human after iv administration2008Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 36, Issue:7
Trend analysis of a database of intravenous pharmacokinetic parameters in humans for 670 drug compounds.
AID1473741Inhibition of human MRP4 overexpressed in Sf9 cell membrane vesicles assessed as uptake of [3H]-estradiol-17beta-D-glucuronide in presence of ATP and GSH measured after 20 mins by membrane vesicle transport assay2013Toxicological sciences : an official journal of the Society of Toxicology, Nov, Volume: 136, Issue:1
A multifactorial approach to hepatobiliary transporter assessment enables improved therapeutic compound development.
AID7615Portion of holoxan excreted in the form of the metabolite from 1200 mL of urine on day 7 was determined in embryonal rhabdomyosarcoma patients treated with ifosfamide1983Journal of medicinal chemistry, May, Volume: 26, Issue:5
Stereospecific synthesis of chiral metabolites of ifosfamide and their determination in the urine.
AID112166Effective dose that produce antitumor activity against L1210 leukemia in mice2002Bioorganic & medicinal chemistry letters, Feb-11, Volume: 12, Issue:3
Studies on the side-chain hydroxylation of ifosfamide and its bromo analogue.
AID7777Percent ratio of the enantiomeric form (-)S extracted from the urine of embryonal rhabdomyosarcoma patients was determined1983Journal of medicinal chemistry, May, Volume: 26, Issue:5
Stereospecific synthesis of chiral metabolites of ifosfamide and their determination in the urine.
AID134723Lethal dose to kill 50% of the mice after single ip injection to healthy female CD2F1 mice1988Journal of medicinal chemistry, Jan, Volume: 31, Issue:1
Synthesis and antitumor activity of analogues of ifosfamide modified in the N-(2-chloroethyl) group.
AID1079944Benign tumor, proven histopathologically. Value is number of references indexed. [column 'T.BEN' in source]
AID135951Number of mice that survived on day 60 at a dose of 180 mg/kg; 6/211988Journal of medicinal chemistry, Jan, Volume: 31, Issue:1
Synthesis and antitumor activity of analogues of ifosfamide modified in the N-(2-chloroethyl) group.
AID1079949Proposed mechanism(s) of liver damage. [column 'MEC' in source]
AID625290Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for liver fatty2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1132149Antileukemic activity against mouse L1210 cells allografted in BDF1 mouse assessed as mean survival time at 530 mg/kg, ip administered 24 hrs (Rvb 4.6 +/- 0.16 days)1978Journal of medicinal chemistry, Feb, Volume: 21, Issue:2
Synthesis and antitumor activity of preactivated isophosphamide analogues bearing modified alkylating functionalities.
AID625289Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for liver disease2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID7770Portion of holoxan excreted in the form of the metabolite from 1500 mL of urine on day 9 was determined in embryonal rhabdomyosarcoma patients treated with ifosfamide1983Journal of medicinal chemistry, May, Volume: 26, Issue:5
Stereospecific synthesis of chiral metabolites of ifosfamide and their determination in the urine.
AID1079941Liver damage due to vascular disease: peliosis hepatitis, hepatic veno-occlusive disease, Budd-Chiari syndrome. Value is number of references indexed. [column 'VASC' in source]
AID1132164Antileukemic activity against mouse L1210 cells allografted in iv dosed BDF1 mouse assessed as maximum tolerated dose for survival over 60 days administered 24 hrs1978Journal of medicinal chemistry, Feb, Volume: 21, Issue:2
Synthesis and antitumor activity of preactivated isophosphamide analogues bearing modified alkylating functionalities.
AID625291Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for liver function tests abnormal2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID625281Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for cholelithiasis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID116289Increased life span against L1210 lymphoid leukemia cells in male BDF1 mice at a dose of 100 mg/kg1986Journal of medicinal chemistry, May, Volume: 29, Issue:5
Synthesis and antitumor activity of cyclophosphamide analogues. 4. Preparation, kinetic studies, and anticancer screening of "phenylketophosphamide" and similar compounds related to the cyclophosphamide metabolite aldophosphamide.
AID625288Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for jaundice2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID97384In vitro antitumor activity against murine leukemic L1210 cells; No activity1999Journal of medicinal chemistry, Jul-15, Volume: 42, Issue:14
Chemical stability and fate of the cytostatic drug ifosfamide and its N-dechloroethylated metabolites in acidic aqueous solutions.
AID588211Literature-mined compound from Fourches et al multi-species drug-induced liver injury (DILI) dataset, effect in humans2010Chemical research in toxicology, Jan, Volume: 23, Issue:1
Cheminformatics analysis of assertions mined from literature that describe drug-induced liver injury in different species.
AID1636356Drug activation in human Hep3B cells assessed as human CYP2C9-mediated drug metabolism-induced cytotoxicity measured as decrease in cell viability at 300 uM pre-incubated with BSO for 18 hrs followed by incubation with compound for 3 hrs in presence of NA2016Bioorganic & medicinal chemistry letters, 08-15, Volume: 26, Issue:16
Development of a cell viability assay to assess drug metabolite structure-toxicity relationships.
AID7971Quantity of the metabolite found in the urine of the embryonal rhabdomyosarcoma patients treated with ifosfamide from 1600 mL of urine tested on day 101983Journal of medicinal chemistry, May, Volume: 26, Issue:5
Stereospecific synthesis of chiral metabolites of ifosfamide and their determination in the urine.
AID7969Quantity of the metabolite found in the urine of the embryonal rhabdomyosarcoma patients treated with ifosfamide from 1300 mL of urine tested on day 81983Journal of medicinal chemistry, May, Volume: 26, Issue:5
Stereospecific synthesis of chiral metabolites of ifosfamide and their determination in the urine.
AID184802acute toxicity against rat after iv administration1999Journal of medicinal chemistry, Jul-15, Volume: 42, Issue:14
Chemical stability and fate of the cytostatic drug ifosfamide and its N-dechloroethylated metabolites in acidic aqueous solutions.
AID588210Human drug-induced liver injury (DILI) modelling dataset from Ekins et al2010Drug metabolism and disposition: the biological fate of chemicals, Dec, Volume: 38, Issue:12
A predictive ligand-based Bayesian model for human drug-induced liver injury.
AID130309Percentage increase in life span of L1210 leukemia implanted mice at a dose of 150 mg/kg1988Journal of medicinal chemistry, Jan, Volume: 31, Issue:1
Synthesis and antitumor activity of analogues of ifosfamide modified in the N-(2-chloroethyl) group.
AID134770acute toxicity against mouse after ip administration1999Journal of medicinal chemistry, Jul-15, Volume: 42, Issue:14
Chemical stability and fate of the cytostatic drug ifosfamide and its N-dechloroethylated metabolites in acidic aqueous solutions.
AID540210Clearance in human after iv administration2008Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 36, Issue:7
Trend analysis of a database of intravenous pharmacokinetic parameters in humans for 670 drug compounds.
AID120471Number of survivors on day 60 at a dose of 200 mg/kg; 0/71986Journal of medicinal chemistry, May, Volume: 29, Issue:5
Synthesis and antitumor activity of cyclophosphamide analogues. 4. Preparation, kinetic studies, and anticancer screening of "phenylketophosphamide" and similar compounds related to the cyclophosphamide metabolite aldophosphamide.
AID1079948Times to onset, minimal and maximal, observed in the indexed observations. [column 'DELAI' in source]
AID1079939Cirrhosis, proven histopathologically. Value is number of references indexed. [column 'CIRRH' in source]
AID7967Quantity of the metabolite found in the urine of the embryonal rhabdomyosarcoma patients treated with ifosfamide from 1200 mL of urine tested on day 71983Journal of medicinal chemistry, May, Volume: 26, Issue:5
Stereospecific synthesis of chiral metabolites of ifosfamide and their determination in the urine.
AID130310Percentage increase in life span of L1210 leukemia implanted mice at a dose of 180 mg/kg1988Journal of medicinal chemistry, Jan, Volume: 31, Issue:1
Synthesis and antitumor activity of analogues of ifosfamide modified in the N-(2-chloroethyl) group.
AID444050Fraction unbound in human plasma2010Journal of medicinal chemistry, Feb-11, Volume: 53, Issue:3
Physicochemical space for optimum oral bioavailability: contribution of human intestinal absorption and first-pass elimination.
AID116293Increased life span against L1210 lymphoid leukemia cells in male BDF1 mice at a dose of 200 mg/kg1986Journal of medicinal chemistry, May, Volume: 29, Issue:5
Synthesis and antitumor activity of cyclophosphamide analogues. 4. Preparation, kinetic studies, and anticancer screening of "phenylketophosphamide" and similar compounds related to the cyclophosphamide metabolite aldophosphamide.
AID1079935Cytolytic liver toxicity, either proven histopathologically or where the ratio of maximal ALT or AST activity above normal to that of Alkaline Phosphatase is > 5 (see ACUTE). Value is number of references indexed. [column 'CYTOL' in source]
AID135970Number of mice that survived on day 60 at a dose of 500 mg/kg; 18/301988Journal of medicinal chemistry, Jan, Volume: 31, Issue:1
Synthesis and antitumor activity of analogues of ifosfamide modified in the N-(2-chloroethyl) group.
AID7968Quantity of the metabolite found in the urine of the embryonal rhabdomyosarcoma patients treated with ifosfamide from 1300 mL of urine tested on day 61983Journal of medicinal chemistry, May, Volume: 26, Issue:5
Stereospecific synthesis of chiral metabolites of ifosfamide and their determination in the urine.
AID1636440Drug activation in human Hep3B cells assessed as human CYP2D6-mediated drug metabolism-induced cytotoxicity measured as decrease in cell viability at 300 uM pre-incubated with BSO for 18 hrs followed by incubation with compound for 3 hrs in presence of NA2016Bioorganic & medicinal chemistry letters, 08-15, Volume: 26, Issue:16
Development of a cell viability assay to assess drug metabolite structure-toxicity relationships.
AID1132159Antileukemic activity against mouse L1210 cells allografted in BDF1 mouse assessed as increase in life span at 330 mg/kg, ip administered 24 hrs relative to control1978Journal of medicinal chemistry, Feb, Volume: 21, Issue:2
Synthesis and antitumor activity of preactivated isophosphamide analogues bearing modified alkylating functionalities.
AID235229Therapeutic index represented as LD50/ED50 was determined2002Bioorganic & medicinal chemistry letters, Feb-11, Volume: 12, Issue:3
Studies on the side-chain hydroxylation of ifosfamide and its bromo analogue.
AID1473739Inhibition of human MRP2 overexpressed in Sf9 cell membrane vesicles assessed as uptake of [3H]-estradiol-17beta-D-glucuronide in presence of ATP and GSH measured after 20 mins by membrane vesicle transport assay2013Toxicological sciences : an official journal of the Society of Toxicology, Nov, Volume: 136, Issue:1
A multifactorial approach to hepatobiliary transporter assessment enables improved therapeutic compound development.
AID120469Number of survivors on day 60 at a dose of 100 mg/kg; 0/71986Journal of medicinal chemistry, May, Volume: 29, Issue:5
Synthesis and antitumor activity of cyclophosphamide analogues. 4. Preparation, kinetic studies, and anticancer screening of "phenylketophosphamide" and similar compounds related to the cyclophosphamide metabolite aldophosphamide.
AID7821Quantity of the metabolite found in the urine of the embryonal rhabdomyosarcoma patients treated with ifosfamide from 1200 mL of urine tested on day 31983Journal of medicinal chemistry, May, Volume: 26, Issue:5
Stereospecific synthesis of chiral metabolites of ifosfamide and their determination in the urine.
AID1079942Steatosis, proven histopathologically. Value is number of references indexed. [column 'STEAT' in source]
AID120477Number of survivors on day 60 at a dose of 400 mg/kg; 7/71986Journal of medicinal chemistry, May, Volume: 29, Issue:5
Synthesis and antitumor activity of cyclophosphamide analogues. 4. Preparation, kinetic studies, and anticancer screening of "phenylketophosphamide" and similar compounds related to the cyclophosphamide metabolite aldophosphamide.
AID625286Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatitis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID625285Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatic necrosis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID135955Number of mice that survived on day 60 at a dose of 200 mg/kg; 16/381988Journal of medicinal chemistry, Jan, Volume: 31, Issue:1
Synthesis and antitumor activity of analogues of ifosfamide modified in the N-(2-chloroethyl) group.
AID211869Dose required to induce cytotoxicity against L1210 leukemia in mice2002Bioorganic & medicinal chemistry letters, Feb-11, Volume: 12, Issue:3
Studies on the side-chain hydroxylation of ifosfamide and its bromo analogue.
AID1636357Drug activation in human Hep3B cells assessed as human CYP3A4-mediated drug metabolism-induced cytotoxicity measured as decrease in cell viability at 300 uM pre-incubated with BSO for 18 hrs followed by incubation with compound for 3 hrs in presence of NA2016Bioorganic & medicinal chemistry letters, 08-15, Volume: 26, Issue:16
Development of a cell viability assay to assess drug metabolite structure-toxicity relationships.
AID625287Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatomegaly2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1474166Liver toxicity in human assessed as induction of drug-induced liver injury by measuring severity class index2016Drug discovery today, Apr, Volume: 21, Issue:4
DILIrank: the largest reference drug list ranked by the risk for developing drug-induced liver injury in humans.
AID625280Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for cholecystitis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID625283Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for elevated liver function tests2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID444054Oral bioavailability in human2010Journal of medicinal chemistry, Feb-11, Volume: 53, Issue:3
Physicochemical space for optimum oral bioavailability: contribution of human intestinal absorption and first-pass elimination.
AID1079934Highest frequency of acute liver toxicity observed during clinical trials, expressed as a percentage. [column '% AIGUE' in source]
AID135942Number of mice that survived on day 60 at a dose of 120 mg/kg; 0/241988Journal of medicinal chemistry, Jan, Volume: 31, Issue:1
Synthesis and antitumor activity of analogues of ifosfamide modified in the N-(2-chloroethyl) group.
AID1132166Antileukemic activity against mouse L1210 cells allografted in po dosed BDF1 mouse assessed as maximum tolerated dose for survival over 60 days administered 24 hrs1978Journal of medicinal chemistry, Feb, Volume: 21, Issue:2
Synthesis and antitumor activity of preactivated isophosphamide analogues bearing modified alkylating functionalities.
AID120479Number of survivors on day 60 at a dose of 50 mg/kg; 0/71986Journal of medicinal chemistry, May, Volume: 29, Issue:5
Synthesis and antitumor activity of cyclophosphamide analogues. 4. Preparation, kinetic studies, and anticancer screening of "phenylketophosphamide" and similar compounds related to the cyclophosphamide metabolite aldophosphamide.
AID130316Percentage increase in life span of L1210 leukemia implanted mice at a dose of 500 mg/kg1988Journal of medicinal chemistry, Jan, Volume: 31, Issue:1
Synthesis and antitumor activity of analogues of ifosfamide modified in the N-(2-chloroethyl) group.
AID7614Portion of holoxan excreted in the form of the metabolite from 1200 mL of urine on day 3 was determined in embryonal rhabdomyosarcoma patients treated with ifosfamide1983Journal of medicinal chemistry, May, Volume: 26, Issue:5
Stereospecific synthesis of chiral metabolites of ifosfamide and their determination in the urine.
AID135966Number of mice that survived on day 60 at a dose of 400 mg/kg; 18/301988Journal of medicinal chemistry, Jan, Volume: 31, Issue:1
Synthesis and antitumor activity of analogues of ifosfamide modified in the N-(2-chloroethyl) group.
AID7774Percent ratio of the enantiomeric form (+)R extracted from the urine of alveolar rhabdomyosarcoma patients was determined1983Journal of medicinal chemistry, May, Volume: 26, Issue:5
Stereospecific synthesis of chiral metabolites of ifosfamide and their determination in the urine.
AID1132167Ratio of Cmax to Cmin for antileukemic activity against mouse L1210 cells allografted in iv dosed BDF1 mouse assessed as survival over 60 days1978Journal of medicinal chemistry, Feb, Volume: 21, Issue:2
Synthesis and antitumor activity of preactivated isophosphamide analogues bearing modified alkylating functionalities.
AID1079931Moderate liver toxicity, defined via clinical-chemistry results: ALT or AST serum activity 6 times the normal upper limit (N) or alkaline phosphatase serum activity of 1.7 N. Value is number of references indexed. [column 'BIOL' in source]
AID444057Fraction escaping hepatic elimination in human2010Journal of medicinal chemistry, Feb-11, Volume: 53, Issue:3
Physicochemical space for optimum oral bioavailability: contribution of human intestinal absorption and first-pass elimination.
AID135948Number of mice that survived on day 60 at a dose of 150 mg/kg; 4/441988Journal of medicinal chemistry, Jan, Volume: 31, Issue:1
Synthesis and antitumor activity of analogues of ifosfamide modified in the N-(2-chloroethyl) group.
AID425653Renal clearance in human2009Journal of medicinal chemistry, Aug-13, Volume: 52, Issue:15
Physicochemical determinants of human renal clearance.
AID1132148Antileukemic activity against mouse L1210 cells allografted in BDF1 mouse assessed as mean survival time at 330 mg/kg, ip administered 24 hrs (Rvb 4.6 +/- 0.16 days)1978Journal of medicinal chemistry, Feb, Volume: 21, Issue:2
Synthesis and antitumor activity of preactivated isophosphamide analogues bearing modified alkylating functionalities.
AID116297Increased life span against L1210 lymphoid leukemia cells in male BDF1 mice at a dose of 400 mg/kg1986Journal of medicinal chemistry, May, Volume: 29, Issue:5
Synthesis and antitumor activity of cyclophosphamide analogues. 4. Preparation, kinetic studies, and anticancer screening of "phenylketophosphamide" and similar compounds related to the cyclophosphamide metabolite aldophosphamide.
AID1079947Comments (NB not yet translated). [column 'COMMENTAIRES' in source]
AID7771Portion of holoxan excreted in the form of the metabolite from 1600 mL of urine on day 10 was determined in embryonal rhabdomyosarcoma patients treated with ifosfamide1983Journal of medicinal chemistry, May, Volume: 26, Issue:5
Stereospecific synthesis of chiral metabolites of ifosfamide and their determination in the urine.
AID444056Fraction escaping gut-wall elimination in human2010Journal of medicinal chemistry, Feb-11, Volume: 53, Issue:3
Physicochemical space for optimum oral bioavailability: contribution of human intestinal absorption and first-pass elimination.
AID152509In vivo antitumor activity against murine P388 leukemia; Effective1999Journal of medicinal chemistry, Jul-15, Volume: 42, Issue:14
Chemical stability and fate of the cytostatic drug ifosfamide and its N-dechloroethylated metabolites in acidic aqueous solutions.
AID7973Quantity of the metabolite found in the urine of the embryonal rhabdomyosarcoma patients treated with ifosfamide from 2310 mL of urine tested on day 41983Journal of medicinal chemistry, May, Volume: 26, Issue:5
Stereospecific synthesis of chiral metabolites of ifosfamide and their determination in the urine.
AID7775Percent ratio of the enantiomeric form (+)R extracted from the urine of embryonal rhabdomyosarcoma patients was determined1983Journal of medicinal chemistry, May, Volume: 26, Issue:5
Stereospecific synthesis of chiral metabolites of ifosfamide and their determination in the urine.
AID7970Quantity of the metabolite found in the urine of the embryonal rhabdomyosarcoma patients treated with ifosfamide from 1500 mL of urine tested on day 91983Journal of medicinal chemistry, May, Volume: 26, Issue:5
Stereospecific synthesis of chiral metabolites of ifosfamide and their determination in the urine.
AID7972Quantity of the metabolite found in the urine of the embryonal rhabdomyosarcoma patients treated with ifosfamide from 1700 mL of urine tested on day 51983Journal of medicinal chemistry, May, Volume: 26, Issue:5
Stereospecific synthesis of chiral metabolites of ifosfamide and their determination in the urine.
AID540213Half life in human after iv administration2008Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 36, Issue:7
Trend analysis of a database of intravenous pharmacokinetic parameters in humans for 670 drug compounds.
AID130315Percentage increase in life span of L1210 leukemia implanted mice at a dose of 400 mg/kg1988Journal of medicinal chemistry, Jan, Volume: 31, Issue:1
Synthesis and antitumor activity of analogues of ifosfamide modified in the N-(2-chloroethyl) group.
AID1132147Antileukemic activity against mouse L1210 cells allografted in BDF1 mouse assessed as mean survival time at 130 mg/kg, ip administered 24 hrs (Rvb 4.6 +/- 0.16 days)1978Journal of medicinal chemistry, Feb, Volume: 21, Issue:2
Synthesis and antitumor activity of preactivated isophosphamide analogues bearing modified alkylating functionalities.
AID625292Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) combined score2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID625279Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for bilirubinemia2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1079932Highest frequency of moderate liver toxicity observed during clinical trials, expressed as a percentage. [column '% BIOL' in source]
AID1132158Antileukemic activity against mouse L1210 cells allografted in BDF1 mouse assessed as increase in life span at 130 mg/kg, ip administered 24 hrs relative to control1978Journal of medicinal chemistry, Feb, Volume: 21, Issue:2
Synthesis and antitumor activity of preactivated isophosphamide analogues bearing modified alkylating functionalities.
AID132249Effective dose that causes 50% increase in life span of mice1988Journal of medicinal chemistry, Jan, Volume: 31, Issue:1
Synthesis and antitumor activity of analogues of ifosfamide modified in the N-(2-chloroethyl) group.
AID1079945Animal toxicity known. [column 'TOXIC' in source]
AID1079943Malignant tumor, proven histopathologically. Value is number of references indexed. [column 'T.MAL' in source]
AID1346986P-glycoprotein substrates identified in KB-3-1 adenocarcinoma cell line, qHTS therapeutic library screen2019Molecular pharmacology, 11, Volume: 96, Issue:5
A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
AID1346987P-glycoprotein substrates identified in KB-8-5-11 adenocarcinoma cell line, qHTS therapeutic library screen2019Molecular pharmacology, 11, Volume: 96, Issue:5
A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
AID588519A screen for compounds that inhibit viral RNA polymerase binding and polymerization activities2011Antiviral research, Sep, Volume: 91, Issue:3
High-throughput screening identification of poliovirus RNA-dependent RNA polymerase inhibitors.
AID540299A screen for compounds that inhibit the MenB enzyme of Mycobacterium tuberculosis2010Bioorganic & medicinal chemistry letters, Nov-01, Volume: 20, Issue:21
Synthesis and SAR studies of 1,4-benzoxazine MenB inhibitors: novel antibacterial agents against Mycobacterium tuberculosis.
AID1159607Screen for inhibitors of RMI FANCM (MM2) intereaction2016Journal of biomolecular screening, Jul, Volume: 21, Issue:6
A High-Throughput Screening Strategy to Identify Protein-Protein Interaction Inhibitors That Block the Fanconi Anemia DNA Repair Pathway.
AID1801808Paraoxonase Activity Assay from Article 10.1111/cbdd.12746: \\Some Anticancer Agents Act on Human Serum Paraoxonase-1 to Reduce Its Activity.\\2016Chemical biology & drug design, Aug, Volume: 88, Issue:2
Some Anticancer Agents Act on Human Serum Paraoxonase-1 to Reduce Its Activity.
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023]

Research

Studies (4,767)

TimeframeStudies, This Drug (%)All Drugs %
pre-1990567 (11.89)18.7374
1990's1548 (32.47)18.2507
2000's1374 (28.82)29.6817
2010's1012 (21.23)24.3611
2020's266 (5.58)2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Market Indicators

Research Demand Index: 61.82

According to the monthly volume, diversity, and competition of internet searches for this compound, as well the volume and growth of publications, there is estimated to be very strong demand-to-supply ratio for research on this compound.

MetricThis Compound (vs All)
Research Demand Index61.82 (24.57)
Research Supply Index8.78 (2.92)
Research Growth Index4.77 (4.65)
Search Engine Demand Index109.66 (26.88)
Search Engine Supply Index2.00 (0.95)

This Compound (61.82)

All Compounds (24.57)

Study Types

Publication TypeThis drug (%)All Drugs (%)
Trials1,430 (28.34%)5.53%
Trials4 (5.13%)5.53%
Reviews561 (11.12%)6.00%
Reviews0 (0.00%)6.00%
Case Studies947 (18.77%)4.05%
Case Studies0 (0.00%)4.05%
Observational19 (0.38%)0.25%
Observational0 (0.00%)0.25%
Other2,088 (41.39%)84.16%
Other74 (94.87%)84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Clinical Trials (384)

Trial Overview

TrialPhaseEnrollmentStudy TypeStart DateStatus
A Phase III Study for the Treatment of Children and Adolescents With Newly Diagnosed Low Risk Hodgkin Disease [NCT00302003]Phase 3287 participants (Actual)Interventional2006-02-28Completed
PHASE I/II TRIAL OF SEQUENTIAL TAXOL/IFOSFAMIDE AND DOSEINTENSIVE CARBOPLATIN/ETOPOSIDE WITH STEM CELL SUPPORT IN CISPLATIN-RESISTANT GERM CELL TUMOR PATIENTS WITH UNFAVORABLE PROGNOSTIC FEATURES [NCT00002558]Phase 1/Phase 2108 participants (Actual)Interventional1994-01-31Completed
A Phase I/II Pilot Study of Ifosfamide, Carboplatin and Etoposide Therapy (ICE) and SGN-30 (NSC# 731636, IND#) in Children With CD30+ Recurrent Anaplastic Large Cell Lymphoma [NCT00354107]Phase 1/Phase 25 participants (Actual)Interventional2007-01-31Terminated
A Multicenter, Randomized, Open-Label Phase 3 Study to Investigate the Efficacy and Safety of Aldoxorubicin Compared to Investigator's Choice in Subjects With Metastatic, Locally Advanced, or Unresectable Soft Tissue Sarcomas Who Either Relapsed or Were R [NCT02049905]Phase 3433 participants (Actual)Interventional2014-01-31Completed
A Pilot Study of Pre-Operative Treatment of Newly-Diagnosed, Surgically-Resectable Osteosarcoma With Doxorubicin, Ifosfamide, Etoposide, and Cisplatin With Early Metabolic Assessment of Response [NCT01258634]Phase 12 participants (Actual)Interventional2010-07-31Terminated(stopped due to PI no longer affiliated with institution; only 2 subjects enrolled)
Tandem High-Dose Chemotherapy (HDCT) With Peripheral-Blood Stem-Cell Rescue for Patients With Metastatic Germ-Cell Tumors Failing First-Line Treatment [NCT01172912]Phase 247 participants (Anticipated)Interventional2010-10-31Recruiting
A Phase 1b Study of Olaratumab, Doxorubicin and Ifosfamide in the Treatment of Patients With Advanced or Metastatic Soft Tissue Sarcoma [NCT03283696]Phase 124 participants (Actual)Interventional2017-10-18Completed
A Pilot Study of G-CSF to Disrupt the Bone Marrow Microenvironment in Relapsed or Refractory Acute Lymphoblastic Leukemia [NCT01331590]Early Phase 113 participants (Actual)Interventional2011-07-31Completed
Anlotinib Hydrochloride Combined With Epirubicin and Ifosfamide for Locally Recurrent or Metastatic Soft Tissue Sarcoma Patients: a One-arm, Multi-center, Prospective Clinical Trial [NCT03815474]Phase 247 participants (Anticipated)Interventional2019-05-20Recruiting
Phase II Study of Neoadyuvant High-dose Ifosfamide and Concurrent Radiotherapy in Soft Tissue Sarcoma and Identification of Response Predictors [NCT01102608]Phase 232 participants (Actual)Interventional2008-03-31Completed
A Phase 2, Open-Label Study of Acalabrutinib in Combination With R-ICE For Relapsed or Refractory Non-Germinal Center Diffuse Large B Cell Lymphoma, Transformed Chronic Lymphocytic Leukemia/Small Lymphocytic Leukemia or Transformed Marginal Zone Lymphoma [NCT04189952]Phase 22 participants (Actual)Interventional2020-09-22Terminated(stopped due to Investigator Decision)
Trial of Chemotherapy Intensification Through Compression in Ewing's Sarcoma and Related Tumors [NCT00006734]Phase 3587 participants (Actual)Interventional2001-05-31Completed
Tandem High-Dose Chemotherapy With Autologous Stem Cell Rescue for Poor-Prognosis Germ Cell Cancer [NCT00002931]Phase 248 participants (Actual)Interventional1997-02-28Completed
A Phase III Multicenter, International, Randomized, Double-blind, Placebo-controlled Study of Doxorubicin Plus Palifosfamide-tris vs. Doxorubicin Plus Placebo in Patients With Front-line Metastatic Soft Tissue Sarcoma. [NCT01168791]Phase 3447 participants (Actual)Interventional2010-07-31Completed
Risk-Adapted Focal Proton Beam Radiation and/or Surgery in Patients With Low, Intermediate and High Risk Rhabdomyosarcoma Receiving Standard or Intensified Chemotherapy [NCT01871766]Phase 298 participants (Actual)Interventional2013-12-04Active, not recruiting
A Phase I Multicenter, Open-label Study of the Effect on QTc, Pharmacokinetics, Safety, and Preliminary Efficacy of Single-agent Palifosfamide-tris in Subjects With Advanced Solid Tumors [NCT01340547]Phase 124 participants (Anticipated)Interventional2011-06-30Active, not recruiting
Apatinib+Ifosfamide and Etoposide (IE) Versus IE Alone for Relapsed or Refractory Osteosarcoma: a Real-world Study in Two Centers in China [NCT04690231]79 participants (Actual)Interventional2020-12-01Completed
A Phase I/II Trial of Neoadjuvant ADI-PEG 20 in Combination With Ifosfamide and Radiotherapy in Soft Tissue Sarcoma (STS) [NCT05813327]Phase 1/Phase 235 participants (Anticipated)Interventional2024-01-31Not yet recruiting
Safety and Efficacy of Combination Chemotherapy With Pazopanib in Children and Adolescents With Relapsed/Refractory Solid Tumors [NCT03628131]Phase 1/Phase 246 participants (Anticipated)Interventional2018-10-31Not yet recruiting
Localized High-Risk Soft Tissue Sarcomas Of The Extremities And Trunk Wall In Adults: An Integrating Approach Comprising Standard Vs Histotype-Tailored Neoadjuvant Chemotherapy [NCT01710176]Phase 3550 participants (Actual)Interventional2011-06-01Active, not recruiting
A Randomized Phase IIb Placebo-controlled Study of R-ICE Chemotherapy With and Without SGN-40 (Anti-CD40 Humanized Monoclonal Antibody) for Second-line Treatment of Patients With Diffuse Large B-Cell Lymphoma (DLBCL) [NCT00529503]Phase 2151 participants (Actual)Interventional2007-09-30Terminated
A Phase II Multicenter, Parallel Group, Randomized Study of Palifosfamide Tris Plus Doxorubicin Versus Doxorubicin in Subjects With Unresectable or Metastatic Soft-tissue Sarcoma [NCT00718484]Phase 267 participants (Actual)Interventional2008-08-31Active, not recruiting
Randomized Phase II Study to Compare Efficacy of CHOP Versus Fractionated ICED in Transplant-eligible Patients With Previously Untreated Peripheral T-cell Lymphoma [NCT02445404]Phase 2134 participants (Anticipated)Interventional2015-09-23Recruiting
A Phase Ib/II Study of Pembrolizumab With Chemotherapy in Patients With Advanced Lymphoma (PembroHeme) [NCT02408042]Phase 1/Phase 20 participants (Actual)Interventional2015-04-30Withdrawn
Combination Chemotherapy Using Cisplatin, Gemcitabine, Ifosfamide, Etoposide, L-asparaginase and Dexamethasone (SIMPLE) for Newly Diagnosed and Relapsed/Refractory NK/T Cell Malignancies [NCT03623087]Phase 368 participants (Anticipated)Interventional2017-07-01Recruiting
Phase I-II Trial of Sunitinib and/or Nivolumab Plus Chemotherapy in Advanced Soft Tissue and Bone Sarcomas [NCT03277924]Phase 1/Phase 2270 participants (Anticipated)Interventional2017-05-31Recruiting
Phase I/II Study of Mesna, Ifosfamide, Teniposide and Weekly Taxol (MITTen) in Relapsed Lymphoma [NCT00004916]Phase 1/Phase 20 participants Interventional1999-02-28Completed
Peripheral Stem Cell Transplantation Protocol for Patients With Previously Treated Advanced Breast Cancer - A Phase II Pilot Study [NCT00004172]Phase 20 participants Interventional1999-10-31Completed
Famitinib Malate (SHR1020) Plus Camrelizumab (SHR 1210) Versus Famitinib Malate Alone Versus Famitinib Malate Plus Ifosfamide Locally Advanced, Unresectable or Metastatic Osteosarcoma Progression Upon Chemotherapy: A Phase Ib/II Randomized and Controlled [NCT04044378]Phase 1/Phase 20 participants (Actual)Interventional2019-08-15Withdrawn(stopped due to toxicity)
Multidisciplinary Approach for Poor Prognosis Sinonasal Tumors: Phase II Study of Chemotherapy, Photon and Heavy Ion Radiotherapy Integration for More Effective and Less Toxic Treatment in Inoperable Patients [NCT02099188]Phase 227 participants (Actual)Interventional2013-11-30Active, not recruiting
Autologous Peripheral Blood Stem Cell Transplant for Germ Cell Tumors [NCT00432094]Phase 223 participants (Actual)Interventional2006-12-19Completed
Phase I/II Feasibility Study of Brentuximab Vedotin in Refractory / Relapsed Hodgkin Lymphoma Patients Who Are Treated by Chemotherapy (ICE) in Second Line and Eligible for Autologous Transplantation [NCT02686346]Phase 1/Phase 253 participants (Actual)Interventional2016-03-31Completed
High-Dose Doxorubicin and Ifosfamide Followed by Melphalan and Cisplatin for Patients With High-Risk and Recurrent Sarcoma [NCT00002601]Phase 213 participants (Actual)Interventional1994-09-30Completed
A Risk-Adapted Strategy of the Use of Dose-Dense Chemotherapy in Patients With Poor-Prognosis Disseminated Non-Seminomatous Germ Cell Tumors [NCT00104676]Phase 3263 participants (Actual)Interventional2003-11-26Active, not recruiting
Chemotherapy Plus Ofatumumab Followed by G-CSF for Mobilization of Peripheral Blood Stem Cells in Patients With Non-Hodgkin's Lymphomas [NCT01329900]Phase 250 participants (Actual)Interventional2011-08-22Completed
International Collaborative Treatment Protocol for Children and Adolescents With Acute Lymphoblastic Leukemia - AIEOP-BFM ALL 2017 [NCT03643276]Phase 35,000 participants (Anticipated)Interventional2018-07-15Recruiting
A Randomized Phase 2 Trial of Brentuximab Vedotin (SGN35, NSC# 749710), or Crizotinib (NSC#749005, Commercially Labeled) in Combination With Chemotherapy for Newly Diagnosed Patients With Anaplastic Large Cell Lymphoma (ALCL) [NCT01979536]Phase 2137 participants (Actual)Interventional2013-11-13Active, not recruiting
Phase 1b Trial Evaluating Idelalisib in Children and Adolescents With Relapsed or Refractory Diffuse Large B-cell Lymphoma or Mediastinal B-cell Lymphoma in Combination With RICE [NCT03349346]Phase 10 participants (Actual)Interventional2019-06-30Withdrawn(stopped due to The European Medical Agency granted a Paediatric Investigational Product-specific waiver on the grounds that idelalisib is likely to be unsafe in paediatrics)
A Pilot Phase II Study for Children With Infantile Fibrosarcoma [NCT00072280]Phase 27 participants (Actual)Interventional2004-11-30Terminated(stopped due to Due to poor accrual)
Multi-center, Phase I Clinical Study to Evaluate the Safety and Tolerability of Multi-antigen Autologous Immune Cell Injection (MASCT-I) in Patients With Advanced Solid Tumor, and to Preliminarily Evaluate the Anti-tumor Efficacy of MASCT-I Alone, in Comb [NCT03034304]Phase 1193 participants (Anticipated)Interventional2017-01-31Recruiting
High-Dose Chemo-Radiotherapy for Patients With Primary Refractory and Relapsed Hodgkin's Disease [NCT00003631]Phase 2118 participants (Actual)Interventional1998-08-31Completed
A Phase III Randomized Trial Investigating Bortezomib (NSC# 681239) on a Modified Augmented BFM (ABFM) Backbone in Newly Diagnosed T-Lymphoblastic Leukemia (T-ALL) and T-Lymphoblastic Lymphoma (T-LLy) [NCT02112916]Phase 3847 participants (Actual)Interventional2014-10-04Active, not recruiting
A Phase 1b/2, Open-Label Trial to Assess the Safety and Preliminary Efficacy of Epcoritamab (GEN3013; DuoBody®-CD3xCD20) in Combination With Other Agents in Subjects With B-cell Non-Hodgkin Lymphoma (B-NHL) [NCT04663347]Phase 1/Phase 2662 participants (Anticipated)Interventional2020-11-03Recruiting
Prospective Phase II Study Evaluating a Multimodal Care of Inguinal Node Metastasis in Squamous Cell Carcinoma of the Penis by Bilateral Lymphadenectomy and Chemotherapy TIP [NCT02817958]Phase 237 participants (Anticipated)Interventional2016-10-17Recruiting
A Phase 2 Trial of Chemotherapy Followed by Response-Based Whole Ventricular &Amp; Spinal Canal Irradiation (WVSCI) for Patients With Localized Non-Germinomatous Central Nervous System Germ Cell Tumor [NCT04684368]Phase 2160 participants (Anticipated)Interventional2021-07-13Recruiting
Treatment of Newly Diagnosed Diffuse Anaplastic Wilms Tumors (DAWT) and Relapsed Favorable Histology Wilms Tumors (FHWT) [NCT04322318]Phase 2221 participants (Anticipated)Interventional2020-10-19Recruiting
Pazopanib Neoadjuvant Trial in Non-Rhabdomyosarcoma Soft Tissue Sarcomas (PAZNTIS): A Phase II/III Randomized Trial of Preoperative Chemoradiation or Preoperative Radiation Plus or Minus Pazopanib (NSC# 737754) [NCT02180867]Phase 2/Phase 3140 participants (Actual)Interventional2014-07-11Active, not recruiting
PEI REGIMEN: A THERAPEUTIC OPTION IN SMALL CELL LUNG CANCER? A MONOINSTITUTIONAL EXPERIENCE OF 46 CONSECUTIVE CASES [NCT02324296]46 participants (Actual)Observational1998-12-31Completed
Combined Systemic and Intrathecal Chemotherapy Followed by High-dose Chemotherapy and Autologous Stem Cell Transplantation for CNS Relapse of Aggressive Lymphomas [NCT01148173]Phase 230 participants (Anticipated)Interventional2007-10-31Recruiting
An Open-Label, Pilot Study To Investigate Feasibility and Safety Of Using Bortezomib, Rituximab, Ifosfamide, Carboplatin, Etoposide As Salvage Regime In Previously Treated Patients With Diffuse Large B-Cell Lymphoma [NCT01226849]Phase 16 participants (Actual)Interventional2010-11-30Completed
Young Adult Acute Lymphoid Leukemia (ALL): Intensification of Pediatric AIEOP LLA-2000 Treatment [NCT01156883]76 participants (Actual)Interventional2010-04-30Completed
Presurgical Chemotherapy Compared With Immediate Surgery and Adjuvant Chemotherapy for Nonmetastatic Osteosarcoma of the Pelvis and Sacrum [NCT03360760]100 participants (Anticipated)Interventional2018-08-01Recruiting
(RICE) Plus Bortezomib (Velcade) in a Dose-Escalating Fashion for Patients With Relapsed or Primary Refractory Aggressive B-Cell NHL [NCT01300793]Phase 16 participants (Actual)Interventional2007-05-31Terminated(stopped due to closed for low accrual and no data is available.)
An International Phase II Trial Assessing Tolerability and Efficacy of Sequential Methotrexate-Aracytin-based Combination and R-ICE Combination, Followed by HD Chemotherapy Supported by ASCT, in Patients With Systemic B-cell Lymphoma With CNS Involvement [NCT02329080]Phase 276 participants (Actual)Interventional2014-12-31Active, not recruiting
Safety and Efficacy Pilot Trial of the Anti-Viral and Anti-Tumor Activity of Velcade Combined With (R)ICE in Subjects With EBV and/or HHV-8 Positive Relapsed/Refractory AIDS-Associated Non-Hodgkin's Lymphoma [NCT00598169]Phase 123 participants (Actual)Interventional2007-11-30Completed
A Non-Randomized Phase III Study of Response Adapted Therapy for the Treatment of Children With Newly Diagnosed High Risk Hodgkin Lymphoma [NCT01026220]Phase 3166 participants (Actual)Interventional2009-12-07Completed
A Multicentre, Phase II, Open Label, Single Arm Study of Pixantrone in Patients With CD20-positive Relapsed or Refractory Aggressive Non-Hodgkin Lymphoma Treated With Rituximab, Ifosfamide and Etoposide. [NCT03458260]Phase 274 participants (Actual)Interventional2018-03-26Active, not recruiting
Therapeutic Trial for Patients With Ewing Sarcoma Family of Tumor and Desmoplastic Small Round Cell Tumors [NCT01946529]Phase 224 participants (Actual)Interventional2013-12-27Active, not recruiting
Phase II Study of Rituximab in Combination With Methotrexate, Doxorubicin, Cyclophosphamide, Leucovorin, Vincristine, Ifosfamide, Etoposide, Cytarabine and Mesna (R-MACLO/VAM) in Patients With Previously Untreated Mantle Cell Lymphoma [NCT00878254]Phase 225 participants (Actual)Interventional2009-03-25Active, not recruiting
Feasibility and Dose Discovery Analysis of Zoledronic Acid With Concurrent Chemotherapy in the Treatment of Newly Diagnosed Metastatic Osteosarcoma [NCT00742924]Phase 124 participants (Actual)Interventional2008-08-31Completed
Randomized Phase II Study of Neoadjuvant Chemotherapy Plus Retifanlimab (INCMGA00012) in Patients With Selected Sarcomas [NCT04968106]Phase 266 participants (Anticipated)Interventional2022-12-07Recruiting
Neoadjuvant Chemotherapy Combined With Targeted Treatment in High-risk Retroperitoneal Sarcoma-- A Nationwide Multicentered Prospective Controlled Study [NCT05844813]Phase 4102 participants (Anticipated)Interventional2022-11-01Enrolling by invitation
A Study of Bevacizumab, a Humanized Monoclonal Antibody Against Vascular Endothelial Growth Factor (VEGF), in Combination With Chemotherapy for Treatment of Osteosarcoma [NCT00667342]Phase 243 participants (Actual)Interventional2008-06-03Completed
International Phase 3 Trial in Philadelphia Chromosome-Positive Acute Lymphoblastic Leukemia (Ph+ALL) Testing Imatinib in Combination With Two Different Cytotoxic Chemotherapy Backbones [NCT03007147]Phase 3475 participants (Anticipated)Interventional2017-08-08Recruiting
A Phase II Study of the Efficacy and Safety of Lenalidomide Plus ICE in the Treatment of Refractory and Relapsed Diffuse Large B-cell Lymphoma [NCT03367143]Phase 239 participants (Anticipated)Interventional2016-12-31Active, not recruiting
A Phase II Trial of Irinotecan and Temozolomide in Combination With Existing High Dose Alkylator Based Chemotherapy for Treatment of Patients With Newly Diagnosed Ewing Sarcoma [NCT01864109]Phase 283 participants (Actual)Interventional2013-05-31Active, not recruiting
Phase II Trial of Pembrolizumab in Combination With ICE Salvage Chemotherapy for Relapsed/Refractory Hodgkin Lymphoma [NCT03077828]Phase 243 participants (Actual)Interventional2017-04-21Active, not recruiting
Combination Chemotherapy Including Cisplatin, Ifosfamide, Gemcitabine, L-asparaginase, Etoposide and Dexamethasone (PIGLETS Regimen) as Treatment of Newly Diagnosed and Relapsed/Refractory Peripheral T Cell Lymphomas (PTCLs) [NCT03071822]Phase 450 participants (Anticipated)Interventional2017-02-24Recruiting
N9: Pilot Study of Novel Shortened Induction Chemotherapy for High-Risk Neuroblastoma [NCT04947501]Early Phase 130 participants (Anticipated)Interventional2021-06-22Recruiting
Multicenter Prospective Randomized Study on NeoAdjuvant Chemotherapy Followed by Radical Hysterectomy (OP) Versus Primary Chemo-RADiation in Patients With Cervical Cancer FIGO Stage IB2 and IIB [NCT02422563]Phase 3534 participants (Anticipated)Interventional2015-10-31Not yet recruiting
A Treatment Strategy of the Use of 1st Line Chemotherapy in Patients With Poor-Prognosis Disseminated Non-Seminomatous Germ Cell Tumors Based on Tumor Marker Decline: A Phase II Trial of Paclitaxel, Ifosfamid and Cisplatin Regimen. [NCT02414685]Phase 219 participants (Actual)Interventional2015-04-30Completed
An Open-label, Non-randomized Phase 2 Study of Ofatumomab (O) in Combination With ICE (Ifosfamide, Carboplatin, Etoposide)-Chemotherapy in Patients With Relapsed/Refractory Diffuse Large B-cell Lymphoma (DLBCL) [NCT02412267]Phase 217 participants (Actual)Interventional2011-04-30Completed
Phase II Study of Intensive Chemotherapy and Rituximab in Burkitt Lymphoma [NCT00126191]Phase 210 participants (Actual)Interventional2005-07-31Terminated(stopped due to closed due to slow accrual)
A Phase I/II, Open-Label, Single-Arm, Two-Part Trial to Evaluate Safety, Tolerability, Pharmacokinetics, and Anti-Tumor Activity of Glofitamab in Monotherapy and in Combination With Chemoimmunotherapy in Pediatric and Young Adult Participants With Relapse [NCT05533775]Phase 1/Phase 265 participants (Anticipated)Interventional2022-11-16Recruiting
A Phase II Single Arm Study of the Use of CODOX-M/IVAC With Rituximab (R-CODOX-M/IVAC) in the Treatment of Patients With Diffuse Large B-Cell Lymphoma (International Prognostic Index High or High-Intermediate Risk) [NCT00974792]Phase 2150 participants (Anticipated)Interventional2006-01-31Recruiting
A Study of Etoposide and Ifosfamide Combined With or Without Sulfatinib on Relapsed or Refractory Drug Resistant Osteosarcoma [NCT05590572]Phase 1/Phase 2148 participants (Anticipated)Interventional2023-01-31Not yet recruiting
A Phase II Study of Bortezomib (Velcade, PS-341) in Combination With Ifosfamide/Vinorelbine in Pediatric Patients and Young Adults With Refractory/Recurrent Hodgkin Disease [NCT00381940]Phase 226 participants (Actual)Interventional2007-01-31Completed
Phase II Study of Rituximab in Combination With Methotrexate, Doxorubicin, Cyclophosphamide, Leucovorin, Vincristine, Ifosfamide, Etoposide, Cytarabine and Mesna (MACLO/IVAM) in Patients With Previously Untreated Mantle Cell Lymphoma [NCT00450801]Phase 222 participants (Actual)Interventional2004-04-30Completed
Phase I/II Study of AMG 531 in Patients With Advanced Malignancy Receiving Treatment With Carboplatin [NCT00147225]Phase 1/Phase 255 participants (Actual)Interventional2005-08-31Completed
"A Pilot Phase II Trial of Adjuvant Radiation Therapy Sandwiched Between Ifosfamide in Patients With Mixed Mesodermal Tumors" [NCT00231842]Phase 230 participants (Actual)Interventional2003-02-28Completed
Multicentric, Randomized Phase II Trial for the Treatment of Patients With Relapsed Osteosarcoma [NCT02718482]Phase 27 participants (Actual)Interventional2016-04-06Terminated(stopped due to Not adequate enrollment (sample size not possible to reach))
A Randomized, Open-label, Safety and Efficacy Study of Ibrutinib in Pediatric and Young Adult Patients With Relapsed or Refractory Mature B-cell Non-Hodgkin Lymphoma [NCT02703272]Phase 372 participants (Actual)Interventional2016-07-01Terminated(stopped due to IDMC recommended that enrolment be stoped, as the EFS hazard ratio and associated p-value crossed the futility boundary specified in protocol (July 2020).)
Chemotherapy, Irradiation, and Surgery for Function-Preserving Curative Therapy of Primary Extremity Soft Tissue Sarcomas: Initial Treatment With I-MAP and GM-CSF; Aerosol GM-CSF During Preoperative Irradiation and Postoperatively [NCT00652860]Phase 239 participants (Anticipated)Interventional2001-08-31Completed
Genomics-Based Target Therapy for Children With Relapsed or Refractory Malignancy [NCT02638428]Phase 290 participants (Anticipated)Interventional2015-12-31Recruiting
Phase I/II Multicentre Trial of Salvage Chemotherapy With Gem-TIP for Relapsed Germ Cell Cancer [NCT00551122]Phase 1/Phase 223 participants (Anticipated)Interventional2006-11-30Recruiting
A Phase II Study of Sorafenib and Ifosfamide as a Treatment for Patients With Sarcoma [NCT00880542]Phase 27 participants (Actual)Interventional2008-08-31Terminated(stopped due to The study lost funding.)
Mitomycin and Ifosfamide (MI) as Salvage Therapy for Metastatic Pancreatic Adenocarcinoma: a Phase II Study. [NCT00967291]Phase 221 participants (Actual)Interventional2006-03-31Terminated(stopped due to lack of activity and G3-4 toxicity at interim analysis)
Treatment of Newly Diagnosed Untreated Osteosarcoma: A Pilot Study of a New Chemotherapeutic Regimen Including Ifosfamide [NCT00645632]60 participants (Anticipated)Interventional1990-11-30Completed
IGEV +/- Bortezomib (Velcade) as Induction Before High Dose Consolidation in Relapsed/Refractory Hodgkin's Lymphoma After First Line Treatment: a Randomized Phase II Trial. On Behalf of Intergruppo Italiano Linfomi [NCT00636311]Phase 213 participants (Actual)Interventional2008-02-29Completed
A Phase I/II Study of Methylselenocysteine (MSC) in Combination With Immunochemotherapy (R-ICE) in Patients With Relapsed/Refractory Diffuse Large B-cell Lymphoma (DLBCL) [NCT00829205]Phase 1/Phase 20 participants (Actual)Interventional2009-01-31Withdrawn
Phase II Study of VIDL (VP-16, Ifosfamide, Dexamethasone, L-asparaginase) Chemotherapy Followed by High-dose Chemotherapy and Autologous Stem Cell Transplantation in Patients With Stage III/IV Extranodal NK-T-Cell Lymphoma [NCT02544425]Phase 227 participants (Anticipated)Interventional2016-02-21Recruiting
A Phase II Study of (Neoadjuvant Chemotherapy Trial Prior to Extirpative Surgery) for Clinical Stage TanyN2-3M0 Squamous Cell Carcinoma of the Penis [NCT00512096]Phase 230 participants (Actual)Interventional1999-08-31Completed
A Phase II Study to Evaluate the Pharmacokinetics, Safety, and Obtain a Preliminary Efficacy Assessment of Palifermin in Patients With Sarcoma Receiving Multicycle Chemotherapy With Doxorubicin and Ifosfamide [NCT00267046]Phase 249 participants (Actual)Interventional2005-12-31Completed
A Phase III Randomised Study Comparing Three Combination Chemotherapy Regimens in Patients With Non Pre-treated Advanced Non-small Cell Lung Cancer [NCT00622349]Phase 3707 participants (Actual)Interventional2004-02-29Completed
Sequential Neoadjuvant Ifosfamide and Doxorubicin in Localized High-grade Soft Tissue Sarcoma of Extremities and Trunk Wall [NCT04776525]Phase 249 participants (Anticipated)Interventional2021-04-27Recruiting
Outpatient Chemotherapy in Pediatric Osteosarcoma: Doxorubicin With Cisplatin, High-Dose Methotrexate, and Additional Risk-Adapted Outpatient Chemotherapy [NCT00673179]7 participants (Actual)Interventional2008-05-31Terminated(stopped due to Low accrual.)
A Randomized Trial of the I-BFM-SG for the Management of Childhood Non-B Acute Lymphoblastic Leukemia [NCT00764907]Phase 34,000 participants (Anticipated)Interventional2002-11-30Recruiting
A Phase I Investigator-Initiated Study of Selinexor (KPT-330) Plus RICE in Patients With Relapsed or Refractory Aggressive B-cell Lymphomas [NCT02471911]Phase 122 participants (Actual)Interventional2015-12-11Completed
Phase I Study To Determine The Safety Of Caelyx (Doxorubin HCI, Pegylated Liposomal) In Combination With Ifosfamide In Previously Untreated Adult Patients With Advanced And/Or Metastatic Soft Tissues Sarcomas [NCT00030784]Phase 128 participants (Actual)Interventional2001-11-30Completed
A Phase I Investigator Sponsored Trial of Selinexor (KPT-330), a Selective Inhibitor of Nuclear Export / SINE™ Compound and Ifosfamide, Carboplatin, Etoposide (ICE) in Patients With Relapsed or Refractory Peripheral T-cell Lymphoma [NCT03212937]Phase 111 participants (Actual)Interventional2016-07-01Completed
Phase II Study of Neoadjuvant Doxorubicin and Ifosfamide, Radiotherapy, and Surgical Resection in Patients With Primary or Recurrent Retroperitoneal Sarcoma [NCT00017160]Phase 20 participants (Actual)InterventionalWithdrawn
A Phase 1/1B Dose-Escalation Study to Determine the Safety and Tolerability of SCH 717454 Administered in Combination With Chemotherapy in Pediatric Subjects With Advanced Solid Tumors (Protocol No. 05883) [NCT00960063]Phase 14 participants (Actual)Interventional2009-11-11Terminated(stopped due to Study was terminated for business reasons.)
Multicenter Study of Safety and Efficacy of PET-adapted Treatment With Nivolumab at the Fixed Dose 40 mg, Ifosfamide, Carboplatin, Etoposide (NICE-40) in Patients With Relapsed/Refractory Hodgkin Lymphoma [NCT04981899]Phase 1/Phase 230 participants (Anticipated)Interventional2021-03-01Recruiting
Randomized Phase 3 Trial Evaluating the Addition of the IGF-1R Monoclonal Antibody Ganitumab (AMG 479, NSC# 750008) to Multiagent Chemotherapy for Patients With Newly Diagnosed Metastatic Ewing Sarcoma [NCT02306161]Phase 3312 participants (Actual)Interventional2014-12-12Active, not recruiting
The Use of Ifosfamide, Doxorubicin and Hypofractionated Radiotherapy in Neoadjuvant Treatment of High-grade Extremity Soft Tissue and Non-metastatic Sarcomas [NCT02812654]Phase 270 participants (Anticipated)Interventional2015-03-31Recruiting
Multi-Cycle High-Dose Chemotherapy Versus Optimized Conventionally-Dosed Chemotherapy in Patients With Metastatic Breast Cancer: A Phase II Prospective Randomized Trial [NCT00012311]Phase 20 participants Interventional2000-01-31Active, not recruiting
Phase II Study of Treatment of Relapsed Agressive Lymphomas [NCT00842595]Phase 250 participants (Actual)Interventional2003-12-31Completed
Mobilization of Autologous Peripheral Blood Stem Cells (PBSC) in CD20+ Lymphoma Patients Using RICE, G-CSF (Granulocyte-Colony Stimulating Factor), and Plerixafor [NCT01097057]Phase 220 participants (Actual)Interventional2010-11-09Completed
A Pilot Study of Chemotherapy Intensification by Adding Vincristine, Topotecan and Cyclophosphamide to Standard Chemotherapy Agents With an Interval Compression Schedule in Newly Diagnosed Patients With Localized Ewing Sarcoma Family of Tumors [NCT00618813]35 participants (Actual)Interventional2008-03-31Completed
A Phase 2 Study of Polatuzumab Vedotin With Rituximab, Ifosfamide, Carboplatin, and Etoposide (PolaR-ICE) as Initial Salvage Therapy for Relapsed/Refractory Diffuse Large B-cell Lymphoma [NCT04665765]Phase 241 participants (Actual)Interventional2021-01-18Active, not recruiting
Study Characterizing the Impact of Different Therapeutic Strategies on Event Occurrence at 2 Years, 5 Years, 10 Years, and 15 Years, According to Prognostic Groups in Patients With Hodgkin Lymphoma [NCT00920153]Phase 3442 participants (Actual)Interventional2008-05-31Terminated(stopped due to Other new drugs)
A Randomized Phase III Trial of Paclitaxel Plus Carboplatin Versus Ifosfamide Plus Paclitaxel in Chemotherapy-Naive Patients With Newly Diagnosed Stage I-IV, Persistent or Recurrent Carcinosarcoma (Mixed Mesodermal Tumors) of the Uterus, Fallopian Tube, P [NCT00954174]Phase 3637 participants (Actual)Interventional2009-08-17Active, not recruiting
Magnetic Resonance Based Non-Invasive Thermometry for Hyperthermic Treatment of Extremity Soft Tissue Sarcomas: A Multimodal Phase I/II Study [NCT00093509]Phase 1/Phase 215 participants (Actual)Interventional1999-11-30Completed
Biologic Evaluation of Renal Toxicity of Cisplatin and Ifosfamide (TOXIPLAT) [NCT00695032]80 participants (Anticipated)Interventional2007-10-31Suspended
A Phase 1/2, Open-label, Multi-center Study to Evaluate theSafety and Efficacy of Selinexor Combined With Chemotherapy orTislelizumab in Relapsed or Refractory Mature T and NK Cell Lymphoma [NCT04425070]Phase 1/Phase 297 participants (Anticipated)Interventional2020-08-18Recruiting
A Phase II Pilot Multicenter Study of Denileukin Diftitox Alone and in Combination With ICE (ICED) Chemotherapy in Children, Adolescents and Young Adults (CAYA) With Relapsed or Refractory Anaplastic Large Cell Lymphoma [NCT00801918]Phase 20 participants (Actual)Interventional2008-12-31Withdrawn(stopped due to Lack of funding)
A Scandinavian Sarcoma Group Treatment Protocol for Adult Patients With Non-metastatic High-risk Soft Tissue Sarcoma of the Extremities and Trunk Wall [NCT00790244]Phase 2188 participants (Anticipated)Interventional2007-10-31Recruiting
Multicenter Trial for Treatment of Acute Lymphoblastic Leukemia in Adults (05/93) [NCT00199069]Phase 4720 participants Interventional1993-04-30Completed
Intensified Tyrosine Kinase Inhibitor Therapy (Dasatinib NSC# 732517) in Philadelphia Chromosome Positive Acute Lymphoblastic Leukemia (ALL) [NCT00720109]Phase 2/Phase 363 participants (Actual)Interventional2008-07-14Completed
A Phase II Study of Intensive-Dose Topotecan, Ifosfamide/Mesna and Etoposide (Vepesid)(TIME) Followed by Autologous Stem Cell Rescue in High Risk Lymphoma [NCT00006373]Phase 227 participants (Actual)Interventional2000-02-29Completed
A Pilot Study of Re-Induction Chemotherapy With Ifosfamide, and Vinorelbine (IV) in Children With Refractory/Relapsed Hodgkin's Disease [NCT00006760]Phase 266 participants (Actual)Interventional2001-05-31Completed
Dose Intensification Phase II Study in Refractory Germ Cell Tumors With Relapse and Bad Prognosis. TICE Protocol : Paclitaxel and Ifosfamide Followed by Carboplatine and Etoposide Intensification With Individual Carboplatine Dose Adjustment. [NCT00864318]Phase 2101 participants (Actual)Interventional2009-03-13Completed
A Phase II Study of Intensive-Dose Topotecan, Ifosfamide/Mesna and Etoposide (TIME) Followed by Autologous Stem Cell Rescue in Metastatic Breast Cancer [NCT00006032]Phase 20 participants Interventional2000-03-31Terminated(stopped due to low accrual)
A Pilot Study Of Tandem High Dose Chemotherapy With Stem Cell Rescue Following Induction Therapy In Children With High Risk Neuroblastoma [NCT00017368]Phase 242 participants (Actual)Interventional2001-04-30Completed
Intensification Therapy of Mature B-ALL, Burkitt and Burkitt Like and Other High Grade Non-Hodgkin's Lymphoma in Adults [NCT00797810]Phase 425 participants (Anticipated)Interventional2006-12-31Recruiting
A Phase II Study of Gemcitabine and Ifosfamide As a Second-Line Systemic Chemotherapy for Cisplatin -Failed Advanced Transitional Cell Carcinoma [NCT00173862]Phase 218 participants (Actual)Interventional2000-05-31Completed
A Multicentre Phase II Study of Risk-adjusted Outpatient-based Salvage Therapy for Patients With Relapsed and Refractory Lymphoma [NCT00163761]Phase 290 participants (Actual)Interventional2002-12-31Completed
An Open, Single-arm, Multi-center Clinical Trial of Molecular Subtype-guided R-MINE+X Regimen in the Treatment of Relapsed/Refractory Diffuse Large B-cell Lymphoma (DLBCL) [NCT05784987]60 participants (Anticipated)Interventional2023-04-15Not yet recruiting
[NCT00541411]10 participants (Anticipated)Interventional2003-06-30Active, not recruiting
Antiangiogenic Potentiation of Preoperative Chemoradiotherapy for High Risk Extremity Soft Tissue Sarcomas: A Phase I Study of Sorafenib With Epirubicin, Ifosfamide, Hypofractionated Radiation, and Surgery [NCT00822848]Phase 118 participants (Actual)Interventional2009-02-28Completed
Phase I/II Trial of Sequential Paclitaxel/Ifosfamide Followed by Dose-Escalated, Dose-Intensive Carboplatin, Paclitaxel and Ifosfamide With Stem Cell Support in Cisplatin-Resistant Germ Cell Tumor Patients [NCT00423852]Phase 1/Phase 226 participants (Actual)Interventional2006-08-31Completed
Phase II Trial of Chemotherapy in Sporadic and Neurofibromatosis Type 1 Associated High Grade Malignant Peripheral Nerve Sheath Tumors [NCT00304083]Phase 248 participants (Actual)Interventional2005-12-31Completed
Intensive Multi-Agent Therapy, Including Dose-Compressed Cycles of Ifosfamide/Etoposide (IE) and Vincristine/Doxorubicin/Cyclophosphamide (VDC) for Patients With High-Risk Rhabdomyosarcoma [NCT00354744]Phase 3109 participants (Actual)Interventional2006-07-31Completed
A Multicenter Phase II Study Incorporating DOXIL® and Rituximab Into the Magrath Regimen for HIV-Negative and HIV-Positive Patients With Newly Diagnosed Burkitt's and Burkitt-like Lymphoma [NCT00392990]Phase 225 participants (Actual)Interventional2007-02-06Completed
Risk-Based Treatment for Non-Rhabdomyosarcoma Soft Tissue Sarcomas (NRSTS) in Patients Under 30 Years of Age [NCT00346164]Phase 3588 participants (Actual)Interventional2007-02-05Completed
Risk-Adapted High Dose Chemoradiotherapy and Autologous Stem Cell Transplantation for Patients With Relapsed and Primary Refractory Hodgkin's Lymphoma [NCT00255723]Phase 298 participants (Actual)Interventional2004-04-30Completed
High-dose Chemotherapy and Autologous Stem Cell Transplant or Consolidating Conventional Chemotherapy in Primary CNS Lymphoma - Randomized Phase III Trial [NCT02531841]Phase 3250 participants (Anticipated)Interventional2014-07-31Recruiting
Treatment of Recurrent or Resistant Pediatric Malignant Germ Cell Tumors With Paclitaxel, Ifosfamide and Carboplatin [NCT00467051]Phase 220 participants (Actual)Interventional2007-11-05Completed
A Phase II Study To Assess The Ability Of Neoadjuvant Chemotherapy Plus/Minus Second Look Surgery To Eliminate All Measurable Disease Prior To Radiotherapy For NGGCT [NCT00047320]Phase 2104 participants (Actual)Interventional2004-01-31Completed
Phase I, Prospective, Open-label, Multi-centric, Dose Finding Trial of Combination of IGEV and Panobinostat Before Autologous Stem Cell Transplant in Patients With Hodgkin's Lymphoma [NCT01884428]Phase 124 participants (Anticipated)Interventional2011-07-31Recruiting
Sequential High-Dose Chemotherapy Combining Two Mobilization and Cyto-Reductive Treatments Followed by Three High-Dose Chemotherapy Regimens Supported by Autologous Stem Cell Transplantation [NCT00231582]Phase 250 participants (Actual)Interventional2004-09-30Completed
A Single Center and Single Arm Study of TIP (Paclitaxel + Ifosfamide + Cisplatin) Combined With Nimotuzumab & Triprilimab as Neoadjuvant Treatment in Locally Advanced Penile Cancer [NCT04475016]Phase 229 participants (Actual)Interventional2020-08-12Completed
Pembrolizumab in Combination With R-ICE Chemotherapy in Relapsed/Refractory Diffuse Large B-cell Lymphoma [NCT05221645]Phase 265 participants (Anticipated)Interventional2022-06-27Recruiting
International Penile Advanced Cancer Trial (International Rare Cancers Initiative Study) [NCT02305654]Phase 3200 participants (Anticipated)Interventional2017-05-12Recruiting
A Multicenter Phase II Clinical Study of Albumin-bound Paclitaxel (Nab-PTX), Ifosfamide and Cisplatin in the Treatment of Pediatric Advanced, Recurrent or Refractory Extracranial Germ Cell Tumor. [NCT04581265]Phase 243 participants (Anticipated)Interventional2020-11-10Not yet recruiting
Randomized Phase II Trial of Paclitaxel, Ifosfamide and Cisplatin (TIP) Versus Bleomycin, Etoposide and Cisplatin (BEP) for Patients With Previously Untreated Intermediate- and Poor-Risk Germ Cell Tumors [NCT01873326]Phase 292 participants (Actual)Interventional2013-06-30Active, not recruiting
A Pilot Study of Dose Intensification of Methotrexate in Patients With Advanced-Stage (III/IV) Small Non-Cleaved Cell Non-Hodgkins Lymphoma and B-Cell All [NCT00005977]Phase 383 participants (Actual)Interventional2000-09-30Completed
A Randomized Phase III Trial of ICE Chemotherapy With or Without Rituximab for the Treatment of Relapsed or Refractory CD20 Expressing Aggressive B-Cell Non-Hodgkin's Lymphomas in Patients Not Suitable for High Dose Therapy and PBSCT [NCT00006708]Phase 37 participants (Actual)Interventional2000-10-31Terminated(stopped due to lack of accrual)
Phase II Trial of Paclitaxel, Ifosfamide, and Cisplatin in Previously Untreated Intermediate and Poor Risk Germ Cell Tumor Patients [NCT00470366]Phase 260 participants (Actual)Interventional2007-03-31Completed
A Phase I Study of Oral Palifosfamide Tris in Advanced, Refractory, Solid Tumors [NCT00607711]Phase 120 participants (Anticipated)Interventional2008-03-31Suspended(stopped due to IND was withdrawn)
A Pilot Study for Soft Tissue Sarcoma [NCT00662233]Early Phase 128 participants (Actual)Interventional1991-10-31Completed
Open-label, Prospective Phase III Clinical Study to Compare Polatuzumab Vedotin Plus Rituximab, Ifosfamide, Carboplatin and Etoposide (Pola-R-ICE) With Rituximab, Ifosfamide, Carboplatin and Etoposide (R-ICE) Alone as Salvage Therapy in Patients With Prim [NCT04833114]Phase 3334 participants (Anticipated)Interventional2021-04-30Recruiting
AIEOP LLA 2000 Multicenter Study for the Diagnosis and Treatment of Childhood Acute Lymphoblastic Leukemia [NCT00613457]Phase 32,039 participants (Actual)Interventional2000-09-30Completed
A Phase III Randomized Study Comparing A Chemotherapy With Cisplatin And Etoposide To A Etoposide Regimen Without Cisplatin For Patients With Extensive Small-Cell Lung Cancer [NCT00658580]Phase 3361 participants (Actual)Interventional2000-04-30Completed
Localized Non-Rhabdomyosarcoma Soft Tissue Sarcomas [NCT00334854]Phase 3250 participants (Anticipated)Interventional2006-03-31Recruiting
A Phase II Evaluation of High Dose Chemotherapy and Autologous Stem Cell Transplantation for Intestinal T-cell Lymphomas [NCT00669812]Phase 260 participants (Anticipated)Interventional2008-02-29Recruiting
Response-based Treatment of High-risk Neuroblastoma [NCT02771743]Phase 254 participants (Anticipated)Interventional2015-04-30Recruiting
Phase II Study of Durvalumab ,Doxorubicin, and Ifosfamide in Pulmonary Sarcomatoid Carcinoma [NCT04224337]Phase 234 participants (Anticipated)Interventional2020-06-11Recruiting
A Clinico-Pathologic Study of Primary Mediastinal B-Cell Lymphoma (IELSG 26) [NCT00689845]120 participants (Anticipated)Interventional2007-06-30Recruiting
Phase I Study of Panobinostat Plus ICE Chemotherapy Followed by a Randomized Phase-II Study of ICE Compared With Panobinostat Plus ICE for Patients With Relapsed and Refractory Classical Hodgkin Lymphoma [NCT01169636]Phase 1/Phase 262 participants (Actual)Interventional2011-01-31Completed
Treatment Intensification With R-ICE and High-Dose Cyclophosphamide for Diffuse Large B-Cell Non-Hodgkin's Lymphoma Based on Early [18F] FDG-PET Scanning [NCT00809341]Phase 227 participants (Actual)Interventional2009-01-31Terminated(stopped due to Low accrual)
"A Phase II Multicenter Study Comparing the Efficacy of the Oral Angiogenesis Inhibitor Nintedanib With the Intravenous Cytotoxic Compound Ifosfamide for Treatment of Patients With Advanced Metastatic Soft Tissue Sarcoma After Failure of Systemic Non-oxaz [NCT02808247]Phase 280 participants (Actual)Interventional2017-07-07Terminated(stopped due to Exceed of pre-specified number of failures in the experimental arm)
[NCT00162695]Phase 3400 participants Interventional1995-07-31Terminated
SIOP CNS GCT II: Prospective Trial for the Diagnosis and Treatment of Children, Adolescents and Young Adults With Intracranial Germ Cell Tumors [NCT01424839]Phase 4400 participants (Anticipated)Interventional2011-10-31Recruiting
A Phase I/II Study of G3139 (Genasense) in Combination With RICE Chemotherapy in Relapsed B-Cell Non-Hodgkin's Lymphoma [NCT00086944]Phase 1/Phase 225 participants (Actual)Interventional2004-05-31Completed
A Phase II Study Of An OutPatient Three Day VIP Regimen With Oral Mesna For Metastatic Breast Cancer [NCT00006260]Phase 236 participants (Actual)Interventional1997-05-31Completed
NB2004 Trial Protocol for Risk Adapted Treatment of Children With Neuroblastoma [NCT00410631]Phase 3642 participants (Anticipated)Interventional2004-10-31Recruiting
A Phase II Trial Of Adjuvant Chemotherapy For High Risk Transitional Cell Carcinoma Of The Urothelium [NCT00028860]Phase 20 participants Interventional2001-10-31Completed
Risk-Adapted Therapy for Patients With Untreated Age-Adjusted International Prognostic Index Low-Intermediate Risk, High-Intermediate Risk, or High Risk Diffuse Large B Cell Lymphoma [NCT00712582]Phase 296 participants (Actual)Interventional2008-07-01Completed
Response-based Treatment for Children With Unresectable Localized Soft Tissue Sarcomas [NCT02784015]Phase 241 participants (Anticipated)Interventional2016-05-31Recruiting
A Randomized, Multicenter, Phase III Trial of Trabectedin (Yondelis) Versus Doxorubicin-based Chemotherapy as First-Line Therapy in Patients With Translocation-Related Sarcomas (TRS) [NCT00796120]Phase 3121 participants (Actual)Interventional2008-11-30Completed
A Phase II Study of Dose Augmented Rituximab and Ice for Patients With Primary Refractory and Poor Risk Relapsed Aggressive B-Cell Non-Hodgkin's Lymphoma Undergoing Second-Line Therapy Prior to Stem Cell Transplantation [NCT00588094]Phase 220 participants (Actual)Interventional2003-10-31Completed
Phase III Study About the Effects of the Addition of Polychemotherapy to Adjuvant Radiotherapy in the Treatment of Non-Metastatic Uterine Sarcomas [NCT00162721]Phase 3270 participants (Anticipated)Interventional2001-09-30Recruiting
SFOP-OS94: Multicentric Randomised Phase III Trial Comparing Efficacy of Preoperative High-Dose Methotrexate Plus Doxorubicin to Efficacy of High-Dose Methotrexate Plus Etoposide and Ifosfamide, in Children and Adolescents Osteosarcoma [NCT00180908]Phase 3226 participants Interventional1994-06-30Completed
Large Cell Lymphoma, Pilot Study III [NCT00187070]8 participants (Actual)Interventional1997-12-31Completed
A Clinical Study of Liposomal Doxorubicin Combined With Ifosfamide Second-line Treatment in Small Cell Lung Cancer: Single Center, Single-arm Study [NCT01872416]Phase 230 participants (Anticipated)Interventional2012-10-31Recruiting
PHASE III MULTICENTRE TRIAL OF TREATMENT OF NEUROBLASTOMA IN CHILDREN AND ADOLESCENTS [NCT00002802]Phase 3500 participants (Anticipated)Interventional1990-07-31Completed
MMT 95 Study For Rhabdomyosarcoma and Other Malignant Soft Tissue Tumors of Childhood [NCT00002898]Phase 3400 participants (Anticipated)Interventional1995-01-31Completed
A Phase II Trial of ICE Chemotherapy Followed by High Dose BEAM Chemotherapy With Autologous Peripheral Blood Progenitor Cell Transplantation in Patients >= 60 Years Old With Refractory or Relapsed Intermediate Grade Non-Hodgkin's Lymphoma [NCT00002982]Phase 20 participants Interventional1997-01-31Completed
A Phase I Dose-Escalation Study of Topotecan and Ifosfamide in Patients With Refractory Non-Hematologic Malignancies. [NCT00003198]Phase 10 participants Interventional1997-11-30Completed
A Major Randomised Trial to Determine the Value of Cisplatin-Based Chemotherapy For All Patients With Non-Small Cell Lung Cancer [NCT00003240]Phase 31,800 participants (Anticipated)Interventional1995-10-31Active, not recruiting
A Phase I Trial of a Combined Regimen of Chemotherapy and 90Y-Labeled, Humanized LL2 (Anti-CD22) Antibody With Peripheral Stem Cell Rescue for the Treatment of Relapsed or Refractory Non-Hodgkin's Lymphoma [NCT00004086]Phase 10 participants Interventional1997-06-30Active, not recruiting
ALL-BFM 2000 Multi-Center Study for the Treatment of Children and Adolescents With Acute Lymphoblastic Leukemia [NCT00430118]Phase 34,559 participants (Actual)Interventional2000-07-31Completed
Phase II Study of Ifosfamide and Doxorubicin in Patients With Refractory Nasopharyngeal Carcinoma [NCT00484601]Phase 29 participants (Actual)Interventional2004-04-15Terminated(stopped due to Low accrual.)
A Phase I Study of Intravenous (IV) Palifosfamide-tris Administered in Combination With IV Etoposide and IV Carboplatin in Patients With Malignancies for Which Etoposide and Carboplatin Are an Appropriate Choice [NCT01242072]Phase 112 participants (Anticipated)Interventional2010-11-30Active, not recruiting
A Phase I Study of a Novel Chemotherapeutic Regimen: Topotecan, Ifosfamide and Carboplatin (TIC) in Children and Young Adults With Solid Tumors-- A Limited Multi-Institution Study [NCT00502892]Phase 12 participants (Actual)Interventional2004-08-31Completed
A Phase IB, Open-Label, Multicenter, Single Arm Study Evaluating the Preliminary Efficacy, Safety, and Pharmacokinetics of Glofitamab in Combination With Rituximab Plus Ifosfamide, Carboplatin Etoposide Phosphate in Patients With Relapsed/Refractory Trans [NCT05364424]Phase 140 participants (Anticipated)Interventional2022-11-04Recruiting
A Pilot Study of Standard-Dose Rituximab, Ifosfamide, Carboplatin and Etoposide (RICE) Plus Bortezomib (Velcade) in a Dose-Escalating Fashion for Patients With Relapsed or Primary Refractory Aggressive B-Cell Non-Hodgkin's Lymphoma Who Are Candidates for [NCT00515138]Early Phase 17 participants (Actual)Interventional2007-05-31Terminated(stopped due to Investigator left institution. 7 patients accrued and there is insufficient data to analyze.)
Modified BFM (Berlin-Frankfurt-Munster)Backbone Therapy for Chinese Children or Adolescents With Newly Diagnosed Lymphoblastic Lymphoma [NCT02845882]Phase 3150 participants (Anticipated)Interventional2016-01-31Active, not recruiting
Acalabrutinib Plus RICE for Patients With Relapsed/Refractory DLBCL Followed by Autologous Hematopoietic Cell Transplantation and Acalabrutinib Maintenance Therapy [NCT03736616]Phase 247 participants (Anticipated)Interventional2019-08-16Recruiting
LBL 2018 - International Cooperative Treatment Protocol for Children and Adolescents With Lymphoblastic Lymphoma [NCT04043494]Phase 3683 participants (Anticipated)Interventional2019-08-23Recruiting
A Multicenter, Open-label, Randomized Phase 2 Study to Compare the Efficacy and Safety of Lenvatinib in Combination With Ifosfamide and Etoposide Versus Ifosfamide and Etoposide in Children, Adolescents and Young Adults With Relapsed or Refractory Osteosa [NCT04154189]Phase 281 participants (Actual)Interventional2020-03-23Completed
A Prospective Multicenter Phase II Trial of Gemcitabine, Cisplatin, and Ifosfamide (GIP) in Patients With Relapsed Non-Seminomatous Germ-Cell Tumors (NSGCT) and a Predicted Favorable Prognosis [NCT00127049]Phase 237 participants Interventional2004-12-31Recruiting
An Open-Label Phase 1/2 Study to Investigate the Preliminary Safety and Activity of Aldoxorubicin Plus Ifosfamide/Mesna in Subjects With Metastatic, Locally Advanced, or Unresectable Soft Tissue Sarcoma [NCT02235701]Phase 1/Phase 270 participants (Actual)Interventional2014-09-02Completed
Phase II Study of Cyclophosphamide, Doxorubicin, Vincristine, Etoposide, and Ifosfamide, Followed by Resection and Radiotherapy in Patients With Peripheral Primitive Neuroectodermal Tumors or Ewing's Sarcoma [NCT00002466]Phase 20 participants Interventional1990-05-31Completed
Continuous 5 Days Infusion of High Dose Ifosfamide and Adriamycin in Patients With Advanced Sarcoma [NCT00002526]Phase 220 participants (Actual)Interventional1993-01-31Completed
TREATMENT OF ADULT PATIENTS WITH RELAPSING ACUTE LYMPHOCYTIC LEUKEMIA, A MULTICENTER TRIAL [NCT00002532]Phase 20 participants Interventional1993-01-31Active, not recruiting
Phase II Study of Intensive Chemotherapy With Autologous Peripheral Blood Stem Cell Support in Patients With Cisplatin Resistant Germ Cell Tumors [NCT00003852]Phase 245 participants (Anticipated)Interventional1998-03-31Terminated(stopped due to lack of patient inclusion)
A Randomized Phase III Study of Paclitaxel, Ifosfamide and Cisplatin Versus Vinblastine, Ifosfamide and Cisplatin as Second-Line Therapy for Patients With Relapsed/Resistant Germ Cell Tumors [NCT00072215]Phase 31 participants (Actual)Interventional2004-04-30Terminated(stopped due to poor accrual)
Treatment of Children and Adolescents With Diffuse Intrinsic Pontine Glioma and High Grade Glioma [NCT00278278]Phase 3150 participants (Anticipated)Interventional2003-09-30Active, not recruiting
A Pilot Study of Aranesp (Darbepoetin Alfa) and Pegfilgrastim (Neulasta) in Patients With Sarcoma Receiving Adriamycin and Ifosfamide [NCT00283621]51 participants (Actual)Interventional2003-06-02Completed
A Phase I Study Of BG In Combination With Ifosfamide For Advanced Solid Tumors [NCT00086970]Phase 132 participants (Actual)Interventional2004-06-30Terminated(stopped due to Administratively complete.)
Phase II Trial of Neoadjuvant, Multi-Agent Chemotherapy For Locally Advanced Urothelial Cancer [NCT00080795]Phase 265 participants (Actual)Interventional2001-07-31Completed
Phase II Study Of Rituximab And Short Duration, High Intensity Chemotherapy With G-CSF Support In Previously Untreated Patients With Burkitt Lymphoma/Leukemia [NCT00039130]Phase 2105 participants (Actual)Interventional2002-05-31Completed
A Phase III Randomized Trial of Adding Vincristine-Topotecan-Cyclophosphamide to Standard Chemotherapy in Initial Treatment of Non-Metastatic Ewing Sarcoma [NCT00334867]Phase 30 participants (Actual)Interventional2005-12-31Withdrawn(stopped due to withdrawn)
A Pilot Study to Evaluate Novel Agents (Temozolomide and Cixutumumab [IMC-A12, Anti-IGF-IR Monoclonal Antibody NSC # 742460]) in Combination With Intensive Multi-agent Interval Compressed Therapy for Patients With High-Risk Rhabdomyosarcoma [NCT01055314]Phase 2175 participants (Actual)Interventional2010-01-31Completed
A Phase I Study Investigating the Combination of RAD001 With Standard Induction and Consolidation Therapy in Older Patients With Newly Diagnosed Acute Myeloid Leukemia (AML) [NCT01154439]Phase 111 participants (Actual)Interventional2010-10-31Completed
A Phase Ⅱ Single-arm Clinical Trial to Investigate the Efficacy and Safety of Vinorelbine-ifosfamide Regimen as Third-line Treatment in Refractory or Recurrent Extensive Small Cell Lung Cancer Patients [NCT01752517]60 participants (Anticipated)Observational2012-12-31Recruiting
Randomized Phase III-Study in Stage IIIb and IV Non-Small-Cell Lung Cancer. Sequential Single-Agent vs. Double-Agent vs. Triple-Agent Therapy. [NCT00148395]Phase 3280 participants Interventional2002-06-30Completed
S9624: Phase II Study of Ifosfamide in Patients With Aggressive Meningeal Tumors [NCT00003292]Phase 27 participants (Actual)Interventional1998-07-31Terminated(stopped due to lack of accrual)
Pilot Study for Treatment of Elderly Patients (>65 Years) With Acute Lymphoblastic Leukemia [NCT00199095]Phase 440 participants Interventional1997-02-28Completed
Multidisciplinary Approach for Poor Prognosis Sinonasal Tumors: Phase II Study of Chemotherapy, Surgery, Photon and Heavy Ion Radiotherapy Integration for More Effective and Less Toxic Treatment in Operable Patients [NCT02099175]Phase 241 participants (Actual)Interventional2013-11-30Active, not recruiting
A Pilot Phase II Trial Of Irinotecan Plus Carboplatin, And Irinotecan Maintenance Therapy (High-Risk Patients Only), Integrated Into The Upfront Therapy Of Newly Diagnosed Patients With Intermediate - And High-Risk Rhabdomyosarcoma [NCT00077285]Phase 265 participants (Anticipated)Interventional2003-10-31Active, not recruiting
Trial Protocol for the Treatment of Children With High Risk Neuroblastoma (NB2004-HR) [NCT00526318]360 participants (Anticipated)Interventional2007-01-31Recruiting
Single-center, Open, Non-randomized, Phase II Prospective Study of Apatinib Combined With Chemotherapy in the Treatment of Unresectable Soft Tissue Sarcoma [NCT04126811]Phase 2120 participants (Anticipated)Interventional2019-06-01Recruiting
Phase 3 Trial to Investigate the Efficacy, Safety, and Tolerability of Blinatumomab as Consolidation Therapy Versus Conventional Consolidation Chemotherapy in Pediatric Subjects With HR First Relapse B-precursor ALL [NCT02393859]Phase 3111 participants (Actual)Interventional2015-11-10Completed
Therapy for Children With Advanced Stage High Risk Neuroblastoma [NCT00186849]Phase 230 participants (Actual)Interventional1997-10-31Completed
Phase II Trial of Ifosfamide/Carboplatin/Etoposide/Rituxan Followed by Zevalin in the Treatment of Patients With Relapsed/Refractory Intermediate Grade B-Cell Lymphoma [NCT00193505]Phase 240 participants Interventional2003-10-31Completed
Phase 1/2 Study of Lenvatinib in Children and Adolescents With Refractory or Relapsed Solid Malignancies and Young Adults With Osteosarcoma [NCT02432274]Phase 1/Phase 2117 participants (Actual)Interventional2014-12-29Completed
Phase-I Study of Bortezomib (VELCADE) Plus ICE (Ifosfamide, Carboplatin, Etoposide) for Patients With Relapsed Classical Hodgkin Lymphoma [NCT00439361]Phase 114 participants (Actual)Interventional2007-02-28Completed
Dose Escalation of Total Marrow Irradiation Added to an Alkylator-Intense Conditioning Regimen for Patients With High Risk or Relapsed Solid Tumors [NCT00623077]Phase 123 participants (Actual)Interventional2005-08-31Terminated(stopped due to Replaced by another study)
A Phase 1/2, Open-Label, Dose Escalation, Safety and Tolerability Study of INCB050465 and Iitacitinib in Subjects With Previously Treated B-Cell Malignancies (CITADEL-101) [NCT02018861]Phase 1/Phase 288 participants (Actual)Interventional2016-09-22Completed
EUROPEAN INTERGROUP COOPERATIVE EWING'S SARCOMA STUDY [EICESS 92] [NCT00002516]Phase 30 participants Interventional1992-07-31Active, not recruiting
A Phase III Randomized Study of Accelerated Hyperfractionated Whole Abdominal Radiotherapy (AHWAR) Versus Combination Ifosfamide-Mesna With Cisplatin in Optimally Debulked Stage I, II, III, or IV Carcinosarcoma (CS) of The Uterus [NCT00002546]Phase 3216 participants (Anticipated)Interventional1993-12-31Completed
A Multi-center, Open-Label, Adaptive, Randomized Study of Palifosfamide-tris, a Novel DNA Crosslinker, in Combination With Carboplatin and Etoposide (PaCE) Chemotherapy Versus Carboplatin and Etoposide (CE) Alone in Chemotherapy Naïve Patients With Extens [NCT01555710]Phase 3548 participants (Anticipated)Interventional2012-05-31Active, not recruiting
A Phase II Trial of Ifosfamide, Carboplatin, and Etoposide (ICE) Chemotherapy in Combination With Rituximab as Salvage Therapy [NCT00007865]Phase 20 participants Interventional2000-09-01Completed
MULTICENTRE TRIAL OF INTENSIFIED THERAPY FOR ADULT ALL (O5/93) [NCT00002531]Phase 20 participants Interventional1993-01-31Active, not recruiting
European Ewing Tumour Working Initiative of National Groups Ewing Tumour Studies 1999 (EURO-E.W.I.N.G.99) [NCT00020566]Phase 31,200 participants (Anticipated)Interventional2001-02-28Recruiting
A Groupwide Phase II Study of Trastuzumab (Herceptin) in Metastatic Osteosarcoma Patients With Tumors That Overexpress HER2 [NCT00023998]Phase 280 participants (Actual)Interventional2001-07-31Completed
A Groupwide Randomized Phase II Window Study of Two Different Schedules of Irinotecan in Combination With Vincristine And Pilot Assessment of Safety and Efficacy of Tirapazamine Combined With Multiagent Chemotherapy for First Relapse or Progressive Diseas [NCT00025363]Phase 2150 participants (Actual)Interventional2001-11-30Completed
MMT 98 Study For Metastatic Disease Rhabdomyosarcoma And Other Malignant Soft Tissue Sarcoma Of Childhood [NCT00025441]Phase 20 participants Interventional1998-11-30Completed
A Randomised Phase III Study On The Effect Of The Chimeric Anti-CD20 Monoclonal Antibody (Mabthera) During Sequential Chemotherapy Followed By Autologous Stem Cell Transplantation In Patients With Relapse B-Cell Non-Hodgkin Lymphoma(HOVON 44 STUDY) [NCT00012051]Phase 3340 participants (Anticipated)Interventional2000-09-30Completed
A Clinicopathological Study In Burkitts's And Burkitt-Like Non-Hodgkin's Lymphoma [NCT00040690]Phase 2120 participants (Anticipated)Interventional2008-11-30Completed
Randomised Trial Of Single Agent Doxorubicin Versus Doxorubicin Plus Ifosfamide In The First Line Treatment Of Advanced Or Metastatic Soft Tissue Sarcoma [NCT00061984]Phase 3455 participants (Actual)Interventional2003-04-30Completed
A Phase I Study of Thrombopoietin (rhTPO) Plus G-CSF in Children Receiving Ifosfamide, Carboplatin, and Etoposide (I.C.E.) Chemotherapy for Recurrent or Refractory Solid Tumors [NCT00003597]Phase 116 participants (Actual)Interventional1998-11-30Completed
Randomized Study of ICE Plus RITUXIMAB Versus DHAP Plus Rituximab in Previously Treated Patients With Diffuse Large B-cell Lymphoma, Followed by Randomized Maintenance With Rituximab [NCT00137995]Phase 3481 participants (Actual)Interventional2003-06-30Completed
International Pleuropulmonary Blastoma (PPB) Treatment and Biology Registry Protocol [NCT01464606]156 participants (Actual)Interventional2009-12-22Active, not recruiting
Phase III Randomized Trial of Sequential High-Dose Chemotherapy Versus Standard Chemotherapy for the Treatment of Small Cell Lung Cancer [NCT00011921]Phase 3430 participants (Anticipated)Interventional1997-09-30Active, not recruiting
Protocol for the Treatment of Extracranial Germ Cell Tumours in Children and Adolescents (GC III) [NCT00274950]Phase 3105 participants (Anticipated)Interventional2005-05-31Active, not recruiting
Neuroblastoma Study Phase II Study of Various Therapies in Patients With Neuroblastoma [NCT00017225]Phase 20 participants Interventional1997-05-31Completed
PILOT MULTINATIONAL PROTOCOLS IN ACUTE LYMPHOBLASTIC LEUKEMIA AND DIFFUSE NON-HODGKIN'S LYMPHOMA [NCT00018954]Phase 20 participants Interventional1992-10-31Completed
A Children's Oncology Group Pilot Study for the Treatment of Very High Risk Acute Lymphoblastic Leukemia in Children and Adolescents (Imatinib (STI571, GLEEVEC) NSC#716051) [NCT00022737]Phase 3220 participants (Actual)Interventional2002-10-31Completed
OS2006 : Protocole de Traitement Des ostéosarcomes de l'Enfant, de l'Adolescent et de l'Adulte Comportant [NCT00470223]Phase 3318 participants (Actual)Interventional2007-03-31Active, not recruiting
Pilot Trial of an Implantable Microdevice for In Vivo Drug Sensitivity Testing in Patients With Sarcomas [NCT04199026]Early Phase 120 participants (Anticipated)Interventional2024-01-31Not yet recruiting
A Phase I/II Study Of Neoadjuvant Chemotherapy, Angiogenesis Inhibitor SU5416 (NSC # 696819; A TK Inhibitor Anti-Angionesises Compound), And Radiation Therapy In The Management Of High Risk, High-Grade, Soft Tissue Sarcomas Of The Extremities And Body Wal [NCT00023738]Phase 1/Phase 20 participants Interventional2001-08-31Completed
Protocol For The Treatment Of Children And Adolescents With Hodgkin's Disease [NCT00025064]Phase 2260 participants (Anticipated)Interventional2000-01-31Active, not recruiting
Docetaxel (DTX) - Ifosfamide (IFX) As First Line Chemotherapy In Metastatic Breast Cancer [NCT00026078]Phase 242 participants (Anticipated)Interventional2001-03-31Recruiting
A Phase II Study of Rituximab (IND #7028) and Ifosfamide, Carboplatin and Etoposide (ICE) Chemotherapy in Children With Recurrent/Refractory B-cell (CD20+) Non-Hodgkin Lymphoma and B-cell Acute Lymphoblastic Leukemia [NCT00058461]Phase 282 participants (Anticipated)Interventional2003-11-30Terminated
Phase II Study of Neoadjuvant Dose-Intensive Chemotherapy With Adriamycin and Ifosfamide Followed by High-Dose ICE in Locally Advanced Soft Tissue Sarcomas [NCT00204646]Phase 20 participants Interventional1999-02-28Completed
A Randomized Phase II/III Trial Comparing Carboplatin-Ifosfamide (IC)-Chemotherapy Vs. IC-Chemotherapy Combined With Extreme Whole Body Hyperthermia In Patients With Recurrence Of Epithelial Ovarian Carcinoma: DOLPHIN-1-STUDY [NCT00045461]Phase 2/Phase 3241 participants (Anticipated)Interventional2000-06-30Recruiting
Osteosarcoma 1999-A Study Of Intensive Chemotherapy Utilizing Ifosfamide, Carboplatin, and Doxorubicin for Adjuvant Chemotherapy for Treatment of Osteosarcoma [NCT00145639]Phase 280 participants (Actual)Interventional1999-05-31Completed
Double Dose Intensive Chemo-Radiotherapy With Peripheral Blood Progenitor Cell Rescue for Children With Advanced Stage Neuroblastoma and Sarcomas [NCT00165139]Phase 220 participants (Actual)Interventional1996-01-31Completed
Phase III Trial Investigating the Potential Benefit of Intensified Peri-operative Chemotherapy With in High-risk CINSARC Patients With Resectable Soft-tissue SARComas [NCT03805022]Phase 3351 participants (Anticipated)Interventional2019-02-14Recruiting
RANDOMISED CLINICAL TRIAL OF IFOSFAMIDE, CARBOPLATIN AND ETOPOSIDE WITH MID-CYCLE VINCRISTINE (VICE) VERSUS STANDARD PRACTICE CHEMOTHERAPY IN PATIENTS WITH LIMITED STAGE SMALL CELL LUNG CANCER (SCLC) AND GOOD PERFORMANCE STATUS [NCT00002822]Phase 3400 participants (Anticipated)Interventional1996-03-31Completed
"Phase II Trial of VIPER Chemotherapy in Relapsed and Refractory Diffuse Large B-cell Lymphoma (NHL)" [NCT00504751]Phase 215 participants (Actual)Interventional2007-05-31Completed
High-dose Chemotherapy for Poor-Prognosis Relapsed Germ-Cell Tumors [NCT00936936]Phase 264 participants (Actual)Interventional2009-06-02Active, not recruiting
A Randomized Study Comparing Chemotherapy Followed by G-CSF Alone Versus G-CSF Plus GM-CSF for Mobilization of Peripheral Blood Stem Cells in Patients With Non-Hodgkin's Lymphomas [NCT00499343]Phase 284 participants (Actual)Interventional2004-01-31Completed
High Dose Samarium-153 With Peripheral Blood Stem Cell Support in High Risk Osteogenic Sarcoma [NCT00245011]Phase 211 participants (Actual)Interventional2004-10-31Completed
A European Treatment Protocol for Bone-sarcoma in Patients Older Than 40 Years [NCT02986503]100 participants (Actual)Observational2002-01-31Completed
Phase II Trial of Neoadjuvant Dose-Dense Doxorubicin, Ifosfamide, and Irinotecan (CPT-11) for Advanced Soft Tissue and Recurrent Bone Sarcomas [NCT00544778]Phase 27 participants (Actual)Interventional2001-08-31Terminated(stopped due to The study was terminated prematurely due to withdrawal of support by the sponsor.)
Phase 2 Trial of Response-Based Radiation Therapy for Patients With Localized Central Nervous System Germ Cell Tumors (CNS GCT) [NCT01602666]Phase 2262 participants (Actual)Interventional2012-05-29Active, not recruiting
Randomized Phase III Trial of Chemotherapy vs. Pembrolizumab Plus Chemotherapy for Relapsed/Refractory Classical Hodgkin Lymphoma [NCT05711628]Phase 30 participants (Actual)Interventional2023-08-10Withdrawn(stopped due to Other - Protocol moved to Withdrawn)
A Randomized Phase III Trial Comparing Conventional-Dose Chemotherapy Using Paclitaxel, Ifosfamide, and Cisplatin (TIP) With High-Dose Chemotherapy Using Mobilizing Paclitaxel Plus Ifosfamide Followed by High-Dose Carboplatin and Etoposide (TI-CE) as Firs [NCT02375204]Phase 3420 participants (Actual)Interventional2015-08-05Active, not recruiting
A Phase III Randomized Trial of Adding Vincristine-Topotecan-Cyclophosphamide to Standard Chemotherapy in Initial Treatment of Non-Metastatic Ewing Sarcoma [NCT01231906]Phase 3642 participants (Actual)Interventional2010-11-22Active, not recruiting
A Randomized Study of the Effect of Adjuvant Chemotherapy With Doxorubicin and Ifosfamide With Mesna in the Treatment of High-Grade Adult Extremity Soft Tissue Sarcoma [NCT00001300]Phase 3150 participants Interventional1992-06-30Completed
A Phase II Trial of Response-Adapted Second-Line Therapy for Hodgkin Lymphoma Using Anti-PD-1 Antibody Nivolumab ? ICE Chemotherapy as a Bridge to Autologous Hematopoietic Cell Transplant (NICE Trial) [NCT03016871]Phase 278 participants (Actual)Interventional2017-04-24Active, not recruiting
A Phase I Study Combining Ibrutinib With Rituximab, Ifosfamide, Carboplatin, and Etoposide (R-ICE) in Patients With Relapsed or Primary Refractory Diffuse Large B-Cell Lymphoma (DLBCL) [NCT02219737]Phase 126 participants (Actual)Interventional2014-09-12Completed
A Pilot Study of Rituximab in Combination With Out-patient Based VGF/F-GIV Salvage Therapies for Relapsed/Refractory CD20+ Lymphomas [NCT00280878]Phase 212 participants (Anticipated)Interventional2006-01-31Completed
A Perspective Phase I and II Trial of Liposome-encapsulated Doxorubicin (TLC D-99) in Combination With Ifosfamide in Patients With Metastatic Soft Tissue Sarcoma [NCT00289809]Phase 1/Phase 236 participants (Anticipated)Interventional2006-09-30Completed
A Phase II Study of Concurrent Chemoradiation for The Localized Nasal NK/T-cell Lymphoma [NCT00292695]Phase 233 participants (Actual)Interventional2006-05-31Completed
SIOP Intracranial Germ Cell Tumours Protocol [NCT00293358]Phase 3500 participants (Anticipated)Interventional1997-01-31Completed
A Multicenter, Open Phase Ib Study of the Safety and Efficacy of BEBT-908 Combined With Drugs in the Treatment of Relapsed/Refractory Diffuse Large B-Cell Lymphoma [NCT06164327]Phase 175 participants (Anticipated)Interventional2023-12-01Recruiting
A Randomized Controlled Multi-center Clinical Trial on Treatment of Stage I/II NK/T Cell Lymphoma With DDGP Regiment (Gemcitabine,Pegaspargase,Cisplatin,Dexamethasone) [NCT01501136]Phase 4200 participants (Anticipated)Interventional2011-01-31Recruiting
A Phase II Study of Sorafenib With Chemotherapy, Radiation, and Surgery for High-Risk Soft Tissue Sarcomas [NCT02050919]Phase 220 participants (Actual)Interventional2013-12-03Completed
A Phase II Randomized, Open Label Study of Ad-RTS-hIL-12 Monotherapy or Combination With Palifosfamide in Subjects With Recurrent/Metastatic Breast Cancer and Accessible Lesions [NCT01703754]Phase 212 participants (Actual)Interventional2013-03-31Completed
An Open-label,Multicenter Randomised Study of CTOP/ITE/MTX Compared With CHOP as the First-line Therapy for the New Diagnosed Young Patients With T Cell Non-hodgkin Lymphoma [NCT01746992]Phase 4200 participants (Anticipated)Interventional2012-09-30Active, not recruiting
A Phase Ⅱ Randomized Clinical Trial Comparing Vinorelbine-ifosfamide With Gefitinib as Third-line Treatment in Advanced EGFR Gene Mutation Negative Non-small Cell Lung Cancer Patients [NCT01749072]Phase 2120 participants (Anticipated)Interventional2012-12-31Recruiting
A Phase Ib/II Trial of Belotecan and Ifosfamide in Patients With Extensive Disease of Small Cell Lung Cancer [NCT01784107]Phase 1/Phase 245 participants (Anticipated)Interventional2011-07-31Recruiting
A Pilot Study for the Treatment of Patients With Metastatic and High Risk Sarcomas and Primitive Neuroectodermal Tumors [NCT00001209]Phase 1120 participants Interventional1986-10-31Completed
PHASE I/II TRIAL OF TAXOL, IFOSFAMIDE, AND CISPLATIN FOR CISPLATIN-RESISTANT GERM CELL TUMOR PATIENTS WITH FAVORABLE PROGNOSTIC FEATURES [NCT00002559]Phase 1/Phase 243 participants (Anticipated)Interventional1994-01-31Completed
"RANDOMIZED COMPARISON OF ALTERNATING TRIPLE THERAPY (ATT) VERUS CHOP IN PATIENTS WITH INTERMEDIATE GRADE LYMPHOMAS AND IMMUNOBLASTIC LYMPHOMAS WITH INTERNATIONAL INDEX 2-5" [NCT00002565]Phase 361 participants (Actual)Interventional1994-05-25Completed
INTENSIVE THERAPY WITH GROWTH FACTOR SUPPORT FOR PATIENTS WITH EWING'S TUMOR METASTATIC AT DIAGNOSIS: A PEDIATRIC ONCOLOGY GROUP PHASE II STUDY [NCT00002643]Phase 2130 participants (Actual)Interventional1995-04-30Completed
HIGH DOSE CHEMORADIOTHERAPY WITH PERIPHERAL BLOOD PROGENITOR CELL TRANSPLANTATION FOR PATIENTS WITH PRIMARY REFRACTORY, RELAPSED AND POOR PROGNOSIS NON-HODGKIN'S LYMPHOMA [NCT00002697]Phase 20 participants Interventional1995-09-30Completed
HIGH INTENSITY, BRIEF DURATION CHEMOTHERAPY FOR RELAPSED OR REFRACTORY ALL: A PHASE II STUDY OF A MULTIDRUG REGIMEN [NCT00002865]Phase 225 participants (Actual)Interventional1995-04-30Completed
A Phase I Study of Avelumab Plus Utomilumab-Based Combination Therapy for Relapsed/Refractory Diffuse Large B-Cell Lymphoma and Mantle Cell Lymphoma [NCT03440567]Phase 116 participants (Anticipated)Interventional2018-04-02Active, not recruiting
Phase I/Ib Study of Carfilzomib Plus Rituximab Plus Ifosfamide Plus Carboplatin Plus Etoposide (C-R-ICE) in Patients With Relapsed/Refractory Diffuse Large B-Cell Lymphoma (DLBCL) [NCT01959698]Phase 129 participants (Actual)Interventional2014-04-17Active, not recruiting
A Randomized Phase II Study of Bortezomib Plus ICE (BICE) Versus Standard ICE for Patients With Relapsed/Refractory Classical Hodgkin Lymphoma [NCT00967369]Phase 220 participants (Actual)Interventional2009-08-24Completed
Pharmacologic Interaction Between Ifosfamide and Aprepitant in Treated Patients With Soft Tissue Sarcoma [NCT03514381]Phase 459 participants (Actual)Interventional2018-05-18Completed
High Dose Conditioning With Ifosfamide, Carboplatin, and Etoposide With Autologous Stem Cell Transplantation for Patients With Recurrent Nasopharyngeal Carcinoma [NCT02137096]Phase 31 participants (Actual)Interventional2014-06-30Terminated(stopped due to This is a rare disease, and enrollment was poor.)
Treatment of Stage IV Breast Cancer With Activated T Cells After Peripheral Blood Stem Cell Transplant (Pilot Phase II) [NCT00020722]Phase 27 participants (Actual)Interventional2007-08-31Terminated(stopped due to Lack of funding to continue study.)
HIGH INTENSITY, BRIEF DURATION CHEMOTHERAPY FOR DIFFUSE SMALL NONCLEAVED CELL LYMPHOMA AND THE L-3 SUBTYPE OF ALL: A PILOT STUDY OF A MULTIDRUG REGIMEN [NCT00002494]Phase 2134 participants (Actual)Interventional1992-05-31Completed
Pilot Study in AIDS-Related Lymphomas [NCT00002524]Phase 246 participants (Actual)Interventional1993-06-30Completed
Multicenter Study to Optimise Therapy of B-ALL, Burkitt's NHL and High-Grade Non-Hodgkin's Lymphoma in Adults (Amend 7) [NCT00199082]Phase 4650 participants (Anticipated)Interventional2002-07-31Completed
METASTASECTOMY AND CHEMOTHERAPY FOR LUNG METASTASES FROM SOFT TISSUE SARCOMA: A RANDOMIZED PHASE III STUDY (AN INTERGROUP STUDY WITH THE SCANDINAVIAN SARCOMA GROUP) [NCT00002764]Phase 3340 participants (Anticipated)Interventional1996-04-30Completed
A Phase I-II Intensive-Dose Ifosfamide, Carboplatin and Taxotere (IC-T) Combination Chemotherapy Followed by Autologous Stem Cell Rescue for Patients With Refractory Malignancies [NCT00003406]Phase 1/Phase 230 participants (Anticipated)Interventional1997-10-31Completed
A Phase II Study of Whole Blood Hyperthermia and Ice Chemotherapy in Sarcoma Patients [NCT00002974]Phase 234 participants (Anticipated)Interventional1996-07-31Completed
Effects of Rolapitant on Nausea/Vomiting in Patients With Sarcoma Receiving Multi-Day Highly Emetogenic Chemotherapy (HEC) With Doxorubicin and Ifosfamide Regimen (AI) [NCT02732015]Phase 237 participants (Actual)Interventional2016-10-12Terminated(stopped due to Terminated per PI's request)
Randomized Study Comparing Neoadjuvant Chemotherapy Etoposide + Ifosfamide + Adriamycin (EIA) Combined With Regional Hyperthermia (RHT) Versus Neoadjuvant Chemotherapy Alone in the Treatment of High-Risk Soft Tissue Sarcomas in Adults [NCT00003052]Phase 3340 participants (Anticipated)Interventional1997-07-31Completed
PHASE I PILOT STUDY OF SEQUENTIAL HIGH DOSE CYCLES OF CISPLATIN, CYCLOPHOSPHAMIDE, ETOPOSIDE AND IFOSFAMIDE, CARBOPLATIN AND TAXOL WITH AUTOLOGOUS STEM CELL SUPPORT [NCT00002854]Phase 133 participants (Actual)Interventional1994-12-31Completed
A Randomized, Double-Blind, Placebo-Controlled Trial of Recombinant Human Keratinocyte Growth Factor (rHuKGF) in Patients With Hematologic Malignancies Undergoing Total Body Irradiation (TBI) and High-Dose Chemotherapy With Autologous Peripheral Blood Pro [NCT00004132]Phase 20 participants Interventional2000-01-31Completed
Multicenter Trial for Treatment of Acute Lymphocytic Leukemia in Adults (Pilot Study 06/99) [NCT00199056]Phase 4225 participants Interventional1999-10-31Completed
Phase I/IIA Study of Sequential Ifosfamide and Topotecan in Patients With Small Cell Lung Cancer [NCT00004186]Phase 1/Phase 255 participants (Anticipated)Interventional1996-12-31Completed
FaR-RMS: An Overarching Study for Children and Adults With Frontline and Relapsed RhabdoMyoSarcoma [NCT04625907]Phase 1/Phase 21,672 participants (Anticipated)Interventional2020-09-17Recruiting
Phase I/II Trial of Venetoclax in Combination With R-ICE (V+RICE) Chemotherapy for Relapsed/Refractory Diffuse Large B-Cell Lymphoma [NCT03064867]Phase 1/Phase 265 participants (Actual)Interventional2017-06-26Active, not recruiting
Pilot Study Using Induction Chemo-immunotherapy Followed by Consolidation With Reduced Toxicity Conditioning and Allogenic Stem Cell Transplant in Advanced Stage Mature Non-anaplastic T-Cell or NK Lymphoma/Leukemia in Children, Adolescents and Young Adult [NCT03719105]Early Phase 140 participants (Anticipated)Interventional2019-03-01Recruiting
A Randomized, Open-Label Phase 2 Study of Denintuzumab Mafodotin (SGN-CD19A) Plus Rituximab, Ifosfamide, Carboplatin, and Etoposide (19A+RICE) Chemotherapy vs. RICE in the Treatment of Patients With Relapsed or Refractory Diffuse Large B-Cell Lymphoma (DL [NCT02592876]Phase 281 participants (Actual)Interventional2015-10-31Terminated(stopped due to Sponsor decision based on portfolio prioritization)
Evaluation of Fosaprepitant's Effect on Drug Metabolism in Sarcoma Patients Receiving Ifosfamide-based Multi-day Chemotherapy Regimen [NCT01490060]47 participants (Actual)Interventional2012-05-31Completed
Risk-Adapted Therapy for Patients With Untreated Age-Adjusted International Prognostic Index II or III Diffuse Large B Cell Lymphoma [NCT00039195]Phase 298 participants (Actual)Interventional2006-11-30Completed
Phase II Evaluation of Ifosfamide Plus Doxorubicin & Filgrastim Versus Gemcitabine Plus Docetaxel & Filgrastim in the Treatment of Localized Poor Prognosis Soft Tissue Sarcoma [NCT00189137]Phase 284 participants (Actual)Interventional2004-08-31Completed
Non-randomized, Phase II, Open-label Study for Efficacy and Safety of Consolidation Paclitaxel/Ifosfamide/Cisplatin (TIP) Chemotherapy for High Risk Pediatric Germ Cell Tumor [NCT05455918]Phase 242 participants (Anticipated)Interventional2020-07-26Recruiting
Dasatinib With Ifosfamide, Carboplatin, Etoposide: A Pediatric Phase I/II Trial [NCT00788125]Phase 1/Phase 27 participants (Actual)Interventional2008-09-03Terminated(stopped due to Terminated early due a shift in resources after lackluster performance of the drug.)
INTERNATIONAL RANDOMIZED STUDY FOR THE SALVAGE TREATMENT OF GERM CELL TUMOURS [NCT00002566]Phase 3280 participants (Anticipated)Interventional1994-02-28Completed
Phase I Study of Romidepsin (ISTODAX®) Plus ICE for Patients With Relapsed or Refractory Peripheral T-Cell Lymphoma [NCT01590732]Phase 122 participants (Actual)Interventional2012-10-29Completed
A Multicenter Study to Evaluate a Risk-adapted Strategy for Treatment of Extra Cranial Non Seminomateous Malignant Germ Cell Tumour in Children and Adolescent [NCT02104986]Phase 2117 participants (Actual)Interventional2014-05-12Completed
Phase III Study on Efficacy of Dose Intensification in Patients With Non-metastatic Ewing Sarcoma. [NCT02063022]Phase 3278 participants (Actual)Interventional2009-01-22Completed
Treatment Regimen or Children or Adolescent With Mature B-cell NHL or B-AL in China [NCT02405676]Phase 2/Phase 3200 participants (Anticipated)Interventional2015-01-31Active, not recruiting
B-NHL 2013 - Treatment Protocol of the NHL-BFM and the NOPHO Study Groups for Mature Aggressive B-cell Lymphoma and Leukemia in Children and Adolescents [NCT03206671]Phase 3650 participants (Anticipated)Interventional2017-08-03Recruiting
Treatment Protocol for Relapsed Anaplastic Large Cell Lymphoma of Childhood and Adolescence [NCT00317408]96 participants (Anticipated)Interventional2004-04-30Active, not recruiting
Phase II Trial Investigating Tailoring First-Line Therapy For Advanced Stage Diffuse Large B-Cell Non-Hodgkin's Lymphoma Based on Mid-Treatment Positron Emission Tomography (PET) Scan Results [NCT00324467]Phase 2150 participants (Actual)Interventional2006-08-31Active, not recruiting
Phase II Trial of Paclitaxel, Cisplatin and Ifosfamide in Patients With Advanced Urothelial Tumors [NCT00002684]Phase 240 participants (Anticipated)Interventional1995-05-31Completed
Phase I/II Study of Samarium 153 as Part of a Double (Sequential) Autologous Bone Marrow Transplant (ABMT) for Patients With Stage IV Breast Cancer [NCT00003086]Phase 1/Phase 212 participants (Anticipated)Interventional1997-03-31Terminated(stopped due to no participants enrolled in a three year period)
A Phase III Trial of Ifosfamide (NSC #109274) Versus Ifosfamide Plus Paclitaxel (NSC #125973) in Patients With Advanced, Persistent or Recurrent Carcinosarcoma (Mixed Mesodermal Tumors) of the Uterus [NCT00003128]Phase 3166 participants (Anticipated)Interventional1997-11-30Completed
Phase II Study of Neoadjuvant Vincristine, Ifosfamide, Doxorubicin, and AND G-CSF in Children With Advanced Stage Non-Rhabdomyosarcoma Soft Tissue Sarcomas [NCT00002804]Phase 243 participants (Actual)Interventional1996-09-30Completed
EXTRAMEDULLARY RELAPSE AND OCCULT BONE MARROW INVOLVEMENT IN CHILDHOOD ACUTE LYMPHOBLASTIC LEUKEMIA: A PHASE III GROUP-WIDE STUDY [NCT00002816]Phase 3120 participants (Anticipated)Interventional1996-12-31Completed
Randomized Phase III Trial of Two Investigational Schedules of Ifosfamide vs. Standard Dose Doxorubicin in Patients With Advanced or Metastatic Soft Tissue Sarcoma [NCT00003212]Phase 3780 participants (Anticipated)Interventional1998-01-31Completed
RANDOMISED TRIAL OF ADJUVANT CHEMOTHERAPY WITH HIGH-DOSE DOXORUBICIN, IFOSFAMIDE AND LENOGRASTIM IN HIGH GRADE SOFT TISSUE SARCOMA [NCT00002641]Phase 3350 participants (Anticipated)Interventional1995-02-28Completed
A PHASE II STUDY OF NEOADJUVANT CHEMOTHERAPY AND RADIATION THERAPY IN THE MANAGEMENT OF HIGH-RISK, HIGH-GRADE, SOFT TISSUE SARCOMAS OF THE EXTREMITIES AND BODY WALL [NCT00002791]Phase 20 participants Interventional1997-02-28Completed
A Phase II Window Study of Trimetrexate With Simultaneous Leucovorin Protection in the Treatment of Newly Diagnosed Patients With Metastatic Osteosarcoma [NCT00003776]Phase 20 participants Interventional1998-12-31Completed
Intensive Chemotherapy With Peripheral Blood Stem Cell Support for Small Cell Lung Cancer [NCT00003860]Phase 236 participants (Anticipated)Interventional1998-09-30Completed
High Dose Combined Modality Therapy With Peripheral Blood Progenitor Cell Transplantation as Primary Treatment for Patients With Mantle Cell Lymphoma [NCT00003541]Phase 1/Phase 224 participants (Anticipated)Interventional1998-06-30Completed
Protocol for Patients With Newly-Diagnosed Non-Metastatic Osteosarcoma - A POG/CCG Pilot Intergroup Study [NCT00003937]Phase 3253 participants (Actual)Interventional1999-09-30Completed
A Randomised, Double-Blind, Double-Dummy, Placebo-Controlled, Three-Way Cross-over Study to Evaluate the Effect of AF-219 on Methacholine Hyper-Reactivity in Subjects With Asthma [NCT01993329]Phase 220 participants (Actual)Interventional2013-12-16Completed
Phase I/II Trial of Sequential Doxorubicin/Gemcitabine (AG) and Ifosfamide, Paclitaxel, and Cisplatin (ITP) Chemotherapy (AG-ITP) in Patients With Metastatic or Locally Advanced Transitional Cell Carcinoma of the Urothelium [NCT00003105]Phase 1/Phase 230 participants (Anticipated)Interventional1997-09-30Completed
Randomized Trial of Surgical Resection With or Without Pre-Operative Chemotherapy in Patients With Operable Non-Small Cell Lung Cancer (NSCLC) of Any Stage [NCT00003159]Phase 3600 participants (Anticipated)Interventional1997-08-31Completed
Response-Adapted Therapy for Aggressive Non-Hodgkin's Lymphomas Based on Early [18F] FDG-PET Scanning [NCT00274924]Phase 2100 participants (Actual)Interventional2006-09-26Completed
A Randomized Prospective Study of Early Intensification Versus Alternating Triple Therapy for Patients With Poor Prognosis Lymphoma [NCT00002835]Phase 3116 participants (Actual)Interventional1995-10-30Completed
A Randomized Phase III Comparative Study of Paclitaxel With Carboplatin Versus Mitomycin, Ifosfamide, Cisplatin (MIC) Chemotherapy in Inoperable Advanced Stage Non-Small Cell Lung Cancer [NCT00004887]Phase 30 participants Interventional1999-01-31Active, not recruiting
A Study of Paclitaxel, Cisplatin and Ifosfamide as Induction Therapy in the Treatment of Patients Relapsing After BEP Chemotherapy for Metastatic Germ Cell Tumors [NCT00004077]Phase 225 participants (Anticipated)Interventional1996-05-31Completed
High Dose Ifosfamide, Carboplatin and Etoposide With Amifostine Chemoprotection [NCT00003657]Phase 224 participants (Actual)Interventional1998-07-31Completed
Cytoreduction and Stem Cell Mobilization With Rituximab and ICE for Patients With Refractory or Relapsed CD20+ B-Cell IGL Eligible for ASCT: The RICE Protocol [NCT00005631]Phase 20 participants Interventional1999-11-30Completed
A Phase 1, Open-Label, Dose-Escalation Study of Olaratumab as a Single Agent and in Combination With Doxorubicin, Vincristine/Irinotecan, or High-Dose Ifosfamide in Pediatric Patients With Relapsed or Refractory Solid Tumors [NCT02677116]Phase 168 participants (Actual)Interventional2016-08-29Completed
Alkylator-Intense Conditioning Followed by Autologous Transplantation for Patients With High Risk or Relapsed Solid or CNS Tumors [NCT01505569]20 participants (Anticipated)Interventional2011-10-20Recruiting
Combination Chemotherapy Followed by Stem Cell Transplant and Isotretinoin in Treating Young Patients With High-risk Neuroblastoma [NCT03042429]Phase 3360 participants (Actual)Interventional2007-01-01Completed
B-cell Mature Non-Hodgkin's Lymphoma Treatment Protocol in Children and Adolescents 2021 (B-NHL-M-2021) [NCT05518383]Phase 4300 participants (Anticipated)Interventional2022-05-25Recruiting
Tandem Autologous Peripheral Blood Stem Cell Transplantation (PBSCT) After High Dose Paclitaxel Followed by Ifosfamide, Carboplatin, and Etoposide (ICE) for the Treatment of Lung Cancer [NCT00003284]Phase 230 participants (Anticipated)Interventional1998-01-31Active, not recruiting
A Protocol For Nonmetastatic Rhabdomyosarcoma [RMS-2005] [NCT00379457]Phase 3600 participants (Anticipated)Interventional2006-06-30Recruiting
A Global Study of Novel Agents in Paediatric and Adolescent Relapsed and Refractory B-cell Non-Hodgkin Lymphoma [NCT05991388]Phase 2/Phase 3210 participants (Anticipated)Interventional2023-10-31Not yet recruiting
A Phase II Trial of Tafasitamab and Lenalidomide Followed by Tafasitamab and ICE as Salvage Therapy for Transplant Eligible Patients With Relapsed/ Refractory Large B-Cell Lymphoma [NCT05821088]Phase 237 participants (Anticipated)Interventional2023-06-29Recruiting
The Effect of Antiangiogenic Therapy With Pazopanib Prior to Preoperative Chemotherapy for Subjects With Extremity Soft Tissue Sarcomas: A Randomized Study to Evaluate Response by Imaging [NCT01446809]23 participants (Actual)Interventional2012-04-30Completed
A Single Arm, Multi Centers, Phase II Study of Sintilimab, Doxorubicin and Ifosfamide at First-line Treatment of Soft Tissue Sarcoma Including Undifferentiated Pleomorphic Sarcoma, Synovial Sarcoma, Myxoid Liposarcoma and De-differentiated Liposarcoma [NCT04356872]Phase 245 participants (Anticipated)Interventional2020-04-08Recruiting
Thrombin Generation and Platelet Activation in Cytoreductive Surgery Combined With Hyperthermic Intraperitoneal Chemotherapy [NCT03034850]27 participants (Actual)Observational2015-04-30Completed
A Randomized Trial of the European and American Osteosarcoma Study Group to Optimize Treatment Strategies for Resectable Osteosarcoma Based on Histological Response to Pre-operative Chemotherapy [NCT00134030]Phase 31,334 participants (Actual)Interventional2005-11-14Completed
A Study of Gemcitabine, L- Asparaginase, Ifosfamide, Dexamethasone and Etoposide Chemotherapy Followed by ASCT for Newly Diagnosed Stage IV, Relapsed or Refractory Extranodal Natural Killer/T-cell Lymphoma, Nasal Type [NCT03154918]Phase 260 participants (Anticipated)Interventional2017-06-01Recruiting
Multicenter Single Arm Phase II Study of Single Agent Palifosfamide in Recurrent and Incurable Germ Cell Tumors [NCT01808534]Phase 25 participants (Actual)Interventional2013-02-28Terminated(stopped due to Due to Low Accrual)
A Phase I/II Trial of Brentuximab Vedotin (BV), Ifosfamide (I), Carboplatin (C), and Etoposide (E) for Patients With Relapsed or Refractory Hodgkin Lymphoma (BV-ICE) [NCT02227199]Phase 1/Phase 245 participants (Actual)Interventional2014-10-10Active, not recruiting
Dose/Schedule Finding Study of Palonosetron in Sarcoma Patients Receiving Multi-Day Chemotherapy With Adriamycin and Ifosfamide (AI) [NCT00410488]51 participants (Actual)Interventional2006-12-31Completed
A Single-arm, Open, Multicenter Study of Apatinib Mesylate Combined With Doxorubicin and Ifosfamide in Advanced Soft-tissue Sarcoma [NCT04012827]Phase 2108 participants (Anticipated)Interventional2019-08-20Recruiting
LS1781: Phase 2 Trial of High Dose Intravenous Ascorbic Acid as an Adjunct to Salvage Chemotherapy in Relapsed / Refractory Lymphoma and Patients With Clonal Cytopenia of Undetermined Significance [NCT03418038]Phase 255 participants (Anticipated)Interventional2018-03-23Recruiting
An Intention-to-Treat Study of Salvage Chemotherapy Followed by Allogeneic Hematopoietic Stem Cell Transplant for the Treatment of High-Risk or Relapsed Hodgkin Lymphoma [NCT00574496]Phase 225 participants (Actual)Interventional2007-11-13Completed
A Pilot Phase II Study of Pre-Operative Radiation Therapy and Thalidomide (IND 48832; NSC 66847) for Low Grade Primary Soft Tissue Sarcoma or Pre-Operative MAID/Thalidomide/Radiation Therapy for High/Intermediate Grade Primary Soft Tissue Sarcoma of the E [NCT00089544]Phase 223 participants (Actual)Interventional2004-06-17Terminated
International Collaborative Treatment Protocol For Children And Adolescents With Acute Lymphoblastic Leukemia [NCT01117441]Phase 36,136 participants (Actual)Interventional2010-06-30Completed
A Pilot Study of Low-Dose Antiangiogenic Chemotherapy in Combination With Standard Multiagent Chemotherapy for Patients With Newly Diagnosed Metastatic Ewing Sarcoma Family of Tumors [NCT00061893]Phase 238 participants (Actual)Interventional2004-04-30Completed
A Randomized Phase III Study of Sequential High-Dose Cisplatinum/Etoposide/Ifosfamide Plus Stem Cell Support Versus BEP in Patients With Poor Prognosis Germ Cell Cancer [NCT00003941]Phase 3222 participants (Anticipated)Interventional1999-04-30Completed
A Randomized Pre-Phase II Trial of Interleukin-2, Interleukin-12, or No Additional Therapy Following Response to Ifosfamide/Etoposide Chemotherapy for Refractory HIV-Associated Non-Hodgkin's Lymphoma [NCT00003575]Phase 240 participants (Actual)Interventional1999-01-31Completed
A Randomized Phase III Study of Chemotherapy and Radiotherapy Versus Radiotherapy Alone as Adjuvant Treatment to Patients With Node Positive Stages IB or IIA Cervix Cancer [NCT00003209]Phase 3700 participants (Anticipated)Interventional1997-12-31Completed
A Randomized Double-Blind, Placebo-Controlled Trial of Recombinant Human Keratinocyte Growth Factor (rHuKGF) in Patients With Hematologic Malignancies Undergoing Total Body Irradiation (TBI) and High-Dose Chemotherapy With Autologous Peripheral Blood [NCT00004061]Phase 2111 participants (Anticipated)Interventional1999-05-31Completed
Treatment of Sarcomatous Kidney Cancer That is Metastatic in Adults With Doxorubicin and Ifosfamide. Phase II Study [NCT00003683]Phase 240 participants (Anticipated)Interventional1998-03-31Completed
An Open, Single Arm, Single Center Phase II Study of Adriamycin and Ifosfamide Combined With Sintilimab in the Treatment of Advanced or Unresectable Soft Tissue Sarcoma [NCT04589754]Phase 269 participants (Anticipated)Interventional2021-07-26Recruiting
Prospective Phase II Study of a High Dose, Short Course Regimen (R-CODOX-M/IVAC) Including CNS Penetration and Intensive IT Prophylaxis in HIV-Associated Burkitt's and Atypical Burkitt's Lymphoma [NCT00392834]Phase 234 participants (Actual)Interventional2006-09-30Completed
A Pilot Study of Whole-body MRI-guided Intensity Modulated Radiation Therapy Combined With Systemic Chemotherapy Followed by High-Dose Chemotherapy With Busulfan, Melphalan and Topotecan and Stem Cell Rescue in Patients With Poor Risk Ewing's Sarcoma [NCT01795430]0 participants (Actual)Interventional2013-07-31Withdrawn(stopped due to No participants enrolled.)
A Phase I/II Study of Vorinostat Plus Rituximab, Ifosphamide, Carboplatin, and Etoposide for Patients With Relapsed or Refractory Lymphoid Malignancies or Untreated T- or Mantle Cell Lymphoma [NCT00601718]Phase 1/Phase 229 participants (Actual)Interventional2007-12-31Completed
A Phase II Trial of Ifosfamide, Etoposide, Cytarabine, and Methotrexate (IVAM) Chemotherapy for Refractory or Relapsed Diffuse Large B Cell Lymphoma [NCT03383406]Phase 230 participants (Anticipated)Interventional2016-12-01Enrolling by invitation
Concurrent Chemotherapy and Radiation Therapy for Newly Diagnosed Patients With Stage I/II Nasal NK Cell Lymphoma [NCT02106988]Phase 240 participants (Anticipated)Interventional2015-01-16Recruiting
Study With High Doses of Chemotherapy, Radiotherapy and Consolidation Therapy With Ciclofosfamide and Anticyclooxygenase 2, for the Metastatic Ewing Sarcoma [NCT02727387]Phase 2155 participants (Actual)Interventional2009-06-01Completed
Chemoimmunotherapy With Obinutuzumab, Ifosfamide, Carboplatin and Etoposide (O-ICE) in Children, Adolescents and Young Adults With Recurrent Refractory CD20+ Mature B-NHL [NCT02393157]Phase 225 participants (Anticipated)Interventional2015-08-21Recruiting
Phase I/II, Open-Label Study of R-ICE (Rituximab-Ifosfamide-Carboplatin-Etoposide) With Lenalidomide (R2-ICE) in Patients With First-Relapse/Primary Refractory Diffuse Large B-Cell Lymphoma (DLBCL) [NCT02628405]Phase 1/Phase 263 participants (Actual)Interventional2016-05-20Active, not recruiting
A Phase III, Multicenter, Randomized, Double-Blind, Placebo-Controlled Trial Comparing the Efficacy and Safety of a Sintilimab Plus ICE Regimen Versus a Placebo Plus ICE Regimen in Classic Hodgkin's Lymphoma Patients With First-line Standard Chemotherapy [NCT04044222]Phase 3240 participants (Anticipated)Interventional2019-10-21Recruiting
High-Risk Neuroblastoma Study 2 of SIOP-Europa-Neuroblastoma (SIOPEN) [NCT04221035]Phase 3800 participants (Anticipated)Interventional2019-11-05Recruiting
International Protocol for the Treatment of Childhood Anaplastic Large Cell Lymphoma [NCT00006455]Phase 3885 participants (Actual)Interventional1999-11-26Completed
The Efficacy of Whole-ventricle Irradiation Plus Primary Boost in Patients With Localized Basal Ganglia Germ Cell Tumors: Prospective Phase II Study [NCT05124951]Phase 2150 participants (Anticipated)Interventional2021-09-15Recruiting
An Evaluation of PET/CT Imaging as a Predictor of Disease Free Survival Following Neo-Adjuvant Chemotherapy for Soft Tissue Sarcoma [NCT00346125]70 participants (Actual)Interventional2006-04-10Completed
ABCB1/P-glycoprotein Expression as Biologic Stratification Factor for Patients With Non Metastatic Osteosarcoma - Prospective Study (ISG/OS-2) [NCT01459484]Phase 2225 participants (Anticipated)Interventional2011-06-23Active, not recruiting
A Randomized Trial Using a Modified COG ABFM Regimen Backbone to Investigate Capizzi Escalating Methotrexate Versus High Dose Methotrexate in Children With Newly Diagnosed T-cell Lymphoblastic Lymphoma (T-LBL) [NCT05681260]Phase 3200 participants (Anticipated)Interventional2023-02-06Recruiting
A Mechanistic Study Of Mifamurtide (MTP-PE) In Patients With Metastatic And/Or Recurrent Osteosarcoma [NCT02441309]Phase 28 participants (Actual)Interventional2014-10-31Terminated(stopped due to Failed to recruit sufficient numbers of patients in the funded period)
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

TrialOutcome
NCT00002558 (1) [back to overview]Overall Objective Response
NCT00002601 (4) [back to overview]5-year Overall Survival
NCT00002601 (4) [back to overview]5-year Progression-free Survival
NCT00002601 (4) [back to overview]Number of Participants With Grade 3 Bilirubin
NCT00002601 (4) [back to overview]Toxicities Counts
NCT00002931 (3) [back to overview]Toxic Effects
NCT00002931 (3) [back to overview]Overall Survival
NCT00002931 (3) [back to overview]Progression-free Survival
NCT00003631 (1) [back to overview]Objective Response
NCT00039130 (3) [back to overview]2 Year Overall Survival
NCT00039130 (3) [back to overview]2 Year Event Free Survival
NCT00039130 (3) [back to overview]Complete Response Rate
NCT00039195 (1) [back to overview]Progression Free Survival
NCT00047320 (6) [back to overview]Number of Patients Experiencing Toxic Death
NCT00047320 (6) [back to overview]Response to Induction Chemotherapy
NCT00047320 (6) [back to overview]The Probability of Event-free Survival (EFS)
NCT00047320 (6) [back to overview]Progression-free Survival (PFS)
NCT00047320 (6) [back to overview]Overall Survival (OS)
NCT00047320 (6) [back to overview]Occurrence of Non-hematological Grade 4 Toxicity Occurrence of Nonhematological Grade 4 Toxicity
NCT00061893 (2) [back to overview]Event Free Survival
NCT00061893 (2) [back to overview]Occurrence of Severe Toxicity
NCT00072280 (1) [back to overview]"Failure-free Survival (FFS) in Chemotherapy Plus Possible Surgery Arm"
NCT00089544 (1) [back to overview]Treatment Delivery With Compliance Defined as Receiving at Least 95% of the Pre-operative Protocol Dose of RT, All 3 Cycles of MAID (if Applicable), and Receive Thalidomide on 75% of the Days During Radiation
NCT00104676 (2) [back to overview]Overall Survival
NCT00104676 (2) [back to overview]Progression-free Survival Rate After 1 Course of Treatment
NCT00126191 (2) [back to overview]Response Rates (CR and PR) in Adults With Burkitt/Atypical Burkitt
NCT00126191 (2) [back to overview]Disease Free Survival
NCT00134030 (3) [back to overview]Event-free Survival (EFS)
NCT00134030 (3) [back to overview]Percentage of Patients With Overall Survival
NCT00134030 (3) [back to overview]Toxicity as Measured by Common Terminology Criteria for Adverse Events (CTCAE) v3.0
NCT00147225 (2) [back to overview]Number of Participants With Adverse Events in Sequential Cohort Dose Escalation Study of AMG 531 Following Chemotherapy
NCT00147225 (2) [back to overview]Number of Participants With Venous Thromboembolism (VTE) Related Serious Adverse Events in Sequential Cohort Dose Escalation Study of AMG 531 Following Chemotherapy
NCT00189137 (2) [back to overview]The Percentage of Patients Alive Without Disease at 2 Years
NCT00189137 (2) [back to overview]Percentage of Patients Hospitalized in Each Arm.
NCT00231842 (1) [back to overview]Cycles With Hematologic Toxicities
NCT00245011 (3) [back to overview]Toxicity at End of Study Treatment
NCT00245011 (3) [back to overview]Tumor Response
NCT00245011 (3) [back to overview]Overall and Progression-free Survival After Study Treatment
NCT00255723 (1) [back to overview]Overall Objective Response
NCT00267046 (2) [back to overview]Cumulative Incidence Rate of Oral Mucositis
NCT00267046 (2) [back to overview]Median Maximum Score for Patient Reported Outcomes in 2 Blinded Cycles
NCT00274924 (2) [back to overview]2-year Progression-Free Survival (PFS)
NCT00274924 (2) [back to overview]5-year Overall Survival
NCT00302003 (4) [back to overview]Event Free Survival Without Receiving Radiation Therapy (EFSnoRT).
NCT00302003 (4) [back to overview]Intensive Therapy Free Survival (ITFS).
NCT00302003 (4) [back to overview]Overall Survival
NCT00302003 (4) [back to overview]Event Free Survival (EFS)
NCT00304083 (5) [back to overview]Provide Epidemiology and Clinical Presentation of the Number of Participants With NF1-associated MPNSTs.
NCT00304083 (5) [back to overview]Perform Pathologic Analysis of Tumor Samples to Analyze the Number of Participants With Markers as Predictors of Response
NCT00304083 (5) [back to overview]Number of Participants With Response Rate (Complete Response and Partial Response)
NCT00304083 (5) [back to overview]Identify the Number of Participants With a Serum Biomarker to Predict the Presence of MPNST Versus Benign Plexiform Neurofibroma
NCT00304083 (5) [back to overview]Construct Tissue Microarray to Identify Novel Targets for Treatment for the Number of Participants With Available Tissue
NCT00346164 (11) [back to overview]Degree of Agreement in Histologic Grade Determined by the Enrolling Institution Versus by Central Pathology Reviewers
NCT00346164 (11) [back to overview]Complete or Partial Response Rate
NCT00346164 (11) [back to overview]Event Free Survival Probability Disease Extent
NCT00346164 (11) [back to overview]Event Free Survival Probability Histologic Grade
NCT00346164 (11) [back to overview]Degree of Agreement in Histologic Grade Between Pediatric Oncology Group (POG) and Fédération Nationale Des Centres de Lutte Contre le Cancer (FNCLCC) Pathologic Grading Systems
NCT00346164 (11) [back to overview]Toxicity Rate
NCT00346164 (11) [back to overview]Probability for Event Free Survival.
NCT00346164 (11) [back to overview]Percent Tumor Necrosis
NCT00346164 (11) [back to overview]Overall Survival Probability Extent of Resection of the Primary Tumor
NCT00346164 (11) [back to overview]Overall Survival Probability Disease Extent
NCT00346164 (11) [back to overview]Incidence of Distant Metastasis
NCT00354107 (1) [back to overview]Response
NCT00354744 (3) [back to overview]Percentage of Patients Event Free at 4 Years Following Study Entry
NCT00354744 (3) [back to overview]Percentage of Patients Experiencing Adverse Events Due to Concurrent Therapy
NCT00354744 (3) [back to overview]Number of Patients With Complete or Partial Response Assessed by RECIST Criteria
NCT00381940 (5) [back to overview]Number of Participants With Grade 3 or 4 Toxicity
NCT00381940 (5) [back to overview]Rate of Successful PBSC Harvest
NCT00381940 (5) [back to overview]Complete Response (CR)
NCT00381940 (5) [back to overview]Overall Response Rate
NCT00381940 (5) [back to overview]Induction Success Rate
NCT00392834 (1) [back to overview]Overall Survival (OS) at 1 Year
NCT00392990 (4) [back to overview]Overall Survival (OS) of Patients With Burkitt's and Burkitt-like Lymphoma/Leukemia Treated With Modified Magrath Regimen
NCT00392990 (4) [back to overview]Safety of Patients With Burkitt's and Burkitt-like Lymphoma/Leukemia Treated With Modified Magrath Regimen (Addition of Rituximab, Subsitution of Adriamycin for Doxil and Using Lower Dose of Methotrexate)
NCT00392990 (4) [back to overview]Progression Free Survival (PFS) of Patients With Burkitt's and Burkitt-like Lymphoma/Leukemia Treated With Modified Magrath Regimen
NCT00392990 (4) [back to overview]Overall Response Rate (ORR) of Patients With Burkitt's and Burkitt-like Lymphoma/Leukemia Treated With Modified Magrath Regimen
NCT00410488 (1) [back to overview]Palonosetron Response Rate in the 10 Day Study Cycle
NCT00423852 (2) [back to overview]Response
NCT00423852 (2) [back to overview]Maximum Tolerated Dose of Ifosfamide
NCT00432094 (5) [back to overview]Overall Survival (OS)
NCT00432094 (5) [back to overview]Disease-free Survival (DFS)
NCT00432094 (5) [back to overview]Engraftment of Neutrophils
NCT00432094 (5) [back to overview]Engraftment of Platelets
NCT00432094 (5) [back to overview]Numbers of Patients Unable to Mobilize Peripheral Blood Stem Cells
NCT00450801 (4) [back to overview]Number of Patients Experiencing Adverse Events.
NCT00450801 (4) [back to overview]Response Rate
NCT00450801 (4) [back to overview]Overall Survival Rate
NCT00450801 (4) [back to overview]Progression-free Survival Rate
NCT00467051 (2) [back to overview]Response Rate as Measured by Response Evaluation Criteria in Solid Tumors (RECIST) Criteria
NCT00467051 (2) [back to overview]The Number of Patients Who Experience at Least One Grade 3 or Higher CTC Version 4 Toxicity.
NCT00470366 (3) [back to overview]Number of Patients With Treatment Related Toxicity
NCT00470366 (3) [back to overview]Percentage of Participants With Progression Free Survival
NCT00470366 (3) [back to overview]Progression-free Survival
NCT00499343 (1) [back to overview]CD34+ Cells/kg in Blood Stem Cells
NCT00504751 (1) [back to overview]Complete Response
NCT00512096 (1) [back to overview]Number of Participants With Pathologic Complete Remission (pCR)
NCT00544778 (1) [back to overview]Response Rate
NCT00574496 (3) [back to overview]Progression-free Survival at 1 Year
NCT00574496 (3) [back to overview]Overall Survival
NCT00574496 (3) [back to overview]Disease Relapse or Progression as Measured by CT Scan or PET
NCT00588094 (1) [back to overview]Improve the Overall Response Rate
NCT00601718 (4) [back to overview]Ability to Proceed to Peripheral Blood Stem Cell Collection Following Treatment
NCT00601718 (4) [back to overview]Safety and Toxicity According to CTCAE v3.0
NCT00601718 (4) [back to overview]Maximum Tolerated Dose of Vorinostat
NCT00601718 (4) [back to overview]Efficacy (Response Rate) of Vorinostat Combined With RICE Chemotherapy
NCT00618813 (5) [back to overview]Incidence Rate (Number of Participants) of Dose-limiting Toxicity (DLT) - Week 29 to Week 37
NCT00618813 (5) [back to overview]Incidence Rate (Number of Participants) of Dose-limiting Toxicity (DLT) - Enrollment to Week 12
NCT00618813 (5) [back to overview]Incidence Rate (Number of Participants) of Dose-limiting Toxicity (DLT) - Week 13 to Week 22
NCT00618813 (5) [back to overview]Incidence Rate (Number of Participants) of Dose-limiting Toxicity (DLT) - Week 23 to Week 28
NCT00618813 (5) [back to overview]Incidence of Death
NCT00667342 (18) [back to overview]2-Year Event Free Survival (EFS) in Patients With Localized Resectable Disease Compared to St. Jude OS99 Protocol.
NCT00667342 (18) [back to overview]2-Year Event Free Survival (EFS) of Patients With Osteosarcoma
NCT00667342 (18) [back to overview]3-Year Event Free Survival
NCT00667342 (18) [back to overview]Mean Duration of Neuropathic Pain
NCT00667342 (18) [back to overview]2-Year Overall Survival (OS) in Patients With Localized Resectable Disease Compared to OS99 Protocol.
NCT00667342 (18) [back to overview]Mean Duration of Neuropathic Pain Medication
NCT00667342 (18) [back to overview]Median Duration of Neuropathic Pain
NCT00667342 (18) [back to overview]Median Duration of Neuropathic Pain Medication
NCT00667342 (18) [back to overview]Mean Vp
NCT00667342 (18) [back to overview]Mean Ktrans
NCT00667342 (18) [back to overview]Number of Participants With Neuropathic Pain (NP) Following Surgery
NCT00667342 (18) [back to overview]Ktrans by Good and Poor Response
NCT00667342 (18) [back to overview]2-Year Overall Survival (OS) of Patients With Osteosarcoma
NCT00667342 (18) [back to overview]Mean Ve
NCT00667342 (18) [back to overview]Difference Between Good and Poor Response by SUVmax
NCT00667342 (18) [back to overview]Number of Participants With Unacceptable Toxicity
NCT00667342 (18) [back to overview]Histologic Response by Stratum
NCT00667342 (18) [back to overview]P95 of Ktrans by Good and Poor Response
NCT00712582 (2) [back to overview]2-year PFS From the Start of Induction Therapy Conditional
NCT00712582 (2) [back to overview]Overall Survival at 1 Year
NCT00720109 (5) [back to overview]Percent of Patients MRD Positive (MRD > 0.01%) at End of Consolidation
NCT00720109 (5) [back to overview]Contribution of Dasatinib on Minimal Residual Disease (MRD) After Induction Therapy
NCT00720109 (5) [back to overview]Event-Free Survival (EFS) of Patients With Standard-risk Disease Treated With Dasatinib in Combination With Intensified Chemotherapy
NCT00720109 (5) [back to overview]Feasibility and Toxicity of an Intensified Chemotherapeutic Regimen Incorporating Dasatinib for Treatment of Children and Adolescents With Ph+ ALL Assessed by Examining Adverse Events
NCT00720109 (5) [back to overview]Overall EFS Rate for the Combined Cohort of Standard- and High-Risk Patients (Who Receive the Final Chosen Dose of Dasatinib)
NCT00742924 (1) [back to overview]Limiting Toxicity
NCT00788125 (1) [back to overview]Maximum Administered Dose of Dasatinib (Phase I)
NCT00796120 (5) [back to overview]Progression - Free Survival (PFS)
NCT00796120 (5) [back to overview]Percentage of Participants With Objective Response
NCT00796120 (5) [back to overview]Overall Survival
NCT00796120 (5) [back to overview]6-month Progression - Free Survival
NCT00796120 (5) [back to overview]Duration of Response (DOR)
NCT00954174 (7) [back to overview]Patient-reported Peripheral Neuropathy Symptoms - Post Baseline
NCT00954174 (7) [back to overview]Patient Reported Quality of Life (QOL) - Post Baseline
NCT00954174 (7) [back to overview]Duration of Progression-free Survival
NCT00954174 (7) [back to overview]Overall Survival
NCT00954174 (7) [back to overview]Patient Reported Peripheral Neuropathy Symptoms - Baseline
NCT00954174 (7) [back to overview]Patient-Reported Quality of Life (QOL) - Baseline
NCT00954174 (7) [back to overview]Incidence of Adverse Events as Assessed by CTCAE Version 3.0
NCT00960063 (3) [back to overview]Number of Participants Who Developed Anti-robatumumab Antibodies
NCT00960063 (3) [back to overview]Best Overall Response Based on Response Evaluation Criteria in Solid Tumors (RECIST)
NCT00960063 (3) [back to overview]Number of Participants With Dose Limiting Toxicities
NCT00967369 (4) [back to overview]Overall Survival (OS) Rate at 24 Months
NCT00967369 (4) [back to overview]Progression Free Survival (PFS) Rate at 12 Months
NCT00967369 (4) [back to overview]Overall Response After 3 Cycles of Botezomib Plus ICE (BICE) Versus Ifosfamide, Carboplatin, Etoposide (ICE) in Patients With Relapsed/Refractory Classical Hodgkin Lymphoma
NCT00967369 (4) [back to overview]PET Scan Response After 3 Cycles of BICE Versus ICE Chemotherapy.
NCT01026220 (7) [back to overview]Grade 3 and 4 Non-hematologic Toxicities During Protocol Therapy
NCT01026220 (7) [back to overview]Relapse-free Survival
NCT01026220 (7) [back to overview]Overall Survival
NCT01026220 (7) [back to overview]Second-event-free Survival
NCT01026220 (7) [back to overview]Safety Analysis and Monitoring of Toxic Death
NCT01026220 (7) [back to overview]Event-free Survival for Rapid Early Response (RER) Positron Emission Tomography(PET)-1 Positive, RER PET-1 Negative
NCT01026220 (7) [back to overview]Event Free Survival
NCT01055314 (5) [back to overview]Feasibility of the Addition of Cixutumumab to Chemotherapy Determined by Patient Enrollment
NCT01055314 (5) [back to overview]Feasibility of the Addition of Temozolomide to Chemotherapy Determined by Patient Enrollment
NCT01055314 (5) [back to overview]Incidence of Adverse Events Assessed by Common Terminology Criteria for Adverse Events Version 4.0
NCT01055314 (5) [back to overview]Event-Free Survival
NCT01055314 (5) [back to overview]Response Rate (CR + PR)
NCT01097057 (4) [back to overview]Total Number of Participants Who Did Not Collect ≥5 x 10^6 CD34 Cells/kg in a Maximum of Four Apheresis Days
NCT01097057 (4) [back to overview]Number of Participants Requiring One or Two Apheresis Collection Days to Reach ≥5 x 10^6 CD34 Cells/kg
NCT01097057 (4) [back to overview]Number of Patients to Mobilize ≥5 x 10^6 CD34 Cells/kg Autologous PBSC (Efficacy)
NCT01097057 (4) [back to overview]Number of Patients Who Achieved ≥5 x 10^6 CD34 Cells/kg in ≤4 Apheresis Days
NCT01169636 (3) [back to overview]Number of Participants With Complete Remission (CR)
NCT01169636 (3) [back to overview]Maximum Tolerated Dose (MTD) of Panobinostat + ICE
NCT01169636 (3) [back to overview]Percentage of Participants With Failure Free Survival (FFS)
NCT01231906 (1) [back to overview]Event-Free Survival
NCT01329900 (1) [back to overview]Mobilization Rate
NCT01446809 (7) [back to overview]Progression Free Survival
NCT01446809 (7) [back to overview]Change in Maximum SUV of Tumors Measured by FDG-PET Pre- and Post Receipt of Pazopanib Versus Placebo
NCT01446809 (7) [back to overview]Number of Participants With Pathologic Response at the Time of Surgery as Measured by % Tumor Viability ( >= 95% Necrosis)
NCT01446809 (7) [back to overview]Overall Survival
NCT01446809 (7) [back to overview]Pharmacokinetic Profile of Pazopanib
NCT01446809 (7) [back to overview]Change in Levels of VEGF and Soluble VEGFR2 Assessed by ELISA on Plasma and Tumor Extracts
NCT01446809 (7) [back to overview]Change in Maximum SUV of Tumors Measured by FDG-PET Post Receipt of 2 Courses of Preoperative Chemotherapy
NCT01490060 (1) [back to overview]Complete Response
NCT01602666 (6) [back to overview]Estimation of the PFS Distribution of Patients With NGGCT Treated With Involved-field Radiation Therapy (IFR)
NCT01602666 (6) [back to overview]Estimation of the PFS Distribution of Patients With Localized Germinoma Patients and Cerebrospinal Fluid (CSF) Serum hCGbeta of 50 mIU/mL or Less or CSF Serum hCGbeta Greater Than 50 mIU/mL and Less Than or Equal to 100 mIU/mL
NCT01602666 (6) [back to overview]Estimation of the OS Distribution of Patients With Localized Germinoma Patients and CSF Serum hCGbeta of 50 mIU/mL or Less or CSF Serum hCGbeta Greater Than 50 mIU/mL and Less Than or Equal to 100 mIU/mL
NCT01602666 (6) [back to overview]Estimation of the Overall Survival (OS) Distribution of Patients With NGGCT Treated With IFR Assessed
NCT01602666 (6) [back to overview]3-year Progression-free Survival (PFS) Rate of Patients With Nongerminomatous Germ Cell Tumor (NGGCT) Who Were Treated With Reduced Dose Whole Ventricular-field Irradiation
NCT01602666 (6) [back to overview]3-year PFS Rate of Patients With Localized CNS Germinoma Who Were Treated With Reduced Dose Radiation Therapy
NCT01808534 (5) [back to overview]Treatment Related Adverse Events Grade 3 or Higher
NCT01808534 (5) [back to overview]Progression Free Survival (PFS)
NCT01808534 (5) [back to overview]Duration of Remission in Patients Who Achieve a Partial or Complete Response
NCT01808534 (5) [back to overview]Overall Response Rate (Defined as Partial Response or Complete Response)
NCT01808534 (5) [back to overview]Overall Survival
NCT01946529 (1) [back to overview]Response to Window Therapy (2 Courses) for Group B (High-risk) - ESFT Participants
NCT01959698 (6) [back to overview]Overall Survival
NCT01959698 (6) [back to overview]Complete Response Rate According to the International Working Group Response Criteria as Reported by the Revised Cheson Criteria
NCT01959698 (6) [back to overview]MTD Defined as the Dose of Carfilzomib Added to Standard R-ICE Chemotherapy Which, if Exceeded, Would Put the Patient at an Undesirable Risk of Medically Unacceptable Dose-limiting Toxicities (Phase I)
NCT01959698 (6) [back to overview]Overall Response Rate (PR + CR)
NCT01959698 (6) [back to overview]Progression-free Survival
NCT01959698 (6) [back to overview]Toxicity of the Addition of Carfilzomib to R-ICE at the MTD, Assessed by the CTEP Version 4.0 of the NCI CTCAE
NCT01979536 (3) [back to overview]Prognostic Significance of Minimal Residual Disease
NCT01979536 (3) [back to overview]Occurrence of Grade 3+ Non-hematologic Adverse Events
NCT01979536 (3) [back to overview]Event Free Survival (EFS)
NCT01993329 (2) [back to overview]Highest FEV1 After Methacholine Challenge
NCT01993329 (2) [back to overview]Provocative Concentration (PC20) After Methacholine Challenge
NCT02018861 (27) [back to overview]Tmax of Itacitinib in Combination With Parsaclisib
NCT02018861 (27) [back to overview]Parts 1 and 2: Cmax of Parsaclisib as Monotherapy and in Combination With Itacitinib
NCT02018861 (27) [back to overview]Parts 1 and 2: Cmin of Parsaclisib as Monotherapy and in Combination With Itacitinib
NCT02018861 (27) [back to overview]Parts 1 and 2: Tmax of Parsaclisib as Monotherapy and in Combination With Itacitinib
NCT02018861 (27) [back to overview]Parts 1 and 2: AUC0-τ of Parsaclisib as Monotherapy and in Combination With Itacitinib
NCT02018861 (27) [back to overview]Parts 1 and 2: AUC0-t of Parsaclisib as Monotherapy and in Combination With Itacitinib
NCT02018861 (27) [back to overview]Part 6: ORR (Sum of Participants With CR and PR) Based on the Revised Response Criteria for HL and NHL, Using PET-CT and CT
NCT02018861 (27) [back to overview]Part 1: ORR (Sum of Participants With CR and PR) Based on the Revised Response Criteria for Hodgkin's Lymphoma (HL) and Non-Hodgkin's Lymphoma (NHL), Using Positron Emission Tomography-computed Tomography (PET-CT) and CT
NCT02018861 (27) [back to overview]Cmin of Itacitinib in Combination With Parsaclisib
NCT02018861 (27) [back to overview]Number of Participants With Treatment-emergent Adverse Events (TEAEs)
NCT02018861 (27) [back to overview]Part 1: ORR Based on the VIth International Workshop on Waldenström Macroglobulinemia (WM) Response Assessment for Participants With WM
NCT02018861 (27) [back to overview]Part 1: Overall Response Rate (Percentage of Participants With Complete Response [CR] and Partial Response [PR]) Based on International Workshop on Chronic Lymphocytic Leukemia (IWCLL) Criteria for Chronic Lymphocytic Leukemia (CLL) for CLL Participants
NCT02018861 (27) [back to overview]Part 3: Tmax of Parsaclisib Monotherapy
NCT02018861 (27) [back to overview]Part 3: Cmin of Parsaclisib Monotherapy
NCT02018861 (27) [back to overview]Part 3: Cmax of Parsaclisib Monotherapy
NCT02018861 (27) [back to overview]Part 3: AUC0-τ of Parsaclisib Monotherapy
NCT02018861 (27) [back to overview]Part 2: Overall Response Rate (Percentage of Participants With CR and PR) Based on IWCLL Criteria for CLL for Participants With CLL
NCT02018861 (27) [back to overview]AUC0-τ of Itacitinib in Combination With Parsaclisib
NCT02018861 (27) [back to overview]AUC0-t of Itacitinib in Combination With Parsaclisib
NCT02018861 (27) [back to overview]Part 2: ORR (Sum of Participants With CR and PR) Based on the Revised Response Criteria for HL and NHL, Using PET-CT and CT
NCT02018861 (27) [back to overview]Part 2: ORR (Sum of Participants With CR and PR) Based on the Revised Response Criteria for HL and NHL, Using PET-CT and CT
NCT02018861 (27) [back to overview]Part 1: ORR (Sum of Participants With CR and PR) Based on the Revised Response Criteria for Hodgkin's Lymphoma (HL) and Non-Hodgkin's Lymphoma (NHL), Using Positron Emission Tomography-computed Tomography (PET-CT) and CT
NCT02018861 (27) [back to overview]Part 1: ORR (Sum of Participants With CR and PR) Based on the Revised Response Criteria for Hodgkin's Lymphoma (HL) and Non-Hodgkin's Lymphoma (NHL), Using Positron Emission Tomography-computed Tomography (PET-CT) and CT
NCT02018861 (27) [back to overview]Part 1: ORR (Sum of Participants With CR and PR) Based on the Revised Response Criteria for Hodgkin's Lymphoma (HL) and Non-Hodgkin's Lymphoma (NHL), Using Positron Emission Tomography-computed Tomography (PET-CT) and CT
NCT02018861 (27) [back to overview]Part 1: ORR (Sum of Participants With CR and PR) Based on the Revised Response Criteria for Hodgkin's Lymphoma (HL) and Non-Hodgkin's Lymphoma (NHL), Using Positron Emission Tomography-computed Tomography (PET-CT) and CT
NCT02018861 (27) [back to overview]Part 3: AUC0-t of Parsaclisib Monotherapy
NCT02018861 (27) [back to overview]Cmax of Itacitinib in Combination With Parsaclisib
NCT02050919 (7) [back to overview]Pathologic Response Rate, Defined as the Percentage of Participants With Greater Than or Equal to 95% Necrosis.
NCT02050919 (7) [back to overview]Overall Survival at 2 Years
NCT02050919 (7) [back to overview]Overall Disease-free Survival (Stage IIB-III Patients)
NCT02050919 (7) [back to overview]Number of Participants With Wound Complications
NCT02050919 (7) [back to overview]Number of Participants With Local Recurrence
NCT02050919 (7) [back to overview]Number of Grade 3-4 Adverse Events
NCT02050919 (7) [back to overview]Distant Disease-free Survival (Stage IIB-III Patients)
NCT02112916 (6) [back to overview]Event-free Survival (EFS) for Modified Augmented Berlin-Frankfurt-Munster Backbone With or Without Bortezomib in All Randomized Patients
NCT02112916 (6) [back to overview]Cumulative Incidence Rates of Isolated Central Nervous System (CNS) Relapse for SR and IR T-ALL Patients on the Non-bortezomib Containing Arm on This Study (no CRT) and Similar Patients on AALL0434 (Receive CRT)
NCT02112916 (6) [back to overview]Toxicity Rates Associated With Modified Standard Therapy, Including Dexamethasone and Additional Pegaspargase
NCT02112916 (6) [back to overview]EFS for Standard (SR) and Intermediate Risk (IR) T-ALL Patients on the Non-bortezomib Containing Arm on This Study (no Cranial Radiation Therapy [CRT]) and Similar Patients on AALL0434 (Received CRT)
NCT02112916 (6) [back to overview]EFS for Very High Risk (VHR) T-ALL Patients Treated With High Risk (HR) Berlin-Frankfurt-Munster (BFM) Intensification Blocks Who Become Minimal Residual Disease (MRD) Negative and Those Who Remain MRD Positive at the End of HR Block 3
NCT02112916 (6) [back to overview]EFS for Very High Risk (VHR) T-LLy Patients Treated With HR Berlin-Frankfurt-Munster (BFM) Intensification Blocks Who Have Complete or Partial Remission and Those Who do Not Respond
NCT02180867 (6) [back to overview]Percentage of Radiotherapy Patients With Positive Pathologic Response at Week 10
NCT02180867 (6) [back to overview]Percentage of Chemoradiotherapy Patients With Positive Pathologic Response at Week 13
NCT02180867 (6) [back to overview]Percentage of Patients Who Experienced Grade 3 or Higher Toxicity Assessed by the National Cancer Institute (NCI) Common Terminology Criteria for Adverse Events (CTCAE)
NCT02180867 (6) [back to overview]Percentage of Patients Who Experienced Grade 3 or Higher Toxicity Assessed by the National Cancer Institute (NCI) Common Terminology Criteria for Adverse Events (CTCAE)
NCT02180867 (6) [back to overview]Feasible Dose: Pediatric
NCT02180867 (6) [back to overview]Feasible Dose: Adult
NCT02227199 (4) [back to overview]2 Year Progression-free Survival
NCT02227199 (4) [back to overview]Percentage of Patients That Achieve a Complete Remission Following Study Treatment
NCT02227199 (4) [back to overview]2 Year Overall Survival
NCT02227199 (4) [back to overview]Maximum Tolerated Dose of Brentuximab Vedotin That Can be Combined With Ifosfamide, Carboplatin, and Etoposide Chemotherapy
NCT02306161 (3) [back to overview]Overall Survival
NCT02306161 (3) [back to overview]Frequency of Toxicity-events
NCT02306161 (3) [back to overview]Event-free Survival
NCT02393859 (12) [back to overview]Pharmacokinetics: Concentration at Steady State (Css) (Blinatumomab Arm Only)
NCT02393859 (12) [back to overview]Kaplan Meier Estimate: Event-Free Survival (EFS; Primary Analysis)
NCT02393859 (12) [back to overview]Number of Participants With Anti-Blinatumomab Antibodies Postbaseline (Blinatumomab Arm Only)
NCT02393859 (12) [back to overview]Number of Participants With Shifts From Baseline Grade 0 or 1 to Worst Postbaseline Grade 3 or 4 Clinical Chemistry and Hematology Values
NCT02393859 (12) [back to overview]Number of Participants With TEAEs of Interest
NCT02393859 (12) [back to overview]Number of Participants With Treatment-Emergent Adverse Events (TEAEs) and Treatment-Related Adverse Events (TRAEs)
NCT02393859 (12) [back to overview]Percentage of Participants With an MRD Response Within 29 Days of Treatment Initiation
NCT02393859 (12) [back to overview]Pharmacokinetics: Clearance (CL) (Blinatumomab Arm Only)
NCT02393859 (12) [back to overview]Kaplan-Meier Estimate of 100-Day Mortality After Allogeneic Hematopoietic Stem Cell Transplantation (alloHSCT)
NCT02393859 (12) [back to overview]Kaplan Meier Estimate: Overall Survival (OS)
NCT02393859 (12) [back to overview]Kaplan Meier Estimate: EFS (Final Analysis)
NCT02393859 (12) [back to overview]Cumulative Incidence of Relapse (CIR)
NCT02432274 (23) [back to overview]Cohorts 1, 2A, 2B, 3A and 3B: Number of Participants With Treatment-emergent Adverse Events (TEAEs) and Serious Adverse Events (SAEs)
NCT02432274 (23) [back to overview]Cohorts 1, 2A, 2B, 3A, and 3B: Number of Participants With Shift From Baseline to Worst Post Baseline Measurements on Urine DipStick for Proteinuria
NCT02432274 (23) [back to overview]Cohorts 1, 2A, 2B, 3A, and 3B: Plasma Concentrations of Lenvatinib
NCT02432274 (23) [back to overview]Cohorts 1, 2A, 2B, 3A, and 3B: Plasma Concentrations of Lenvatinib
NCT02432274 (23) [back to overview]Cohorts 1, 2B, 3A, and 3B: Number of Participants With Best Overall Response (BOR)
NCT02432274 (23) [back to overview]Cohorts 1, 2A, 2B, 3A and 3B: Overall Survival (OS)
NCT02432274 (23) [back to overview]Cohort 2B, 3B: Percent Change From Baseline in Serum Biomarkers Level
NCT02432274 (23) [back to overview]Cohorts 1, 2A, 2B, 3A and 3B: Number of Participants Who Experienced Disease Control
NCT02432274 (23) [back to overview]Cohorts 1, 2A, 2B, 3A and 3B: Number of Participants Experienced Clinical Benefit
NCT02432274 (23) [back to overview]Cohorts 1, 2A, 2B, 3A and 3B: Duration of Response (DOR)
NCT02432274 (23) [back to overview]Cohort 3A: Recommended Dose (RD) of Lenvatinib When Given in Combination With Etoposide and Ifosfamide
NCT02432274 (23) [back to overview]Cohort 2A: Number of Participants With Objective Response (OR) of Complete Response (CR) or Partial Response (PR)
NCT02432274 (23) [back to overview]Cohort 1: Recommended Dose (RD) of Lenvatinib
NCT02432274 (23) [back to overview]Cohorts 1, 2A, 2B, 3A and 3B: Progression-free Survival (PFS)
NCT02432274 (23) [back to overview]Cohorts 1, 2A, 2B, 3A and 3B: Time to Progression (TTP)
NCT02432274 (23) [back to overview]Cohorts 1, 2B, 3A, and 3B: Objective Response Rate (ORR)
NCT02432274 (23) [back to overview]Cohorts 2B and 3B: Progression-free Survival (PFS) Rate at Month 4
NCT02432274 (23) [back to overview]Cohort 2A: Number of Participants With Best Overall Response (BOR)
NCT02432274 (23) [back to overview]Cohort 2B, 3B: Percent Change From Baseline in Serum Biomarkers Level
NCT02432274 (23) [back to overview]Cohorts 1, 2A, 2B, 3A and 3B: Number of Participants Categorized Based on Overall Acceptability Questionnaire Responses for Suspension of Lenvatinib
NCT02432274 (23) [back to overview]Cohorts 1, 2A, 2B, 3A and 3B: Number of Participants With Most Frequent Treatment-emergent Adverse Events (TEAEs) Related to Lenvatinib Exposure
NCT02432274 (23) [back to overview]Cohorts 1, 2A, 2B, 3A and 3B: Number of Participants With Shift From Baseline to Worst Post Baseline Score in Karnofsky Performance Status (KPS) Scores
NCT02432274 (23) [back to overview]Cohorts 1, 2A, 2B, 3A and 3B: Number of Participants With Shift From Baseline to Worst Post Baseline Score in Lansky Performance Play Score
NCT02441309 (5) [back to overview]Number of Patients Experiencing a Laboratory Abnormality (Grade 3-4)
NCT02441309 (5) [back to overview]Number of Patients Experiencing a Grade 3 or More Severe Adverse Event (Graded According to CTCAE Criteria v4.0)
NCT02441309 (5) [back to overview]Disease Specific Overall Survival
NCT02441309 (5) [back to overview]Progression Free Survival
NCT02441309 (5) [back to overview]Objective Radiological Response Based on RECIST v1.1
NCT02592876 (10) [back to overview]Number of Participants With Laboratory Abnormalities
NCT02592876 (10) [back to overview]Number of Patients Achieving Peripheral Blood Stem Cell (PBSC) Mobilization
NCT02592876 (10) [back to overview]Number of Patients Receiving Autologous Stem Cell Transplant (ASCT)
NCT02592876 (10) [back to overview]Objective Response Rate (ORR)
NCT02592876 (10) [back to overview]Complete Remission Rate Per Independent Review Facility
NCT02592876 (10) [back to overview]Duration of Complete Response (CR)
NCT02592876 (10) [back to overview]Duration of Objective Response (OR)
NCT02592876 (10) [back to overview]Overall Survival (OS)
NCT02592876 (10) [back to overview]Progression-free Survival (PFS)
NCT02592876 (10) [back to overview]Number of Participants With Adverse Events (AEs)
NCT02677116 (16) [back to overview]PK: Maximum Concentration (Cmax) of Olaratumab Part B
NCT02677116 (16) [back to overview]PK: Maximum Concentration (Cmax) of Olaratumab Part B
NCT02677116 (16) [back to overview]PK: Maximum Concentration (Cmax) of Olaratumab Part C
NCT02677116 (16) [back to overview]PK: Maximum Concentration (Cmax) of Olaratumab Part C
NCT02677116 (16) [back to overview]PK: Maximum Concentration (Cmax) of Olaratumab Part C
NCT02677116 (16) [back to overview]PK: Trough Serum Minimum Concentration (Cmin) of Olaratumab Part A
NCT02677116 (16) [back to overview]PK: Trough Serum Minimum Concentration (Cmin) of Olaratumab Part A
NCT02677116 (16) [back to overview]PK: Trough Serum Minimum Concentration (Cmin) of Olaratumab Part A
NCT02677116 (16) [back to overview]PK: Trough Serum Minimum Concentration (Cmin) of Olaratumab Part B
NCT02677116 (16) [back to overview]Percentage of Participants With Treatment Emergent (TE) Positive Anti-Olaratumab Antibodies
NCT02677116 (16) [back to overview]PK: Trough Serum Minimum Concentration (Cmin) of Olaratumab Part C
NCT02677116 (16) [back to overview]Number of Participants With Olaratumab Dose Limiting Toxicities (DLTs)
NCT02677116 (16) [back to overview]Percentage of Participants With a Complete Response (CR) or Partial Response (PR) (Objective Response Rate [ORR])
NCT02677116 (16) [back to overview]Progression Free Survival (PFS)
NCT02677116 (16) [back to overview]Pharmacokinetics (PK): Maximum Concentration (Cmax) of Olaratumab Part A
NCT02677116 (16) [back to overview]Pharmacokinetics (PK): Maximum Concentration (Cmax) of Olaratumab Part A
NCT02703272 (37) [back to overview]Part 1: Apparent (Oral) Plasma Clearance (CL/F) of Ibrutinib
NCT02703272 (37) [back to overview]Part 1 and Part 2: Gene Expression Evaluated by Disease-specific Biomarkers at Baseline
NCT02703272 (37) [back to overview]Part 2: Tumor Volume Reduction Rate at Day 14
NCT02703272 (37) [back to overview]Part 2: Time to Response
NCT02703272 (37) [back to overview]Part 2: Percentage of Participants With EFS at 3 Years
NCT02703272 (37) [back to overview]Part 2: Percentage of Participants With EFS at 2 Years
NCT02703272 (37) [back to overview]Part 2: Percentage of Participants Who Achieved Partial Response (PR)
NCT02703272 (37) [back to overview]Part 2: Percentage of Participants Who Achieved Complete Response (CR)
NCT02703272 (37) [back to overview]Part 2: Overall Survival
NCT02703272 (37) [back to overview]Part 2: Number of Participants With c-MYC Gene Rearrangement
NCT02703272 (37) [back to overview]Part 1: Apparent (Oral) Volume of Distribution (Vd/F) of Ibrutinib
NCT02703272 (37) [back to overview]Part 1: Apparent (Oral) Volume of Distribution (Vd/F) of Ibrutinib
NCT02703272 (37) [back to overview]Part 1: Apparent (Oral) Plasma Clearance (CL/F) of Ibrutinib
NCT02703272 (37) [back to overview]Part 2: Apparent (Oral) Plasma Clearance (CL/F) of Ibrutinib
NCT02703272 (37) [back to overview]Part 1 and Part 2: Visual Analog Scale (VAS) Score for Palatability
NCT02703272 (37) [back to overview]Part 1 and Part 2: Number of Participants With Adverse Events as Measure of Safety and Tolerability
NCT02703272 (37) [back to overview]Part 2: Apparent (Oral) Plasma Clearance (CL/F) of Ibrutinib
NCT02703272 (37) [back to overview]Part 2: Number of Participants With CD79B, CARD11, and MYD Mutations
NCT02703272 (37) [back to overview]Part 2: Apparent (Oral) Volume of Distribution (Vd/F) of Ibrutinib
NCT02703272 (37) [back to overview]Part 2: Apparent (Oral) Volume of Distribution (Vd/F) of Ibrutinib
NCT02703272 (37) [back to overview]Part 2: Apparent (Oral) Volume of Distribution (Vd/F) of Ibrutinib
NCT02703272 (37) [back to overview]Part 2: Area Under the Plasma Concentration-time Curve (AUC) of Ibrutinib
NCT02703272 (37) [back to overview]Part 2: Area Under the Plasma Concentration-time Curve (AUC) of Ibrutinib
NCT02703272 (37) [back to overview]Part 2: Area Under the Plasma Concentration-time Curve (AUC) of Ibrutinib
NCT02703272 (37) [back to overview]Part 2: Maximum Observed Plasma Concentration (Cmax) of Ibrutinib
NCT02703272 (37) [back to overview]Part 2: Maximum Observed Plasma Concentration (Cmax) of Ibrutinib
NCT02703272 (37) [back to overview]Part 2: Maximum Observed Plasma Concentration (Cmax) of Ibrutinib
NCT02703272 (37) [back to overview]Part 1 and Part 2: Number of Participants With Greater Than (>) 90% Bruton's Tyrosine Kinase (BTK) Occupancy
NCT02703272 (37) [back to overview]Part 1 and Part 2: Overall Response Rate (ORR)
NCT02703272 (37) [back to overview]Part 2: Duration of Response
NCT02703272 (37) [back to overview]Part 2: Event Free Survival (EFS) Between the 2 Treatment Groups
NCT02703272 (37) [back to overview]Part 2: Number of Participants Who Proceeded to Stem Cell Transplantation
NCT02703272 (37) [back to overview]Part 2: Apparent (Oral) Plasma Clearance (CL/F) of Ibrutinib
NCT02703272 (37) [back to overview]Part 1: Maximum Observed Plasma Concentration (Cmax) of Ibrutinib
NCT02703272 (37) [back to overview]Part 1: Maximum Observed Plasma Concentration (Cmax) of Ibrutinib
NCT02703272 (37) [back to overview]Part 1: Area Under the Plasma Concentration-time Curve (AUC) of Ibrutinib
NCT02703272 (37) [back to overview]Part 1: Area Under the Plasma Concentration-time Curve (AUC) of Ibrutinib
NCT02732015 (1) [back to overview]Number of Participants With Complete Response (CR) of Rolapitant Hydrochloride Administered as a Single-dose
NCT03283696 (11) [back to overview]Disease Control Rate (DCR): Percentage of Participants With a Best Overall Response of CR, PR, or Stable Disease (SD)
NCT03283696 (11) [back to overview]Number of Participants With Olaratumab Dose Limiting Toxicities (DLTs)
NCT03283696 (11) [back to overview]PK: Trough Serum Concentration (Cmin,ss) of Olaratumab at Steady-state
NCT03283696 (11) [back to overview]PK: Trough Serum Concentration (Cmin)
NCT03283696 (11) [back to overview]Number of Participants With Anti-Olaratumab Antibodies
NCT03283696 (11) [back to overview]Duration of Response (DoR)
NCT03283696 (11) [back to overview]Objective Response Rate (ORR): Number of Participants Who Achieve Best Overall Tumor Response of Complete Response (CR) or Partial Response (PR)
NCT03283696 (11) [back to overview]Overall Survival (OS)
NCT03283696 (11) [back to overview]Progression Free Survival (PFS)
NCT03283696 (11) [back to overview]Pharmacokinetics (PK): Maximum Serum Concentration (Cmax) of Olaratumab
NCT03283696 (11) [back to overview]PK: Maximum Serum Concentration (Cmax,ss) of Olaratumab at Steady-state
NCT04154189 (10) [back to overview]Percentage of Participants With Overall Survival at 1 Year or Month 12 (OS-1y)
NCT04154189 (10) [back to overview]Percentage of Participants With PFS at 1 Year or Month 12 (PFS-1y Rate) by IIR Assessment
NCT04154189 (10) [back to overview]Percentage of Participants With PFS at Month 4 (PFS-4m Rate) by IIR Assessment
NCT04154189 (10) [back to overview]Progression-free Survival (PFS) by Independent Imaging Review (IIR) Assessment
NCT04154189 (10) [back to overview]Number of Participants Categorized Based on Overall Palatability and Acceptability Questionnaire Responses for Suspension of Lenvatinib
NCT04154189 (10) [back to overview]Change From Baseline in Pediatric Quality of Life Inventory (PedsQL) Scale: Generic Core Scale Score at Month 4
NCT04154189 (10) [back to overview]Change From Baseline in PedsQL Scale: Cancer Module Scale Score at Month 4
NCT04154189 (10) [back to overview]Objective Response Rate at Month 4 (ORR-4m) by IIR Assessment
NCT04154189 (10) [back to overview]Treatment Arm A: Plasma Concentration of Lenvatinib
NCT04154189 (10) [back to overview]ORR by IIR Assessment
NCT04189952 (8) [back to overview]Event-Free Survival (EFS)
NCT04189952 (8) [back to overview]Number of Treatment-Emergent Adverse Events
NCT04189952 (8) [back to overview]Overall Survival (OS)
NCT04189952 (8) [back to overview]Percentage of Participants Achieving Complete Response (CR)
NCT04189952 (8) [back to overview]Percentage of Participants Achieving Mobilization Rate Greater Than or Equal to 2x10^6 CD34+ Cells/kg Body Weight
NCT04189952 (8) [back to overview]Percentage of Participants Achieving Overall Response
NCT04189952 (8) [back to overview]Percentage of Participants Achieving Partial Response (PR)
NCT04189952 (8) [back to overview]Progression-Free Survival (PFS)

Overall Objective Response

Overall Objective Response will be assessed prior to dose-intensive therapy and at the completion of therapy. Complete disappearance of all clinical, radiographic and biochemical (normal AFP and HCG) evidence of disease for a minimum of 4 weeks (CR to chemotherapy). Patients must be free of disease for a minimum of 4 weeks. Partial Response: Complete disappearance of all biochemical evidence of disease in patients without a surgical procedure for a residual radiographic mass. Patients must demonstrate no biochemical recurrence or progression of radiographic masses for a minimum of four weeks (PR to chemotherapy} (NCT00002558)
Timeframe: 2 years

,
Interventionparticipants (Number)
Complete Response (CR)Incomplete Response (IR)Partial Response (PR)
Group A50365
Group B483

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5-year Overall Survival

Estimated using the product-limit method of Kaplan and Meier. (NCT00002601)
Timeframe: Until death from any cause, up to 5 years

Interventionpercentage of participants (Number)
Doxorubicin/Ifosfamide + Melphalan/CDDP + PSCT31

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5-year Progression-free Survival

Estimated using the product-limit method of Kaplan and Meier. Progression is defined using Response Evaluation Criteria In Solid Tumors Criteria (RECIST), as a 25% increase in the sum of the longest diameter of target lesions, or the appearance of new lesions. (NCT00002601)
Timeframe: Until disease progression, up to 5 Years

Interventionpercentage of participants (Number)
Doxorubicin/Ifosfamide + Melphalan/CDDP + PSCT23

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Number of Participants With Grade 3 Bilirubin

Criteria for early termination of this feasibility study: > 2 patients experience grade 4 or 5 hematologic toxicity or more that 3 patients experience grade 3 hematologic toxicity; > 2 patients experience grade 3 hepatic or gastrointestinal toxicity or > 3 patients are unable to receive the second cycle of treatment; > 2 patients experience grade 5 toxicity related to treatment regimen. (NCT00002601)
Timeframe: 2 years after completion of treatment

Interventionparticipants with Grade 3 Bilirubin (Number)
Doxorubicin/Ifosfamide + Melphalan/CDDP + PSCT3

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Toxicities Counts

Number of patients with grade 3 and 4 toxicities observed during cycles 1 & 2 using the Common Toxicity Criteria Version for Chemotherapy. (NCT00002601)
Timeframe: 2 months after completion of second cycle of treatment.

,
InterventionParticipants (Count of Participants)
AnemiaLeukopeniaNeutropeniaFebrile neutropeniaThrombocytopeniaMucositisBacteremia/sepsisHyperglycemiaPulmonary function impairment (FEV1)Pulmonary infiltratesDiarrheaArrhythmiaHematuriaMoodElevated PTT
Cycle 181313131313251011111
Cycle 2311119111410201010

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Toxic Effects

Number of Participants with Grade 3 and 4 Adverse Events Related to Protocol-based Therapy (NCT00002931)
Timeframe: From date of randomization until death of any cause, assessed up to 12 weeks

Interventionparticipants (Number)
HyperglycemiaTransaminase aloneMucositis/stomatitisNausea/vomitingFebrile neutropeniaDiarrheaHyperbilirubinemiaFever w/o neutropeniaHypocalcemiaHemorrhageElevated INR/Prothrombin timeRenal FailureConstipationEsophagitis
HD Chemo and Auto Stem Cells461051332212111

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Overall Survival

Estimated using the product-limit method of Kaplan and Meier. (NCT00002931)
Timeframe: Until death from any cause, up to 5 years.

InterventionMonths (Median)
HD Chemo and Auto Stem Cells21.7

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Progression-free Survival

Estimated using the product-limit method of Kaplan and Meier. Progression is defined as an increase o any radiologically measureable tumor by greater than 25% or a greater than 10% increase of elevated tumor markers. (NCT00002931)
Timeframe: Until disease progression, up to 5 years.

InterventionMonths (Mean)
HD Chemo and Auto Stem Cells11.8

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Objective Response

Determine the overall objective response. CR rate [as measured from the start of ICE, (or high dose CTX) to the end of transplant for those who receive it, or the end of ICE for those who do not].Complete response (CR): No evidence of Hodgkin's disease determined clinically, radiologically or pathologically when indicated (NCT00003631)
Timeframe: 2 years

,,
Interventionparticipants (Number)
FailureMinor Response (MR)Partial Response (PR)Progression Free (P-Free)Complete Response (CR)Progression of Disease (POD)
Group A - Favorable Prognostic Group3214100
Group B - Intermediate Prognostic Group6123121
Group C - Unfavorable Prognostic Group304710

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2 Year Overall Survival

Percentage of participants who were alive at 2 years. The 2 year survival, with 95% confidence interval, was estimated using the Kaplan Meier method. (NCT00039130)
Timeframe: 2 years

Interventionpercentage of participants (Number)
Rituximab With High Intensity Chemotherapy80

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2 Year Event Free Survival

Percentage of patients who were event free at 2 years. The 2-year event free rate was estimated using the Kaplan Meier method. An event is defined as death, progression or treatment failure. (NCT00039130)
Timeframe: 2 years

Interventionpercentage of participants (Number)
Rituximab With High Intensity Chemotherapy78

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Complete Response Rate

Response is assessed by investigator according to Revised Response Criteria for Malignant Lymphoma. Complete response requires disappearance of all evidence of disease. (NCT00039130)
Timeframe: 6 months

Interventionpercentage of participants (Number)
Rituximab With High Intensity Chemotherapy83

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Progression Free Survival

Kaplan-Meier estimates will be used to verify the progression free survival. (NCT00039195)
Timeframe: 2 years

Interventionpercentage of patients progression free (Number)
Induction R-CHOPac Therapy79

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Number of Patients Experiencing Toxic Death

Toxic death, defined as death predominantly attributable to treatment-related causes. (NCT00047320)
Timeframe: During chemotherapy (up to 18 weeks)

InterventionParticipants (Count of Participants)
Radiation Therapy (CR From Induction)0

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Response to Induction Chemotherapy

A patient who achieves a complete or partial response, defined a reduction of at least 65% in tumor size after induction chemotherapy will be considered to have experienced response. (NCT00047320)
Timeframe: 18 weeks

InterventionParticipants (Count of Participants)
ResponderNon-Responder
Radiation Therapy (CR From Induction)7411

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The Probability of Event-free Survival (EFS)

Event-free Survival was defined as time from study entry to death from any cause, disease progression or recurrence, or second malignant neoplasm. Event-free survival was estimated by KM estimate. (NCT00047320)
Timeframe: At 3 years from study entry

InterventionProbability (Number)
Radiation Therapy (CR From Induction)0.837

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Progression-free Survival (PFS)

Progression-free Survival was defined as time from study entry to disease progression or recurrence. Deaths that are clearly unrelated to disease progression, and second neoplasms are censored in this analysis. Progression -free survival was estimated by KM estimate. (NCT00047320)
Timeframe: At 3 years from study entry

InterventionProbability (Number)
Radiation Therapy (CR From Induction)0.837

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Overall Survival (OS)

Overall Survival was defined as time from study entry to death from any cause. Overall survival was estimated by KM estimate. (NCT00047320)
Timeframe: At 3 years from study entry

InterventionProbability (Number)
Radiation Therapy (CR From Induction)0.927

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Occurrence of Non-hematological Grade 4 Toxicity Occurrence of Nonhematological Grade 4 Toxicity

The number of patients who experienced non-hematological grade 4 toxicities anytime during chemotherapy. (NCT00047320)
Timeframe: During chemotherapy(up to 18 weeks)

Interventionparticipants (Number)
Radiation Therapy (CR From Induction)22

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Event Free Survival

(NCT00061893)
Timeframe: 24 months after start of protocol therapy

Interventionpercentage of participants (Number)
Combination Chemotherapy35

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Occurrence of Severe Toxicity

An incidence of severe toxicity is defined to be the occurrence of grade 3 or higher infection or grade 3 or higher sensory neuropathy during cycles 1-2 of protocol therapy. If 12 or more patients experience grade 3 or higher infection or five or more patients experience grade 3 or higher sensory neuropathy during cycles 1-2 of protocol therapy, the regimen will be flagged as being associated with an excessive rate of severe toxicity. (NCT00061893)
Timeframe: The first two cycles (6 weeks) of protocol chemotherapy

Interventionparticipants (Number)
Grade 3 or Higher InfectionGrade 3 or Higher Sensory Neuropathy
Combination Chemotherapy11

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"Failure-free Survival (FFS) in Chemotherapy Plus Possible Surgery Arm"

Failure is defined as the occurrence of one of the following: disease progression, defined as at least a 20% increase in the disease measurement, taking as reference the smallest disease measurement recorded since the start of treatment, or the appearance of one or more new lesions; relapse (defined with same criteria as for disease progression) after response; or death as a first event. Data will be summarized as number of eligible patients in each of the following categories at the time of data cutoff for analyses of 5-year FFS: 1)Failed; 2)Failure-free through 5 years of follow-up; 3)Failure-free until data cutoff (if less than 5 years of follow-up); 4)Withdrew from study; 5)Lost to follow-up. NOTE: Reported data are through March 2008 (see Caveats section). (NCT00072280)
Timeframe: Study enrollment until failure, completion of follow-up, or completion of 5-year FFS analyses (up to 5 years)

Interventionparticipants (Number)
FailedFailure-free through 5 years of follow-upFailure-free at cutoff (if < 5 years follow-up)Withdrew from studyLost to follow-up
Chemotherapy Plus Possible Surgery10100

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Treatment Delivery With Compliance Defined as Receiving at Least 95% of the Pre-operative Protocol Dose of RT, All 3 Cycles of MAID (if Applicable), and Receive Thalidomide on 75% of the Days During Radiation

Was to be estimated using a binomial distribution and accompanied by the associated 95% confidence interval. Due to early study closure, this endpoint could not be fully evaluated per the protocol plan. (NCT00089544)
Timeframe: Duration of treatment (which can continue up to approximately 15 months).

,
Interventionparticipants (Number)
Not CompliantCompliant
Cohort A (Chemotherapy, Radiation, Thalidomide, Surgery)510
Cohort B (Thalidomide, Radiation, Surgery)25

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Overall Survival

To evaluated the overall survival in both groups in participants presenting fast and slow decrease in serum levels of tumor markers. The median overall survival was defined as the median percentage of participants alive after 1 course of treatment. (NCT00104676)
Timeframe: 3 years from randomization

Interventionpercentage of participants (Number)
Arm I65
Arm II73

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Progression-free Survival Rate After 1 Course of Treatment

Primary objective is to compare the progression-free survival of participants after 1 cycle of treatment, treated randomly by 3 additional cycles of BEP (Arm I) or by T-BEP-Oxaliplatin/cisplatin-ifosfamide-Bleomycin (Arm II). The median progression-free survival rate was defined as the median percentage of participants alive without disease progression after 1 course of treatment. (NCT00104676)
Timeframe: 3 years from randomization

Interventionpercentage of participants (Number)
Arm I48
Arm II59

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Response Rates (CR and PR) in Adults With Burkitt/Atypical Burkitt

"Complete Response (CR): Disappearance of all measurable or evaluable disease confirmed.~Partial Response (PR): Reduction of 50% or greater in the sum of the products of the perpendicular diameters of all measurable.~Of 8 High Risk participants, 7 met the primary response outcome. 1 High Risk participant did not meet protocol defined primary outcome response and died two months following enrollment." (NCT00126191)
Timeframe: 3 years

Interventionparticipants (Number)
Low Risk2
High Risk7

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Disease Free Survival

Participants are followed after completion of protocol therapy until disease progression to determine disease free survival. (NCT00126191)
Timeframe: Until disease progression up to 120 months

InterventionMonths (Mean)
Low Risk84
High Risk52

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Event-free Survival (EFS)

"EFS is defined as time from randomisation to the first of: death, detection of local recurrence or metastasis, progression of metastatic disease, or detection of a secondary malignancy.~EFS will be assessed using the logrank test and expressed using hazard ratios with appropriate confidence intervals. Follow up per participant will be assessed for up to 10 years. The 3 year EFS is provided as a summary." (NCT00134030)
Timeframe: From date of randomization to date of the event.

InterventionPercentage EFS (Number)
MAP-GR74
MAPifn77
MAP-PR55
MAPIE53

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Percentage of Patients With Overall Survival

"Overall survival is time from randomization until death from any cause.~Will be assessed using the logrank test and expressed using hazard ratios with appropriate confidence intervals. Participants will be assessed for up to 10 years. 5 year overall survival is provided as a summary." (NCT00134030)
Timeframe: From date of randomization to date of death.

InterventionPercentage of participants (Number)
MAP-GR84
MAPifn84
MAP-PR68
MAPIE68

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Toxicity as Measured by Common Terminology Criteria for Adverse Events (CTCAE) v3.0

Percentages of patients experiencing grade 3 and 4 adverse events. These will be compared using chi-square tests or Fisher's exact tests where appropriate. (NCT00134030)
Timeframe: Adverse events are assessed for up to 10 years per participant.

InterventionParticipants (Count of Participants)
MAP-GR348
MAPifn340
MAP-PR287
MAPIE281

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Number of Participants With Adverse Events in Sequential Cohort Dose Escalation Study of AMG 531 Following Chemotherapy

Number of participants experiencing an adverse event (AE) or serious adverse event (SAE) during study treatment, possible or probable related to study drug. All toxicities graded using the Common Terminology Criteria for Adverse Events version 3.0. Participation has a maximum of 6 cycles of chemotherapy on the study. (NCT00147225)
Timeframe: Toxicity assessments with each dose level/cycle (21-28 day cycle) up to 6 cycles

,,,,,
Interventionparticipants (Number)
Adverse Events, Possible or ProbableSerious Adverse Events, Possible or ProbableTotal Adverse Events
1 mcg/kg AMG 531 Post Chemotherapy000
10 mcg/kg AMG 531 Post Chemotherapy112
10 mcg/kg AMG 531 Pre/Pre/Post/Post Chemotherapy808
10 mcg/kg Pre/Post Chemotherapy404
3 mcg/kg AMG 531 Post Chemotherapy000
5 mcg/kg AMG 531 Pre/Pre/Post/Post Chemotherapy527

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The Percentage of Patients Alive Without Disease at 2 Years

Disease-free survival (NCT00189137)
Timeframe: 2 years

Interventionpercentage of patients (Number)
Doxorubicin and Ifosfamide57
Gemcitabine and Docetaxel74

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Percentage of Patients Hospitalized in Each Arm.

To contrast the proportion of treated patients hospitalized subsequent to treatment with gemcitabine and docetaxel as compared to doxorubicin and ifosfamide as neoadjuvant or adjuvant therapy of poor prognosis soft tissue sarcoma. (NCT00189137)
Timeframe: 12 weeks

Interventionpercentage of patients hospitalized (Number)
Doxorubicin and Ifosfamide35
Gemcitabine and Docetaxel26

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Cycles With Hematologic Toxicities

Out of 162 planned cycles, a total of 138 cycles (85%) were administered. Number of cycles during which participants with grades 3 and 4 experienced hematologic toxicities are reported. Most of the toxicities were self-limiting. (NCT00231842)
Timeframe: 2 years

,
InterventionCycles (Number)
NeutropeniaAnemiaThrombocytopenia
Grade 3 Toxicity1166
Grade 4 Toxicity1402

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Toxicity at End of Study Treatment

(NCT00245011)
Timeframe: Continual and at End of Study

InterventionParticipants (Count of Participants)
Delayed numbness and tinglingMild hypocalcemiaMild - Moderate pancytopeniaLymphopeniaFever
Samarium-153/Stem Cell Transplant/Radiation3111115

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Tumor Response

WHO (World Health Organization) tumor measurement criteria used to determine response. (NCT00245011)
Timeframe: 1 week after study treatment

Interventionparticipants (Number)
Samarium-153/Stem Cell Transplant/Radiation10

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Overall and Progression-free Survival After Study Treatment

(NCT00245011)
Timeframe: up to 4 years

Interventiondays (Median)
Overall SurvivalProgression-free Survival
Samarium-153/Stem Cell Transplant/RadiationNA79

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Overall Objective Response

"Overall objective response to therapy Complete remission/unconfirmed (CRu)~This includes patients who meet criteria for CR with the following exceptions:~1. A residual lymph node mass > 1.5 cm in the short axis with normalization of 18Ffluorodeoxyglucose- PET scan Partial remission/minimal response (PR and MR)~Any decrease in lymph nodes and nodal-based masses~Any decrease in PET avidity (however, residual FDG uptake is present)~Involving organs involved prior to therapy must have diminished in size.~No new sites of disease Stable disease Response is less than that which constitutes a PR and disease does not meet criteria for progressive disease Progressive disease~1. Increase in lymph nodes or nodal-based masses, or other measurable disease from pretreatment observations. 2. Appearance of any new lesion at the end of therapy" (NCT00255723)
Timeframe: 3 years

,
Interventionparticipants (Number)
Complete RemissionPartial Remission (PR)Progression of Disease (POD)
Arm A4563
Arm B3117

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Cumulative Incidence Rate of Oral Mucositis

"Cumulative incidence of World Health Organization (WHO) grade 2 or > mucositis (moderate to severe) in participants completing up to 6 blinded cycles. Rate defined as participants who had Grade 2 or > divided by total number of participants who completed up to 6 blinded cycles.~WHO Criteria of Grade 1: possible buccal mucosal scalloping with/without erythema; No ulcers; swallows solid diet. Grade 2: ulcers with or without erythema; swallow solid diet. Grade 3: ulcers with/without (extensive) erythema; swallow liquid, not solid diet. Grade 4: mucositis to extent alimentation not possible." (NCT00267046)
Timeframe: Within 6 blinded cycles (3-week cycles), up to 18 weeks.

,
InterventionPercentage of Participants (Mean)
Cumulative incidence of WHO grade 2 or higher mucoCumulative Incidence of WHO Grade 3 or 4 Mucositis
Palifermin4413
Placebo8851

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Median Maximum Score for Patient Reported Outcomes in 2 Blinded Cycles

Median maximum score (0 to 10, with 10 being the worst) for participant-reported outcomes in the first 2 blinded cycles for Mouth Pain, Overall Mouth and Throat Soreness, and Rectal Soreness while median maximum score for Swallowing, Drinking and Eating Difficulty (0 to 4, with 4 being the difficult). (NCT00267046)
Timeframe: Within the first 2 blinded cycles (3-week cycles), up to 6 weeks.

,
InterventionUnits on a scale (Median)
Mouth PainOverall Mouth and Throat SorenessRectal SorenessDrinking DifficultyEating DifficultySwallowing Difficulty
Palifermin110000
Placebo55.541.522

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2-year Progression-Free Survival (PFS)

2-year progression-free survival is defined as the probability of patients who remain alive and progression free at 2 years from study entry. The method of Kaplan and Meier (1958) was used to estimate PFS. (NCT00274924)
Timeframe: Assessed every 4 months if patient is < 2 years from study entry, every 6 months if patient is 2-5 years from study entry, then every 12 months if patient is 5-10 years from study entry.

Interventionprobability (Number)
Group I (PET Negative)0.76
Group II (PET Positive)0.42

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5-year Overall Survival

5-year overall survival is defined as the probability of patients who remain alive at 5 years from study entry. The method of Kaplan and Meier (1958) was used to estimate overall survival. (NCT00274924)
Timeframe: Every 4 months if patient is < 2 years from study entry, every 6 months if patient is 2-5 years from study entry, then every 12 months if patient is 5-10 years from study entry.

Interventionprobability (Number)
Group I (PET Negative)0.77
Group II (PET Positive)0.69

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Event Free Survival Without Receiving Radiation Therapy (EFSnoRT).

Survival is defined as the minimum time from study entry to requirement for additional chemotherapy and IFRT for retrieval, occurrence of a second malignant neoplasm, or death from any cause. Patients without report of such events where censored at last contact. Patients who achieve less than CR after 3 cycles of AV-PC will require IFRT and hence will satisfy this definition at the time of response evaluation. Patients who achieve a CR but who relapse will receive addition chemotherapy and IFRT or intense retrieval and hence will satisfy this definition at the time of the first relapse of Hodgkin disease. This endpoint will be used to compute event free survival without receiving radiation therapy (EFSnoRT). (NCT00302003)
Timeframe: At 60 months

InterventionProbability of survival (Number)
Group 10.49

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Intensive Therapy Free Survival (ITFS).

Survival is defined as the minimum time from study entry to a relapse of higher risk at any time, any relapse following treatment with protocol mandated IFRT, death from any cause, or the occurrence of a second malignant neoplasm. This will be used to compute intensive therapy free survival (ITFS). Patients without report of such events where censored at last contact. This differs from traditional EFS in that relapse after AVPC* x3 therapy alone that does not place the patient in a higher risk category is not considered a treatment failure. In this definition, higher-risk relapse refers to relapse involving sites and extent of disease that place the patient in the current COG definition of intermediate or high-risk disease. If a patient with CR who experiences a LR relapse is not retreated with protocol-mandated chemotherapy and IFRT, subsequent disease relapses will nevertheless be counted in the analysis of the treatment strategy. (NCT00302003)
Timeframe: At 60 months

InterventionProbability of survival (Number)
Group 10.89

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Overall Survival

Survival is defined as time from study entry to death due to any cause. Patients alive at last contact where censored at last contact. (NCT00302003)
Timeframe: At 60 months

InterventionProbability of survival (Number)
Group 10.99

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Event Free Survival (EFS)

Survival is defined as the minimum time from study entry to a relapse of any kind, death from any cause, or occurrence of a second malignant neoplasm. Patients without report of such events where censored at last contact. This will be used to compute event free survival (EFS). (NCT00302003)
Timeframe: At 60 months

InterventionProbability of survival (Number)
Group 10.79

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Provide Epidemiology and Clinical Presentation of the Number of Participants With NF1-associated MPNSTs.

Increase the knowledge of the epidemiology and clinical presentation of NF1-associated MPNSTs. (NCT00304083)
Timeframe: After 4 cycles

InterventionParticipants (Count of Participants)
≥10 subcutaneous neurofibromas6 or more CALIntertriginous frecklingNeurofibromasPlexiform neurofibromaParaspinal neurofibromas≥10 cutaneous neurofibromasOptic gliomaGliomaScoliosisIntellectual delayHypertension
NF1 MPNST1017192612121311588

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Perform Pathologic Analysis of Tumor Samples to Analyze the Number of Participants With Markers as Predictors of Response

Evaluate the molecular biology of sporadic and NF1-associated MPNSTs by performing a detailed pathologic analysis of tumor samples with the goal to analyze if markers can be identified that predict for response to chemotherapy or outcome. (NCT00304083)
Timeframe: After 4 cycles

,
InterventionParticipants (Count of Participants)
Histologic Variant- ConventionalHistologic Variant- PerineuralHistologic Variant- EpithelioidHistologic Variant- DivergentHistologic Variant- Mixed histologyLow CellularityModerate CellularityHigh CellularityNecrosis- absentNecrosis 1-10%Necrosis 10-50%Necrosis >50%
NF1 MPNST151019052158103
Sporadic MPNST702020471253

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Number of Participants With Response Rate (Complete Response and Partial Response)

WHO criteria was used to determine responses due to the nonspherical shape of most MPNST. Complete Response (CR), Disappearance of all target lesions; Partial response (PR), >=50% decrease of target lesions. (NCT00304083)
Timeframe: After 4 Cycles (1 cycle=21 days)

,
InterventionParticipants (Count of Participants)
Partial responseComplete responseStable DiseaseProgressive Disease
NF1 MPNST50203
Sporadic MPNST4041

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Identify the Number of Participants With a Serum Biomarker to Predict the Presence of MPNST Versus Benign Plexiform Neurofibroma

Assess if a serum biomarker can be identified that predicts for the presence of a MPNST versus benign plexiform neurofibroma. (NCT00304083)
Timeframe: After 4 cycles

InterventionParticipants (Count of Participants)
NF1 patients with gene amplifiedSporadic patients with gene amplified
NF1 and Sporadic MPNST32

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Construct Tissue Microarray to Identify Novel Targets for Treatment for the Number of Participants With Available Tissue

Construct a tissue microarray from submitted tumor samples that will be used in the future to identify novel targets for treatment of MPNSTs. The tissue microarray looked at various gene deletions and amplifications. (NCT00304083)
Timeframe: After 4 cycles

,
Interventionparticipants (Number)
EGFR (7p12) amplificationTOPO2A (17q21-q22) amplificationHer2/Neu (17q11-q12) amplificationCyclin D1 (11q13) amplificationc-MYC (8q24) amplificationN-MYC (2p24) amplificationNF1 (17q11) deletionp16 (9p21) deletionRB (13q14) deletionp53 (17q13) deletion
NF1 MPNST35215371016
Sporadic MPNST1202010322

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Degree of Agreement in Histologic Grade Determined by the Enrolling Institution Versus by Central Pathology Reviewers

Histologic grades were determined by the central pathology reviewers and institutional pathologists based on published standards. A higher grade is associated with a more severe disease. (NCT00346164)
Timeframe: At Diagnosis

,,
InterventionParticipants (Number)
Histologic grade 1 by central pathology reviewersHistologic grade 2 by central pathology reviewersHistologic grade 3 by central pathology reviewers
Histologic Grade 1 by Enrolling Institution3843
Histologic Grade 2 by Enrolling Institution55610
Histologic Grade 3 by Enrolling Institution19268

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Complete or Partial Response Rate

Tumor response by imaging. Complete Response (CR): Complete disappearance of the tumor. Partial Response (PR): At least 64% decrease in volume compared to the measurement obtained at study enrollment. Overall Response (OR)=CR+PR. (NCT00346164)
Timeframe: 13 weeks

Interventionpercentage of patients (Number)
Arm D33.1

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Event Free Survival Probability Disease Extent

Probability of no relapse, secondary malignancy or death after 5 years since enrollment. (NCT00346164)
Timeframe: 5 years

InterventionProbability (Number)
Non-metastatic0.7758
Metastatic0.1960

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Event Free Survival Probability Histologic Grade

Probability of no relapse, secondary malignancy or death after 5 years since enrollment (NCT00346164)
Timeframe: 5 years

InterventionProbability (Number)
Histologic Grade 10.9636
Histologic Grade 20.8505
Histologic Grade 30.6136

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Degree of Agreement in Histologic Grade Between Pediatric Oncology Group (POG) and Fédération Nationale Des Centres de Lutte Contre le Cancer (FNCLCC) Pathologic Grading Systems

POG and FNCLCC grades were determined by pathologists based on published standards. A higher grade is associated with a more severe disease. (NCT00346164)
Timeframe: At diagnosis

,,
InterventionParticipants (Count of Participants)
Histologic grade 1 by POGHistologic grade 2 by POGHistologic grade 3 by POG
Histologic Grade 1 by FNCLCC46249
Histologic Grade 2 by FNCLCC869145
Histologic Grade 3 by FNCLCC10240

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Toxicity Rate

Percentage of Arm D patients experiencing grade 4+ adverse events. (NCT00346164)
Timeframe: 13 weeks

Interventionpercentage of participants (Number)
Arm D3.06

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Probability for Event Free Survival.

Probability of no relapse, secondary malignancy or death after 5 years since enrollment. (NCT00346164)
Timeframe: 5 years

InterventionProbability of EFS at 5 years (Number)
Arm A: No Adjuvant Treatment0.8984
Arm B: Low Risk; Adjuvant Radiotherapy0.7647
Arm C: Intermediate & High Risk; Adjuvant Chemoradiotherapy0.6079
Arm D: Intermediate & High Risk; Neoadjuvant Chemoradiotherapy0.4873

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Percent Tumor Necrosis

Percent tumor necrosis by pathology review. (NCT00346164)
Timeframe: 13 weeks

Interventionpercentage of tumor necrosis (Mean)
Arm D59.4

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Overall Survival Probability Extent of Resection of the Primary Tumor

Probability of survival after 5 years since enrollment. (NCT00346164)
Timeframe: 5 years

InterventionProbability (Number)
Less Than Total Resection0.5975
Negative Margins0.9353
Positive Margins0.7764

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Overall Survival Probability Disease Extent

Probability of survival after 5 years since enrollment. (NCT00346164)
Timeframe: 5 years

InterventionProbability (Number)
Non-metastatic0.8752
Metastatic0.3153

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Incidence of Distant Metastasis

Percent of patients who had distant metastasis. (NCT00346164)
Timeframe: Up to 10 years

InterventionPercentage of participants (Number)
Non-metastatic10.59
Metastatic60.87
Histologic Grade 10.00
Histologic Grade 25.06
Histologic Grade 323.38

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Response

Anti tumor activity as assessed by computed tomography of neck/chest/abdomen/pelvis, positron emission tomography scan and/or gallium scan. Assessed by physical examination appropriate imaging studies. Bone marrow aspirate/biopsy must be normal and any macroscopic nodules in any organs detectable on imaging techniques should no longer be present. Gallium scans must be negative if initially positive. (NCT00354107)
Timeframe: Week 4

Interventionpercent (Number)
Treatment (Monoclonal Antibody Therapy, Chemotherapy)50

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Percentage of Patients Event Free at 4 Years Following Study Entry

Event-free survival: Time to recurrence, second malignancy, or death as a first event, estimated from a Kaplan Meier curve (NCT00354744)
Timeframe: 4 years

InterventionPercentage of patients (Number)
High_Risk_Rhabdomyosarcoma36

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Percentage of Patients Experiencing Adverse Events Due to Concurrent Therapy

Adverse events are reported for patients receiving concurrent irinotecan hydrochloride and radiotherapy. (NCT00354744)
Timeframe: From enrollment to up to 2 years

Interventionpercentage of patients (Number)
Course 1Course 2Course 3Course 4
High_Risk_Rhabdomyosarcoma53.368.479.355.7

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Number of Patients With Complete or Partial Response Assessed by RECIST Criteria

"Volumetric measurements of the primary tumor using an elliptical model (0.5 x the product of the 3 largest perpendicular diameters) to assess response to neoadjuvant therapy. The RECIST (Response Evaluation Criteria in Solid Tumors) from the NCI will be used for assessment of the size of measurable metastases, including nodal metastases. Primary Tumor Measurement: Technical guidelines for cross-sectional imaging computed tomography (CT) slice thickness should be 5mm or less and the diameter of the measurable mass should be at least twice the reconstructed slice thickness. Smaller masses are considered detectable, but will be counted as non-measurable. Complete Response (CR): Complete disappearance of the tumor confirmed at >4 weeks. Partial Response (PR): At least 64% decrease in volume compared to the measurement obtained at study enrollment. Progressive Disease (PD): At least 40% increase in tumor volume compared to the smallest volume obtained since the beginning." (NCT00354744)
Timeframe: Protocol week 6 evaluation

Interventionpercentage of participants (Number)
High_Risk_Rhabdomyosarcoma63

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Number of Participants With Grade 3 or 4 Toxicity

Grade 3 and 4 non-hematologic toxicity during protocol therapy. The number of patients that experience CTC Version 4 grade 3 or higher non-hematologic at any time during protocol therapy (NCT00381940)
Timeframe: 4 weeks following completion of therapy

InterventionParticipants (Count of Participants)
Treatment (Ifosfamide, Vinorelbine, Bortezomib)9

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Rate of Successful PBSC Harvest

Success is defined as the ability to harvest 2x10^6 CD34+ cells/kg within 5 collection days. (NCT00381940)
Timeframe: After 2 cycles

InterventionParticipants (Count of Participants)
Treatment (Ifosfamide, Vinorelbine, Bortezomib)19

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Complete Response (CR)

CR is defined as at least 80% reduction in the sum of the products of the perpendicular diameters of each of the nodal masses or return to normal size, along with negative nuclear medicine imaging. (NCT00381940)
Timeframe: After 2 cycles of treatment

Interventionparticipants (Number)
With CRWithout CR
Treatment (Ifosfamide, Vinorelbine, Bortezomib)221

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Overall Response Rate

Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0) for target lesions and assessed by MRI: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Overall Response (OR) = CR + PR (NCT00381940)
Timeframe: After 2 cycles and 4 cycles

InterventionParticipants (Count of Participants)
Overall Response Rate (After 2 cycles)Overall Response Rate (After 4 cycles)
Treatment (Ifosfamide, Vinorelbine, Bortezomib)1912

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Induction Success Rate

Induction success is defined as achieving CR or PR without a targeted primary toxicity. Primary toxicity includes toxic death (which is any death predominantly attributable to treatment-related toxicities or complications, occurring during or within one month of the completion of therapy), Non-hematologic grades 3 or 4 toxicities attributable to drug (with the specific exclusion of 1) Grade 3 or 4 nausea or vomiting, 2) grade 3 transaminases (AST/ALT) elevations which return to < grade 1 prior to the time of the next treatment course, 3) grade 3 or 4 fever or infection, and 4) Grade 3 mucositis.) and Hematologic toxicity (Delay of >2 weeks in the start of re-induction cycle 2 or in hematologic recovery after cycle 2 secondary to severe myelosuppression, infection, or sepsis.) (NCT00381940)
Timeframe: After 2 cycles and 4 cycles

InterventionParticipants (Count of Participants)
Induction Success Rate (After 2 cycles)Induction Success Rate (After 4 cycles)
Treatment (Ifosfamide, Vinorelbine, Bortezomib)1912

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Overall Survival (OS) at 1 Year

(NCT00392834)
Timeframe: 1 year post treatment

InterventionCumulative proportion surviving at 1 yr (Number)
Regimen A (R-CODOX-M Chemotherapy)1.0
Regimen B (Rituximab and IVAC Chemotherapy)0.82

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Overall Survival (OS) of Patients With Burkitt's and Burkitt-like Lymphoma/Leukemia Treated With Modified Magrath Regimen

Overall Survival (OS) of patients with Burkitt's and Burkitt-like Lymphoma/Leukemia treated with modified Magrath regimen. OS is defined from the first dose of study drug to the time of death for any reason. (NCT00392990)
Timeframe: At 2 years from treatment initiation Median follow up 34 months (range 15-45)

Interventionpercentage of patients alive (Number)
High Risk - Treated With Alternating R-CODOX-M/R-IVAC81
Low Risk - Treatment With 3 Cycles of R-CODOX-M100

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Safety of Patients With Burkitt's and Burkitt-like Lymphoma/Leukemia Treated With Modified Magrath Regimen (Addition of Rituximab, Subsitution of Adriamycin for Doxil and Using Lower Dose of Methotrexate)

"Adverse events (AE) graded as either 3 or 4 and determined to be at least possibly related to study treatment will be collected in patients Burkitt's and Burkitt-like Lymphoma/Leukemia treated with modified Magrath regimen to assess the safety and toxicity profile of the addition of rituximab, subsitution of adriamycin for doxil and lower dose of methotrexate. AEs will be assessed as follows at the following time points: At the end of each cycle or monthly whichever is less frequent and 30 days post last dose of study treatment for a maximum of 3 cycles for regimen A and 4 cycles for regimen B and up to 12 months.~In general AEs will be assessed according to the National Cancer Institute's Common Toxicity Criteria for adverse events version 3.0 (CTCAE v 3.0). In general adverse events (AEs) will be graded according to the following:~Grade 1 Mild AE Grade 2 Moderate AE Grade 3 Severe AE Grade 4 Life-threatening or disabling AE Grade 5 Death related to AE" (NCT00392990)
Timeframe: After each cycle or monthly (whichever is less frequent), 30 days post last dose. Treatment duration was at a median of 13 weeks (range 11-20) for high-risk patients and 10 weeks (range 9-12) for low-risk patients.

,
Interventionparticipants (Number)
Anemia : Grade 3Anemia : Grade 4Neutropenia : Grade 3Neutropenia : Grade 4Thrombocytopenia : Grade 3Thrombocytopenia : Grade 4Mucositis : Grade 3Mucositis : Grade 4Infection : Grade 3Infection : Grade 4Elevated Transaminases : Grade 3Elevated Transaminases : Grade 4Fever (Neutropenic) : Grade 3Fever (Neutropenic) : Grade 4Low Phosphate : Grade 3Low Phosphate : Grade 4Sodium Abnormalities : Grade 3Sodium Abnormalities : Grade 4Hyperglycemia : Grade 3Hyperglycemia : Grade 4Hypoalbuminemia : Grade 3Hypoalbuminemia : Grade 4Hypokalemia : Grade 3Hypokalemia : Grade 4Cardiac : Grade 3Cardiac : Grade 4Diarrhea : Grade 3Diarrhea : Grade 4Elevated Creatinine : Grade 3Elevated Creatinine : Grade 4Nausea/Vomiting : Grade 3Nausea/Vomiting : Grade 4Low Blood Pressure : Grade 3Low Blood Pressure : Grade 4Rash : Grade 3Rash : Grade 4Edema : Grade 3Edema : Grade 4Low Magnesium : Grade 3Low Magnesium : Grade 4
High Risk - Treated With Alternating R-CODOX-M/R-IVAC131561137380604050401540103020201010101010
Low Risk - Treatment With 3 Cycles of R-CODOX-M3022122010203010203000200000000000000000

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Progression Free Survival (PFS) of Patients With Burkitt's and Burkitt-like Lymphoma/Leukemia Treated With Modified Magrath Regimen

Progression Free Survival (PFS) will be defined from the first dose of study drug to the first documentation of progressive disease or death for any reason. Patients that are lost to follow-up before progression will be censored at the point of last documentation of not experiencing the event. (NCT00392990)
Timeframe: At 2 years from treatment initiation. Median follow up 34 months (range 15-45)

Interventionpercentage of patients progression free (Number)
High Risk - Treated With Alternating R-CODOX-M/R-IVAC76
Low Risk - Treatment With 3 Cycles of R-CODOX-M100

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Overall Response Rate (ORR) of Patients With Burkitt's and Burkitt-like Lymphoma/Leukemia Treated With Modified Magrath Regimen

"Response Rate is defined as combined number of patients with Complete Remission (CR) Complete Remission undetermined (Cru) and Partial Remission (PR) for patients with Burkitt's and Burkitt-like Lymphoma/Leukemia. Response will be measured by CT scans following treatment completion and assessed using Response Criteria for Non-Hodgkin's Lymphoma where:~CR=complete disappearance of all detectable clinical and radiographic evidence of disease and disappearance of all disease-related symptoms.~CRu=same as above but allowing for 75% decrease in lymph node masses and indeterminate or normal bone marrow.~PR=50% decrease in SPD of the six largest dominant nodes or nodal masses with no increase in size or other nodes, liver, spleen and no new sites of disease." (NCT00392990)
Timeframe: After two cycles of treatment and at completion of treatment (4 cycles for high risk and 3 cycles for low risk) up to approximately 20 weeks.

,
Interventionpercentage of patients (Number)
ORR after two cycles of treatmentORR at completion of treatment
High Risk - Treated With Alternating R-CODOX-M/R-IVAC100100
Low Risk - Treatment With 3 Cycles of R-CODOX-M100100

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Palonosetron Response Rate in the 10 Day Study Cycle

Number of participants with dose of palonosetron who experienced response (no emesis) during acute and delayed time period of the study (10 days) divided by number of participants. Complete response defined as no emesis and no rescue medicines in 10 days from the start of chemotherapy in the first chemotherapy cycle. (NCT00410488)
Timeframe: 10 days

Interventionpercentage of participants (Number)
Palonosetron - 1 Dose31.25
Palonosetron - 3 Doses50

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Response

"Response assessed at the completion of therapy (after four to five cycles of chemotherapy and after surgery if necessary)~Complete Response (CR): A complete response is defined as one of the following:~Complete disappearance of all clinical and radiographic and biochemical (normal AFP and HCG) evidence of disease for a minimum of 4 weeks (CR to chemotherapy).~Complete disappearance of all biochemical evidence of disease with resection of residual radiographic masses that prove to be negative for residual GCT; this includes both mature teratoma and necrotic debris (CR to chemotherapy) for a minimum of 4 weeks.~Complete disappearance of all biochemical evidence of disease with complete surgical excision of all residual radiographic masses that, if pathologically positive for residual malignant GCT, show margins to microscopically free of disease (CR to chemotherapy + surgery). Patients must be free of disease for a minimum of 4 weeks." (NCT00423852)
Timeframe: 2 year

Interventionparticipants (Number)
Complete Response (CR)Incomplete Response (IR)Partial Response (PR)
Chemotherapy With Stem Cell Support1265

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Maximum Tolerated Dose of Ifosfamide

(NCT00423852)
Timeframe: 4 years

Interventionmg/m2 (Number)
Chemotherapy With Stem Cell Support9990

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Overall Survival (OS)

The percentage of people in a study or treatment group who are alive for a certain period of time after they were diagnosed with or treated for a disease, such as cancer. Also called survival rate. (NCT00432094)
Timeframe: 1 Year

Interventionpercentage of participants (Mean)
2 Transplants86
1 Transplant56

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Disease-free Survival (DFS)

The number of patients who survive without any signs of symptions of that cancer or any other cancer. (NCT00432094)
Timeframe: 1 Year

Interventionpercentage of participants (Mean)
2 Transplants64
1 Transplant44

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Engraftment of Neutrophils

Neutrophil engraftment is defined as the first day of three consecutive days where the neutrophil count (absolute neutrophil count) is 500 cells/mm3 (0.5 x 109/L) or greater. (NCT00432094)
Timeframe: Day 42

InterventionParticipants (Count of Participants)
2 Transplants13
1 Transplant9

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Engraftment of Platelets

Platelet engraftment is defined as 20,000/mm^3 (20 x 10^9/L) for 3 consecutive days unsupported by a platelet transfusion. (NCT00432094)
Timeframe: Day 100

Interventionparticipants (Number)
2 Transplants13
1 Transplant8

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Numbers of Patients Unable to Mobilize Peripheral Blood Stem Cells

Number of patients unable to achieve adequate stem cell mobilization, need to undergo one or tandem transplantation. Stem cell mobilization = A process in which certain drugs are used to cause the movement of stem cells from the bone marrow into the blood. The stem cells can be collected and stored. They may be used later to replace the bone marrow during a stem cell transplant. (NCT00432094)
Timeframe: Pre-Transplant

InterventionParticipants (Count of Participants)
2 Transplants0
1 Transplant0

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Number of Patients Experiencing Adverse Events.

Number of patients experiencing adverse events during the course of protocol therapy. (NCT00450801)
Timeframe: Up to 5 years

Interventionparticipants (Number)
R-MACLO Cycles22
R-IVAM Cycles22
Thalidomide Therapy19

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Response Rate

Percentage of participants achieving complete response (CR) to protocol therapy according to International Working Group Response Criteria for Non-Hodgkin's Lymphoma (NHL) using the CT imaging method. Patients were classified by best tumor response; CR was defined as normalization of the lactate dehydrogenase (LDH), complete disappearance of disease-related symptoms and lymph nodes, and clearance of lymphoma from involved organs; complete response unconfirmed (CRu) as a residual lymph node greater than 1.5 cm in greatest transverse diameter that had regressed by more than 75% or an indeterminate bone marrow examination; partial response (PR) as greater than 50% reduction in the involved lymph nodes, or disappearance of the involved lymph nodes but persistent bone marrow involvement; relapse/progression as new or increased lymph nodes, organomegaly, or reappearance of bone marrow involvement. (NCT00450801)
Timeframe: Up to 5 years

Interventionpercentage of participants (Number)
R-MACLO-IVAM-T100

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Overall Survival Rate

Percentage of participants who are alive up to five years after receipt of protocol therapy. (NCT00450801)
Timeframe: Up to 5 years

Interventionpercentage of participants (Number)
1-year rate overall survival Rate2-year overall survival Rate3-year overall survival rate4-year overall survival rate5-year overall survival rate
R-MACLO-IVAM-T9696968787

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Progression-free Survival Rate

Percentage of participants achieving progression-free survival at 1, 3 and 5 years after the start of protocol therapy, based upon the International Working Group Response Criteria for Non-Hodgkin's Lymphoma (NHL). Progression is defined as a ≥ 50% increase from nadir in the product of the two largest perpendicular diameters (PPD-size) of any previously identified abnormal node, or appearance of any new lesion. (NCT00450801)
Timeframe: Up to 5 years

Interventionpercentage of participants (Number)
1 year progression-free survival3 year progression-free survival5-year progression-free survival
R-MACLO-IVAM-T917869

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Response Rate as Measured by Response Evaluation Criteria in Solid Tumors (RECIST) Criteria

Patients who demonstrate a PR or CR, as defined below, will be considered as responders. RECIST criteria: CR (complete response) = disappearance of all target lesions, PR (partial response) = 30% decrease in the sum of the longest diameter of target lesions, PD (progressive disease) = 20% increase in the sum of the longest diameter of target lesions and SD (stable disease) = small changes that do not meet above criteria. (NCT00467051)
Timeframe: At baseline (day 1) and after completion of protocol therapy (2 cycles or 42 days)

Interventionparticipants (Number)
ResponderNon-Responder
Treatment (Chemotherapy, Biological Therapy)128

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The Number of Patients Who Experience at Least One Grade 3 or Higher CTC Version 4 Toxicity.

(NCT00467051)
Timeframe: Two cycles of chemotherapy; expected to be 42 days of treatment.

InterventionParticipants (Count of Participants)
Experimental18

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Percentage of Participants With Progression Free Survival

Progression Free Survival at 3 years. Progression is defined using Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0), as a 20% increase in the sum of the longest diameter of target lesions, or a measurable increase in a non-target lesion, or the appearance of new lesions (NCT00470366)
Timeframe: 3 years

Interventionpercentage of patients (Number)
Paclitaxel, Ifosfamide, and Cisplatin72

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Progression-free Survival

Progression is defined using Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0), as a 20% increase in the sum of the longest diameter of target lesions, or a measurable increase in a non-target lesion, or the appearance of new lesions (NCT00470366)
Timeframe: Up to 8 years

Interventionyears (Median)
Paclitaxel, Ifosfamide, and Cisplatin4.4

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CD34+ Cells/kg in Blood Stem Cells

After blood counts return to normal, stem cell collection (takes approximately 4 hours) up to 6 sessions. (NCT00499343)
Timeframe: The process of stem cell collections take about 4 hours, 1-6 sessions may be needed.

InterventionCD34+ cells/kg (Median)
Rituximab + Ifosfamide + Etoposide + 2 Growth Factors7.5
Rituximab + Ifosfamide + Etoposide + 1 Growth Factor10.34

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Complete Response

Complete Response (NCT00504751)
Timeframe: 26 months

Interventionparticipants (Number)
Study Treatment3

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Number of Participants With Pathologic Complete Remission (pCR)

Histopathologic assessment of surgical resection to confirm Pathologoic Complete Remission. Complete remission defined as disappearance of all target lesions. (NCT00512096)
Timeframe: restaging with second and fourth 21-day cycles followed by surgery

Interventionparticipants (Number)
Cisplatin + Ifosfamide + Paclitaxel3

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Response Rate

Response rate defined as the proportion of subjects with confirmed partial or complete response as defined by the RECIST criteria. (NCT00544778)
Timeframe: First disease evaluation one month after the start of treatment and every 3 months there after, up to 2 years.

Interventionpercentage of patients responding (Number)
Arm 10

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Progression-free Survival at 1 Year

Progression is defined using Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0), as a 20% increase in the sum of the longest diameter of target lesions, or a measurable increase in a non-target lesion, or the appearance of new lesions (NCT00574496)
Timeframe: 1 year

Interventionproportion of progression-free pts (Number)
High-Risk or Relapsed Hodgkin Lymphoma33.3

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Overall Survival

(NCT00574496)
Timeframe: up to 8 years

Interventionmonths (Median)
High-Risk or Relapsed Hodgkin Lymphoma70.3

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Disease Relapse or Progression as Measured by CT Scan or PET

(NCT00574496)
Timeframe: 3 years

Interventionmonths (Median)
High-Risk or Relapsed Hodgkin Lymphoma34.3

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Improve the Overall Response Rate

assessing the response rate (CR+PR) (NCT00588094)
Timeframe: 2 years

Interventionparticipants (Number)
Complete RemissionComplete Remission/UnconfirmedPartial RemissionProgression of Disease
R-ICEesc4274

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Ability to Proceed to Peripheral Blood Stem Cell Collection Following Treatment

(NCT00601718)
Timeframe: 1-3 weeks post end of treatment

InterventionParticipants (Count of Participants)
Treatment (Enzyme Inhibitor, Monoclonal Antibody, Chemotherapy20

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Safety and Toxicity According to CTCAE v3.0

Common dose limiting toxicities. (NCT00601718)
Timeframe: 3-5 weeks post end of treatment

InterventionParticipants (Count of Participants)
InfectionHypokalemiaTransaminitisGrade 3 related gastrointestinal toxicity
Treatment (Enzyme Inhibitor, Monoclonal Antibody, Chemotherapy2229

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Maximum Tolerated Dose of Vorinostat

(NCT00601718)
Timeframe: 28 days post last dose of study drug

Interventionmg twice daily X 5 days (Number)
Treatment (Enzyme Inhibitor, Monoclonal Antibody, Chemotherapy500

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Efficacy (Response Rate) of Vorinostat Combined With RICE Chemotherapy

(NCT00601718)
Timeframe: 3-5 weeks post end of treatment

InterventionParticipants (Count of Participants)
Treatment (Enzyme Inhibitor, Monoclonal Antibody, Chemotherapy19

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Incidence Rate (Number of Participants) of Dose-limiting Toxicity (DLT) - Week 29 to Week 37

The incidence rate of DLT while on protocol therapy where DLT is defined as (1) Grade 3 or greater nonhematological adverse event that is possibly, probably, or likely related to therapy with the specific exception of Grade 3 or greater nausea or vomiting controlled by standard supportive care measures, Grade 3 infection and Grade 3 alopecia; or (2) Grade 4 or higher hematological AE that delays the administration of therapy at least 2 weeks. (NCT00618813)
Timeframe: Week 29 to week 37

Interventionparticipants (Number)
Treatment (Combination Chemotherapy)14

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Incidence Rate (Number of Participants) of Dose-limiting Toxicity (DLT) - Enrollment to Week 12

The incidence rate of DLT while on protocol therapy where DLT is defined as (1) Grade 3 or greater nonhematological adverse event that is possibly, probably, or likely related to therapy with the specific exception of Grade 3 or greater nausea or vomiting controlled by standard supportive care measures, Grade 3 infection and Grade 3 alopecia; or (2) Grade 4 or higher hematological AE that delays the administration of therapy at least 2 weeks. (NCT00618813)
Timeframe: Enrollment to week 12

Interventionparticipants (Number)
Treatment (Combination Chemotherapy)12

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Incidence Rate (Number of Participants) of Dose-limiting Toxicity (DLT) - Week 13 to Week 22

The incidence rate of DLT while on protocol therapy where DLT is defined as (1) Grade 3 or greater nonhematological adverse event that is possibly, probably, or likely related to therapy with the specific exception of Grade 3 or greater nausea or vomiting controlled by standard supportive care measures, Grade 3 infection and Grade 3 alopecia; or (2) Grade 4 or higher hematological AE that delays the administration of therapy at least 2 weeks. (NCT00618813)
Timeframe: Week 13 to week 22

Interventionparticipants (Number)
Treatment (Combination Chemotherapy)9

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Incidence Rate (Number of Participants) of Dose-limiting Toxicity (DLT) - Week 23 to Week 28

The incidence rate of DLT while on protocol therapy where DLT is defined as (1) Grade 3 or greater nonhematological adverse event that is possibly, probably, or likely related to therapy with the specific exception of Grade 3 or greater nausea or vomiting controlled by standard supportive care measures, Grade 3 infection and Grade 3 alopecia; or (2) Grade 4 or higher hematological AE that delays the administration of therapy at least 2 weeks. (NCT00618813)
Timeframe: Week 23 to week 28

Interventionparticipants (Number)
Treatment (Combination Chemotherapy)9

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Incidence of Death

Incidence of death from complications of therapy while the patient is on protocol therapy or within one month of terminating protocol therapy (NCT00618813)
Timeframe: Length of protocol therapy (up to 37 weeks) plus 30 days

Interventionparticipants (Number)
Treatment (Combination Chemotherapy)0

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2-Year Event Free Survival (EFS) in Patients With Localized Resectable Disease Compared to St. Jude OS99 Protocol.

The current protocol OS2008 (NCT00667342) was closed early due to slow accrual. Thus, with the limited number of patients, the comparison of EFS of OS20008 to that of OS99 (NCT00145639) participants was not done. The 2-year EFS of OS2008 participants is reported here. (NCT00667342)
Timeframe: After all patients have completed therapy, up to 2 years after last patient is enrolled

Interventionprobability (Number)
A: Localized Resectable Disease0.642

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2-Year Event Free Survival (EFS) of Patients With Osteosarcoma

Kaplan-Meier method was used to estimate the EFS of patients with osteosarcoma treated with chemotherapy and Bevacizumab. (NCT00667342)
Timeframe: After all patients have completed therapy, up to 2 years after last patient is enrolled

Interventionprobability (Number)
All Participants0.617

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3-Year Event Free Survival

To study the effect of adding bevacizumab to chemotherapy comprised of cisplatin, doxorubicin, and high-dose methotrexate (HDMTX) on the event-free survival (EFS) in patients with localized resectable osteosarcoma. The Kaplan-Meier (K-M) method was used to estimate survival rate. (NCT00667342)
Timeframe: After all patients have completed therapy, up to 4 years after last patient is enrolled

InterventionProbability (Number)
A: Localized Resectable Disease0.575

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Mean Duration of Neuropathic Pain

Thirty participants who underwent surgery (31 surgeries) were determined to have neuropathic pain (NP). Four participants received only opioids for NP and 26 participants (for 27 surgeries) were treated with NP specific medications including gabapentin, tricyclic antidepressant, methadone. One participant had 2 different surgical procedures and was analyzed both in the limb sparing group and in the amputation group. (NCT00667342)
Timeframe: From surgery until resolution of NP symptoms, up to 6 months

InterventionWeeks (Mean)
Amputation Group4.9
Limb Sparing Group7.2
Entire Study Group6.5

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2-Year Overall Survival (OS) in Patients With Localized Resectable Disease Compared to OS99 Protocol.

The current protocol OS2008 (NCT00667342) was closed early due to slow accrual. Thus, with the limited number of patients, the comparison of EFS of OS2008 to that of OS99 (NCT00145639) participants was not done. The 2-year OS of OS2008 participants is reported here. (NCT00667342)
Timeframe: After all patients have completed therapy, up to 2 years after last patient is enrolled

Interventionprobability (Number)
A: Localized Resectable Disease0.934

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Mean Duration of Neuropathic Pain Medication

Thirty participants who underwent surgery (31 surgeries) were determined to have neuropathic pain. Four participants received only opioids for NP and 26 participants (for 27 surgeries) were treated with NP specific medications including gabapentin, tricyclic antidepressant, methadone. One participant had 2 different surgical procedures and was analyzed both in the limb sparing group and in the amputation group. (NCT00667342)
Timeframe: From surgery until resolution of NP symptoms, up to 6 months

InterventionWeeks (Mean)
Amputation Group9.0
Limb Sparing Group9.8
Entire Study Group9.5

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Median Duration of Neuropathic Pain

Thirty participants who underwent surgery (31 surgeries) were determined to have neuropathic pain. Four participants received only opioids for NP and 26 participants (for 27 surgeries) were treated with NP specific medications including gabapentin, tricyclic antidepressant, methadone. One participant had 2 different surgical procedures and was analyzed both in the limb sparing group and in the amputation group. (NCT00667342)
Timeframe: From surgery until resolution of NP symptoms, up to 6 months

InterventionWeeks (Median)
Amputation Group3.5
Limb Sparing Group4.9
Entire Study Group4.4

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Median Duration of Neuropathic Pain Medication

Thirty participants who underwent surgery (31 surgeries) were determined to have neuropathic pain (NP). Four participants received only opioids for NP and 26 participants (for 27 surgeries) were treated with NP specific medications including gabapentin, tricyclic antidepressant, methadone. One participant had 2 different surgical procedures and was analyzed both in the limb sparing group and in the amputation group. (NCT00667342)
Timeframe: From surgery until resolution of NP symptoms, up to 6 months

InterventionWeeks (Median)
Amputation Group6.5
Limb Sparing Group7.0
Entire Study Group7.0

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Mean Vp

The fractional blood plasma volume (Vp) was used to evaluate clinical outcomes. The average for the distribution across the whole region of interest (ROI) was calculated as a summary measure for each data set. (NCT00667342)
Timeframe: Baseline through Week 10

,
Intervention(unitless) (Mean)
BaselineDay -2Day 1Day 5Week 5Week 10
A: Localized Resectable Disease0.00810.00670.00700.00660.00630.0060
C: Metastatic Tumors0.00940.00770.00950.00890.00690.0055

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Mean Ktrans

The volume transfer constant (Ktrans) was used to evaluate clinical outcomes. The average for the distribution across the whole region of interest (ROI) was calculated as a summary measure for each data set. (NCT00667342)
Timeframe: Baseline through Week 10

,
Interventionmin(-1) (Mean)
BaselineDay -2Day 1Day 5Week 5Week 10
A: Localized Resectable Disease0.130.110.120.140.080.07
C: Metastatic Tumors0.150.140.160.160.100.07

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Number of Participants With Neuropathic Pain (NP) Following Surgery

Of the 43 participants enrolled on this trial, 37 met criteria for evaluation of neuropathic pain (NP) following definitive surgery. The 37 participants underwent 38 surgeries: one participant had a limb-sparing surgery followed by an amputation surgery. Six of 43 participants were excluded from evaluation for NP: 1 due to deep vein thrombosis, 2 removed from study prior to surgery, 1 removed immediately after surgery to receive radiation therapy, 1 had non-extremity osteosarcoma, and 1 patient had a fibula resection. Patients were followed for neuropathic pain daily for the first week postoperatively and weekly for up to 6 months postoperatively. (NCT00667342)
Timeframe: Up to 6 months postoperatively

Interventionparticipants (Number)
Amputation Group10
Limb Sparing Group20
Entire Study Group30

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Ktrans by Good and Poor Response

The response is based on the Huvos grade of histologic response for DCE-MRI comparisons and is defined as good for ≥90% necrosis and poor for less than 90%. (NCT00667342)
Timeframe: at week 10 after start of therapy

Interventionmin(-1) (Mean)
Poor ResponseGood Response
All Participants0.07750.0491

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2-Year Overall Survival (OS) of Patients With Osteosarcoma

Kaplan-Meier method was used to estimate the OS of patients with osteosarcoma treated with chemotherapy and Bevacizumab. (NCT00667342)
Timeframe: After all patients have completed therapy, up to 2 years after last patient is enrolled

Interventionprobability (Number)
All Participants0.880

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Mean Ve

The fractional volume of extravascular extracellular space (Ve) was used to evaluate clinical outcomes. The average for the distribution across the whole region of interest (ROI) was calculated as a summary measure for each data set. (NCT00667342)
Timeframe: Baseline through Week 10

,
Intervention(unitless) (Mean)
BaselineDay -2Day 1Day 5Week 5Week 10
A: Localized Resectable Disease0.25430.24440.25640.28540.30550.2776
C: Metastatic Tumors0.26710.26230.26020.31260.31050.2726

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Difference Between Good and Poor Response by SUVmax

The response is based on the Huvos grade of histologic response for DCE-MRI comparisons and is defined as good for ≥90% necrosis and poor for less than 90%. (NCT00667342)
Timeframe: at week 10 after start of therapy

Intervention(unitless) (Mean)
Poor ResponseGood Response
All Participants6.28943.2720

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Number of Participants With Unacceptable Toxicity

"Objective: To study the feasibility of combining: 1) bevacizumab with cisplatin, doxorubicin, and high-dose methotrexate (MAP) in patients with localized resectable osteosarcoma; and 2) bevacizumab with MAP and ifosfamide, and etoposide in patients with unresectable or metastatic osteosarcoma.~The target unacceptable toxicity is defined as grade 4 hypertension, proteinuria, or bleeding excluding petechiae/purpura, grade 3/4 thrombosis/embolism excluding catheter-related thrombosis. The unacceptable toxicity for major wound complication is defined as grade 2, 3, or 4 major wound complications.~A six-stage group sequential stopping rule was developed for monitoring unacceptable toxicity." (NCT00667342)
Timeframe: After all patients have completed therapy, up to 1 year after last patient is enrolled

,
Interventionparticipants (Number)
Grade 4 HypertensionGrade 4 ProteinuriaGrade 4 BleedingGrade 3/4 Thrombosis/EmbolismGrade 2, 3 or 4 Major Wound Complication
A: Localized Resectable Disease00017
C: Metastatic Tumors00002

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Histologic Response by Stratum

"The effect of adding bevacizumab to preoperative chemotherapy comprised of cisplatin, doxorubicin, and HDMTX on the histologic response in patients with localized resectable osteosarcoma compared to historical controls treated with preoperative cisplatin, doxorubicin, and HDMTX without bevacizumab on the Intergroup Study 0133.~Histologic response at week 10 of therapy was evaluated by Huvos grading systems as grade I: tumor not responding to therapy, no effect identified; grade IIA: more than 50% viable tumor left; grade IIB: 5-50% viable tumor remaining; grade III: only scattered foci of viable tumor seen (less than 5% of tumor); grade IV: no viable tumor seen in extensive sampling (at least a full cross-section of the tumor).~The study did not enroll an adequate number of participants, therefore, the comparison to Intergroup Study 0133 participants was not done." (NCT00667342)
Timeframe: After 6 cycles of chemotherapy, up to 1 year after the start of therapy

,
Interventionparticipants (Number)
Grade IGrade IIAGrade IIBGrade III
A: Localized Resectable Disease15178
C: Metastatic Tumors0173

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P95 of Ktrans by Good and Poor Response

The response is based on the Huvos grade of histologic response for DCE-MRI comparisons and is defined as good for ≥90% necrosis and poor for less than 90%. P95 denotes the level of each kinetic parameter exceeding 95% of its values in each tumor. (NCT00667342)
Timeframe: at week 10 after start of therapy

Interventionmin(-1) (Mean)
Poor ResponseGood Response
All Participants0.20470.1228

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2-year PFS From the Start of Induction Therapy Conditional

2-year PFS from the start of induction therapy conditional on attaining either a negative FDG-PET or a negative biopsy at the interim evaluation. (NCT00712582)
Timeframe: 2 years

Interventionpercentage of patients (Number)
Consolidation A86.6
Consolidation B90.6
Consolidation C0.4

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Overall Survival at 1 Year

Overall survival from the start of induction therapy conditional on attaining either a negative FDG-PET or a negative biopsy at the interim evaluation. (NCT00712582)
Timeframe: 1 year

InterventionPercent of patients (Number)
Consolidation A98.3
Consolidation B96.9
Consolidation C50.0

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Percent of Patients MRD Positive (MRD > 0.01%) at End of Consolidation

A 1-sample Z-test of proportions (alpha=5%, 1-sided test) will be used. (NCT00720109)
Timeframe: At end of consolidation (at 11 weeks)

InterventionPercentage of participants (Number)
Treatment Induction (Enzyme Inhibitor Therapy & Chemotherapy)10.5
Standard-risk0
High-risk66.7

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Contribution of Dasatinib on Minimal Residual Disease (MRD) After Induction Therapy

Percent of patients MRD Positive (MRD > 0.01%) at End of Induction. (NCT00720109)
Timeframe: At the end of induction therapy (at 5 weeks)

InterventionPercentage of participants (Number)
Treatment Induction (Enzyme Inhibitor Therapy & Chemotherapy)40.7
Standard-risk29.2
High-risk100.0

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Event-Free Survival (EFS) of Patients With Standard-risk Disease Treated With Dasatinib in Combination With Intensified Chemotherapy

Event-Free Survival (EFS) curves will be constructed using the Kaplan-Meier life table method with standard errors computed using the method of Peto and Peto. A 1-sided 95% confidence interval for EFS will be constructed. (NCT00720109)
Timeframe: At 3 years

InterventionPercent probability (Number)
Treatment Induction (Enzyme Inhibitor Therapy & Chemotherapy)79.8
Standard-risk83.2
High-risk66.7

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Feasibility and Toxicity of an Intensified Chemotherapeutic Regimen Incorporating Dasatinib for Treatment of Children and Adolescents With Ph+ ALL Assessed by Examining Adverse Events

Number of patients in safety cohort with dose limiting toxicity (DLT)(including treatment delay) (NCT00720109)
Timeframe: Weeks 3 through 23 of treatment (From week 3 Induction through Intensification Block 1)

InterventionPts with DLTs (Number)
Treatment Induction (Enzyme Inhibitor Therapy & Chemotherapy)1

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Overall EFS Rate for the Combined Cohort of Standard- and High-Risk Patients (Who Receive the Final Chosen Dose of Dasatinib)

An event is defined as: Induction failure, relapse at any site, secondary malignancy, or death. (NCT00720109)
Timeframe: From the time entry on study to first event or date of last follow-up, assessed up to 7 years

Interventionpercentage of patients (Number)
Treatment Induction (Enzyme Inhibitor Therapy & Chemotherapy)79.8
Standard-risk83.2
High-risk66.7

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Limiting Toxicity

"The occurrence of Limiting Toxicity defined as Any CTC AE version 4 Grade 3 and 4 non-hematologic toxicity thought to be possibly, probably or definitely related to zoledronic acid with the specific exclusion of:~Grade 3 nausea and vomiting controlled with adequate antiemetic prophylaxis.~Grade 3 transaminase (AST/ALT) that occurs during the evaluation period but resolves to ≤ Grade 2, before the planned dose of therapy after definitive surgery.~Grade 3 fever or infection.~Grade 3 or 4 hypocalcemia (see Section 5.1.1)~Grade 3 mucositis.~Grade 3 fatigue that returns to ≤ Grade 2, before the planned dose of therapy after definitive surgery.~Grade 3 joint range of motion, decreased or joint effusion that is related to the primary tumor." (NCT00742924)
Timeframe: Enrollment through the first 12 weeks of therapy.

Interventionparticipants (Number)
Arm 1- Chemotherapy and 1.2 mg/m2 Zoledronic Acid1
Arm 2 - Chemotherapy and 2.3 mg/m2 Zoledronic Acid1
Arm 3 - Chemotherapy and 3.5 mg/m2 Zoledronic Acid3
Chemotherapy and 2.3 mg/m2 Zoledronic Acid After MTD2

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Maximum Administered Dose of Dasatinib (Phase I)

This field captured the maximum dose of dasatinib administered. (NCT00788125)
Timeframe: 28 days after start of course 1

Interventionmg/m2 dose BID (Number)
Period 1: 35 mg/m^2/Dose BID PO Dasatinib x 17 Days35

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Progression - Free Survival (PFS)

The PFS was assessed as median number of days from the date of randomization until the first documented sign of disease progression (increase in disease; radiographic, clinical, or both) or death due to any cause, whichever occurred earlier. (NCT00796120)
Timeframe: Every 6 weeks from randomization during the first 9 months and thereafter, every 9 weeks up to 20 months

Interventionmonths (Median)
Trabectedin19.6
Doxorubicin Plus Ifosfamide8.3

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Percentage of Participants With Objective Response

Tumor response was assessed according to Response Evaluation Criteria In Solid Tumors (RECIST) criteria: Partial Response (PR)=at least 30% reduction in the sum of the longest dimensions (LD) of all target lesions in reference to the baseline sum LD, Complete Response (CR) =Disappearance of all non-target lesions. Percentage of participants with objective tumor response was determined by the number of participants with PR or CR divided by the total number of response-evaluable participants. (NCT00796120)
Timeframe: Every 6 weeks during first 9 months of the study and thereafter every 9 weeks up to 20 months

Interventionpercentage of participants (Number)
Trabectedin5.9
Doxorubicin Plus Ifosfamide27.0

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Overall Survival

Overall survival defined as time from the date of randomization to the date of death. For participants who were alive at the time of analysis, overall survival was censored at the last contact date. (NCT00796120)
Timeframe: Baseline up to End of Study (an average of 4 years)

Interventionmonths (Median)
Trabectedin46.6
Doxorubicin Plus Ifosfamide33.5

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6-month Progression - Free Survival

Percentage of participants survived for 6 months from the start of study treatment without progression of disease. Progression of the disease was associated with increasing symptoms, including pain from new or progressing lesions. Delay in disease progression generally represents a clinical benefit to the participant. (NCT00796120)
Timeframe: 6 months

Interventionpercentage of participants (Number)
Trabectedin66.7
Doxorubicin Plus Ifosfamide78.3

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Duration of Response (DOR)

The DOR is defined as the time from date of first documentation of response (CR or PR, whichever comes first) to the date of documented PD or death. PR=at least 30% reduction in the sum of the longest dimensions (LD) of all target lesions in reference to the baseline sum LD, CR =Disappearance of all non-target lesions. (NCT00796120)
Timeframe: Up to 20 months

Interventiondays (Median)
TrabectedinNA
Doxorubicin Plus IfosfamideNA

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Patient-reported Peripheral Neuropathy Symptoms - Post Baseline

Patient reported peripheral neuropathy symptoms was measured with the Functional Assessment of Cancer Therapy/Gynecologic Oncology Group - neurotoxicity subscale (short version) (FACT/GOG-Ntx subscale). The FACT/GOG-Ntx subscale contains 11 items. Each item was scored using a 5-point scale (0=not at all; 1=a little bit; 2=somewhat; 3=quite a bit; 4=very much). The Ntx score ranges 0-44 with a large score suggesting less peripheral neuropathy symptoms.Quality of Life was analyzed across cohorts since disease site was considered independent of Quality of Life. (NCT00954174)
Timeframe: Prior to cycle 3, Prior to cycle 6, 30 weeks post cycle 1

,
Interventionunits on a scale (Least Squares Mean)
Prior to cycle 3Prior to cycle 630 weeks post cycle 1
Regimen I - Uterine and Non-Uterine Subjects37.234.134.8
Regimen II - Uterine and Non-Uterine Subjects37.034.234.9

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Patient Reported Quality of Life (QOL) - Post Baseline

Patient reported quality of life was measured with the Treatment Outcome Index (TOI) of the Functional Assessment of Cancer Therapy for endometrial cancer (FACT-En TOI). The FACT-En TOI is a scale for assessing general QOL of endometrial cancer patients. The FACT-En TOI score ranges 0-120 with a large score suggesting better QOL. Quality of Life was analyzed across cohorts since disease site was considered independent of Quality of Life. (NCT00954174)
Timeframe: Prior to cycle 3, Prior to cycle 6, 30 weeks post cycle 1.

,
Interventionunits on a scale (time point) (Least Squares Mean)
Pre-cycle 3Pree-cycle 630 weeks post cycle 1
Regimen I - Uterine and Non-Uterine Subjects93.391.698.0
Regimen II - Uterine and Non-Uterine Subjects93.391.697.6

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Duration of Progression-free Survival

Measured in months from randomization to last contact or the earlier of the date of progression or death. (NCT00954174)
Timeframe: Approximately 9 years and 7 months

Interventionmonths (Median)
Regimen I - Uterine Carcinsarcoma Subjects16.3
Regimen II - Uterine Carcinsarcoma Subjects11.7
Regimen III - Non-uterine Carcinsarcoma Subjects14.6
Regimen IV - Non-uterine Carcinsarcoma Subjects10.3

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Overall Survival

Measured in months from randomization to last contact or death. Primary analysis was restricted to the eligible uterine carcinosarcoma cohort. (NCT00954174)
Timeframe: From date of randomization until the date of first documented progression or date of death from any cause, whichever came first, assessed up to 115 months.

Interventionmonths (Median)
Regimen I- Uterine Carcinsarcoma Subjects37.3
Regimen II - Uterine Carcinsarcoma Subjects29

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Patient Reported Peripheral Neuropathy Symptoms - Baseline

Patient reported peripheral neuropathy symptoms was measured with the Functional Assessment of Cancer Therapy/Gynecologic Oncology Group - neurotoxicity subscale (short version) (FACT/GOG-Ntx subscale). The FACT/GOG-Ntx subscale contains 11 items. Each item was scored using a 5-point scale (0=not at all; 1=a little bit; 2=somewhat; 3=quite a bit; 4=very much). . The Ntx score ranges 0-44 with a large score suggesting less peripheral neuropathy symptoms. Quality of Life was analyzed across cohorts since disease site was considered independent of Quality of Life. (NCT00954174)
Timeframe: Baseline (Pre cycle 1)

Interventionunits on a scale-baseline (Mean)
Regimen I - Uterine and Non-Uterine Subjects40.2
Regimen II - Uterine and Non-Uterine Subjects41.0

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Patient-Reported Quality of Life (QOL) - Baseline

Patient reported quality of life was measured with the Treatment Outcome Index (TOI) of the Functional Assessment of Cancer Therapy for endometrial cancer (FACT-En TOI). The FACT-En TOI is a scale for assessing general QOL of endometrial cancer patients. The FACT-En TOI score ranges 0-120 with a large score suggesting better QOL. Quality of Life was analyzed across cohorts since disease site was considered independent of Quality of Life. (NCT00954174)
Timeframe: Baseline - Prior to study treatment

Interventionunits on a scale (time point) (Mean)
Regimen I - Uterine and Non-Uterine Subjects96.2
Regimen II - Uterine and Non-Uterine Subjects97.5

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Incidence of Adverse Events as Assessed by CTCAE Version 3.0

Maximum grade experienced among all treated and eligible patients. The grades are described by severity. Grade 1 is the lowest (most mild) and Grade 5 being death (most severe). Adverse events were analyzed across cohorts since disease site was considered independent of AEs. (NCT00954174)
Timeframe: Patients were assessed for adverse events during active protocol treatment and up to 30 days after the last cycle of treatment on the protocol.

,
InterventionParticipants (Count of Participants)
Grade 1Grade 2Grade 3Grade 4Grade 5
Regimen I - Uterine and Non-Uterine Subjects3221071306
Regimen II - All Uterine and Non-Uterine Subjects38097613

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Number of Participants Who Developed Anti-robatumumab Antibodies

The incidence of anti-robatumumab antibodies was to be assessed. Only participants who had a negative pre-treatment sample and a post-treatment sample were considered to be evaluable. If a participant had a single sample considered positive in the anti-robatumumab antibody assay (with the exception of pre-treatment positive participants), then they would be counted as positive in the immunogenicity assessment. (NCT00960063)
Timeframe: Prior to 1st and 8th doses of robatumumab, ~30 days after last dose of study drug, and 4 months after last dose of study drug (Up to ~13.3 months)

InterventionParticipants (Number)
Temozolomide+Irinotecan+Robatumumab0
Ifosfamide+Etoposide+Robatumumab0

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Best Overall Response Based on Response Evaluation Criteria in Solid Tumors (RECIST)

All measurable lesions up to a maximum of 5 lesions per organ and 10 lesions in total, representative of all involved organs were to be identified as target lesions. Data were to be collected at Screening, every 6 weeks and at 30 days after the final dose of robatumumab or the standard treatment assigned (whichever was last). The best overall response was to be the best response recorded from the start of the treatment until disease progression/recurrence. Complete Response (CR): Disappearance of all target lesions; Partial Response (PR): >30% decrease in the sum of the longest diameter (LD) of target lesions; Progressive Disease (PD): >20% increase in the sum of the LD of target lesions or the appearance of one or more new lesions; or Stable Disease (SD): Neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD. (NCT00960063)
Timeframe: Screening, every 6 weeks and at ~30 days after last dose of study drug (Up to ~10.3 months)

,
InterventionParticipants (Number)
Complete Response (CR)Partial Response (PR)Stable Disease (SD)Progressive Disease (PD)
Ifosfamide+Etoposide+Robatumumab0201
Temozolomide+Irinotecan+Robatumumab0100

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Number of Participants With Dose Limiting Toxicities

Dose-limiting toxicity was defined by the following adverse events (AEs) that were considered possibly or probably related to either robatumumab or to its interaction with the chemotherapy regimen assigned: neutropenia (Grade 4 for >1 week that did not resolve prior to Day 1 of the next cycle; Grade 3-4 neutropenia with Grade ≥2 fever lasting 3 days; neutropenic infection; failure to recover to study entry/eligibility criteria laboratory requirement levels that resulted in a delay of 14 days between treatment cycles), thrombocytopenia (Grade 4 for >1 week that did not resolve prior to Day 1 of the next cycle; Grade 3-4 requiring a platelet transfusion on 2 separate days within a cycle) or all other AEs (Grade ≥3 [any duration] not ameliorable by supportive or symptomatic measures). The National Cancer Institute Common Terminology Criteria for Adverse Events (NCI-CTCAE version 4.0) was to be used to grade AEs. (NCT00960063)
Timeframe: Up to ~30 days after last dose of study drug (Up to ~10.3 months)

InterventionParticipants (Number)
Temozolomide+Irinotecan+Robatumumab1
Ifosfamide+Etoposide+Robatumumab3

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Overall Survival (OS) Rate at 24 Months

Overall Survival is time from date of treatment start until date of death due to any cause or last Follow-up within 24 months. (NCT00967369)
Timeframe: 24 months

Interventionpercentage of participants (Number)
BICE (Bortezomib, Ifosfamide, Carboplatin, Etoposide)70
ICE (Ifosfamide, Carboplatin, Etoposide)89

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Progression Free Survival (PFS) Rate at 12 Months

Progression free survival time is defined as the time interval from treatment start to progression or death due to any cause whichever happens first. Participants will be censored at the last follow-up date, if an event(progression/death) is not observed during the follow-up. (NCT00967369)
Timeframe: From date of randomization until the date of first documented progression or date of death from any cause, whichever came first, assessed up to 100 months

Interventionpercentage of participants (Number)
BICE (Bortezomib, Ifosfamide, Carboplatin, Etoposide)50
ICE (Ifosfamide, Carboplatin, Etoposide)70

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Overall Response After 3 Cycles of Botezomib Plus ICE (BICE) Versus Ifosfamide, Carboplatin, Etoposide (ICE) in Patients With Relapsed/Refractory Classical Hodgkin Lymphoma

Response rates for Bortezomib, Ifosfamide, Carboplatin, Etoposide (BICE) and Ifosfamide, Carboplatin, Etoposide (ICE) treatment groups were assessed by the 1999 International Working Group (IWG)(CT alone) (Cheson et al., 1999) and compared to 2007 IWG (CT plus PET) (Cheson et al., 2007) criteria. Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0) for target lesions and assessed by MRI: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Overall Response (OR) = CR + PR (NCT00967369)
Timeframe: From baseline to 3 cycles of treatment

,
InterventionParticipants (Count of Participants)
Overall ResponseComplete Response (CR)Partial Response (PR)Progressive Disease (PD)Stable Disease (SD)
BICE (Bortezomib, Ifosfamide, Carboplatin, Etoposide)73401
ICE (Ifosfamide, Carboplatin, Etoposide)61503

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PET Scan Response After 3 Cycles of BICE Versus ICE Chemotherapy.

Response rates for BICE and ICE treatment groups will be assessed by 1999 IWG (CT alone) (Cheson et al., 1999) and compared to 2007 IWG (CT plus PET) (Cheson et al., 2007) criteria. (NCT00967369)
Timeframe: Baseline up to 1 year

,
InterventionParticipants (Count of Participants)
PET negativity : Complete Response (CR)PET negativity : Partial Response (PR)PET negativity : Stable Disease (SD)PET positivity : Partial Response (PR)PET positivity : Stable Disease (SD)PET positivity : Progressive Disease (PD)
BICE (Bortezomib, Ifosfamide, Carboplatin, Etoposide)300412
ICE (Ifosfamide, Carboplatin, Etoposide)641220

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Grade 3 and 4 Non-hematologic Toxicities During Protocol Therapy

The number of patients that experience Common Terminology Criteria (CTC) Version 4 grade 3 or higher non-hematologic toxicity at any time during protocol therapy. (NCT01026220)
Timeframe: During and after completion of study treatment.

Interventionparticipants (Number)
Group 172

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Relapse-free Survival

A description, survival to relapse, of patterns of relapse after Doxorubicin, Bleomycin, Vincristine, Etoposide - Prednisone, Cyclophosphamide (ABVE-PC) and risk-adapted radiotherapy. (NCT01026220)
Timeframe: 3 years from enrollment

InterventionProbability of survival (Number)
Group 10.82
Group 60.83
Group 70.79

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Overall Survival

Survival from enrollment to death. (NCT01026220)
Timeframe: At 3 years from enrollment

InterventionProbability of survival (Number)
Group 10.97
Group 20.97
Group 30.97

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Second-event-free Survival

Second event here is defined as any relapse/progression of Hodgkin Lymphoma (HL) or a previously reported second malignant neoplasm (SMN), a new SMN, or death after a first event which can be relapse/progression of HL, SMN, biopsy-proven HL following completion of Consolidation for Slow Early Response (SER) patient, positive bilateral bone marrow biopsy following completion of Consolidation for Stage IV patient, or death. If death occurs as the 1st event, it also counts as the 2nd event. (NCT01026220)
Timeframe: At 4 years from enrollment

,
InterventionProbability of survival (Number)
Group 10.91
Group 20.94
Group 30.88

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Safety Analysis and Monitoring of Toxic Death

The primary endpoint for safety analysis and monitoring is toxic death, which is death primarily attributable to treatment. (NCT01026220)
Timeframe: Within 30 days of protocol treatment at median follow-up of 48 months (range: 1 to 70 months).

Interventionparticipants (Number)
Group 10

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Event-free Survival for Rapid Early Response (RER) Positron Emission Tomography(PET)-1 Positive, RER PET-1 Negative

To investigate whether very early response assessment measured by Fluorodeoxyglucose-PET after 1 cycle of chemotherapy identifies a subject cohort that can be studied in future trials and that is distinguishable from currently defined RER after 2 cycles. (NCT01026220)
Timeframe: 3 years from enrollment

InterventionProbability of survival (Number)
Group 10.84
Group 40.82
Group 50.90

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Event Free Survival

Survival from enrollment to first event: relapse/progression, second malignancy, or death. (NCT01026220)
Timeframe: At 3 years from enrollment

InterventionProbability of survival (Number)
Group 10.81
Group 20.83
Group 30.78

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Feasibility of the Addition of Cixutumumab to Chemotherapy Determined by Patient Enrollment

Proportion of no Grade 3+ cardiac toxicity. (NCT01055314)
Timeframe: From start to week 26 of therapy

InterventionProportion of Participants (Number)
IMC-A120.9390

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Feasibility of the Addition of Temozolomide to Chemotherapy Determined by Patient Enrollment

Proportion of no Grade 4+ non-hematologic toxicity. (NCT01055314)
Timeframe: From start to week 26 of therapy

InterventionProportion of Participants (Number)
Temozolomide0.7097

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Incidence of Adverse Events Assessed by Common Terminology Criteria for Adverse Events Version 4.0

Number of patients with grade 3+ adverse events (AE) during therapy. (Grade 3+) = (Grade 3 + Grade 4 + Grade 5) . Grade 3: Severe and undesirable AE; Grade 4: Life threatening or disabling AE; Grade 5: Death related to AE. (NCT01055314)
Timeframe: Up to 54 weeks

InterventionParticipants (Number)
IMC-A1289
Temozolomide61

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Event-Free Survival

Probability of no relapse, secondary malignancy, or death after 3 years in the study. (NCT01055314)
Timeframe: 3 years

InterventionProbability (Number)
IMC-A120.1627
Temozolomide0.1919

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Response Rate (CR + PR)

Proportion of patients with complete or partial response. Complete Response (CR): Complete disappearance of the tumor confirmed at > 4 weeks. Partial Response (PR): At least 64% decrease in volume compared to the measurement obtained at study enrollment; Overall Response (OR) = CR + PR. (NCT01055314)
Timeframe: From the start of treatment until a maximum of 2 cycles (21 days per cycle) of treatment in the absence of disease progression or unacceptable toxicities

InterventionProportion of Participants (Number)
IMC-A120.7667
Temozolomide0.7846

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Total Number of Participants Who Did Not Collect ≥5 x 10^6 CD34 Cells/kg in a Maximum of Four Apheresis Days

Number of participants who did not collect ≥5 x 10^6 CD34 cells/kg in up to four apheresis days (NCT01097057)
Timeframe: Up to Four Apheresis Days

InterventionParticipants (Count of Participants)
Treatment (Rituximab, Etoposide, Carboplatin, Ifosfamide)0

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Number of Participants Requiring One or Two Apheresis Collection Days to Reach ≥5 x 10^6 CD34 Cells/kg

Number of participants requiring one or two apheresis collection days to reach collection goal. (NCT01097057)
Timeframe: Up to Four Apheresis Days

InterventionParticipants (Count of Participants)
One apheresis collection dayTwo apheresis collection daysThree apheresis collection daysFour apheresis collection days
Treatment (Rituximab, Etoposide, Carboplatin, Ifosfamide)15200

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Number of Patients to Mobilize ≥5 x 10^6 CD34 Cells/kg Autologous PBSC (Efficacy)

Number of patients who achieved ≥5 x 10^6 CD34 cells/kg autologous PBSC collection by apheresis. (NCT01097057)
Timeframe: One Month

InterventionParticipants (Count of Participants)
Treatment (Rituximab, Etoposide, Carboplatin, Ifosfamide)17

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Number of Patients Who Achieved ≥5 x 10^6 CD34 Cells/kg in ≤4 Apheresis Days

Number of patients to collect at least 5 x 10^6 CD34 cells/kg in under 4 apheresis procedures. (NCT01097057)
Timeframe: Up to Four Apheresis Days

InterventionParticipants (Count of Participants)
Treatment (Rituximab, Etoposide, Carboplatin, Ifosfamide)17

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Number of Participants With Complete Remission (CR)

Will be assessed by Kaplan-Meier methods. (NCT01169636)
Timeframe: Assessed after 3 cycles of ICE (2 months)

,,
InterventionParticipants (Count of Participants)
Complete ResponsePartial ResponseStable DiseaseProgressive Disease
Phase I: Panobinostat + ICE (Maximal Tolerated Dose (MTD)21422
Phase II Panobinostat + ICE9020
Phase II: Standard of Care (ICE)8121

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Maximum Tolerated Dose (MTD) of Panobinostat + ICE

Maximum Tolerated Dose (MTD) of Panobinostat + ICE (NCT01169636)
Timeframe: From first dose of panobinostat (or chemotherapy, in the arm of ICE alone) until 30 days after last dose, up to 6 years

Interventionmg (Number)
Phase I: Panobinostat + ICE (Maximal Tolerated Dose (MTD)30

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Percentage of Participants With Failure Free Survival (FFS)

FFS duration was calculated from date of study entry to date of progression or death or change of therapy, whichever came first. (NCT01169636)
Timeframe: 16 months

Interventionpercentage of participants (Number)
Phase I: Panobinostat + ICE (Maximal Tolerated Dose (MTD)61
Phase II: Standard of Care (ICE)82
Phase II Panobinostat + ICE75

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Event-Free Survival

Estimated 5-year EFS where EFS is calculated as the time from study enrollment to disease progression, disease relapse, occurrence of a second malignant neoplasm, death from any cause or last follow-up whichever occurs first. Kaplan-Meier method is used for estimation. Patients without an event are censored at last contact. (NCT01231906)
Timeframe: 5 years after enrollment

InterventionPercent Probability (Number)
Arm A (Combination Chemotherapy)77.64
Arm B (Combination Chemotherapy, Topotecan Hydrochloride)78.79

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Mobilization Rate

Feasibility of mobilization with ofatumumab + chemotherapy is defined as successful collection of 2 x 10^6CD34+ stem cell/kg and successful purging of the apheresis product of all the markers (i.e., monoclonal B-cells, bcl-2, bcl-1 and/or JH) that were found to be positive on pretreatment evaluation. Mobilization rate is number of participants with successful collection out of total study participants. (NCT01329900)
Timeframe: Mobilization rate measured on Day 21

InterventionParticipants (Count of Participants)
Ofatumumab + Stem Cell Collection50

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Progression Free Survival

Defined as the duration of time from randomization to progressive disease (per RECIST), local recurrence, distant metastatic disease (exclusive of stage IV subjects), or death, whichever occurs first. (NCT01446809)
Timeframe: Up to 3 years

InterventionParticipants (Count of Participants)
Arm I (Pazopanib Hydrochloride)10
Arm II (Placebo)4

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Change in Maximum SUV of Tumors Measured by FDG-PET Pre- and Post Receipt of Pazopanib Versus Placebo

Change in maximum SUV (standardized uptake value) of tumors measured by FDG-PET. Comparison conducted using a two-sided Wilcoxon rank sum test. (NCT01446809)
Timeframe: From baseline to 15 days

InterventionStandardized uptake value-SUV (Median)
Pazopanib-0.1
Placebo-0.1

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Number of Participants With Pathologic Response at the Time of Surgery as Measured by % Tumor Viability ( >= 95% Necrosis)

Estimate the amount of viable tumor, and report the percentage of necrosis. Analysis was only completed on a subset of participants. (NCT01446809)
Timeframe: An expected average of 12 weeks

InterventionParticipants (Count of Participants)
Pazopanib6
Placebo6

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Overall Survival

Defined as the interval of time from randomization until death from any cause. (NCT01446809)
Timeframe: Up to 3 years

InterventionParticipants (Count of Participants)
Pazopanib12
Placebo4

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Pharmacokinetic Profile of Pazopanib

Trough plasma pazopanib concentration measured during the 14 day run-in period on days 10 through 14. (NCT01446809)
Timeframe: Up to 14 days

Interventionng/mL (Mean)
Pazopanib56.38
Placebo0

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Change in Levels of VEGF and Soluble VEGFR2 Assessed by ELISA on Plasma and Tumor Extracts

Plasma will be collected for measurement of VEGF and soluble VEGFR2 (sVEGFR2) at baseline, after the 14 day Run-in period of pazopanib, after completion of neoadjuvant chemotherapy and approximately every 3 months thereafter until completion of pazopanib maintenance therapy, when indicated. Quantitative enzyme-linked immunosorbent assays (ELISA) for VEGF and sVEGFR2 will be performed on plasma and tumor extracts. Plasma will also be collected for micro RNA at baseline, after the 14 day Run-in period of pazopanib, following neoadjuvant chemotherapy and every 3 months thereafter until completion of pazopanib maintenance therapy, when indicated. (NCT01446809)
Timeframe: At baseline and after 14 days

Interventionpercentage of concentration (Number)
PazopanibNA
PlaceboNA

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Change in Maximum SUV of Tumors Measured by FDG-PET Post Receipt of 2 Courses of Preoperative Chemotherapy

Change in maximum SUV of tumors measured by FDG-PET. Comparison conducted using a two-sided Wilcoxon rank sum test. (NCT01446809)
Timeframe: From baseline to 8 weeks

InterventionSUV (Median)
Pazopanib-1.1
Placebo-4.0

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Complete Response

Complete response (CR) defined as: No emetic episodes and no rescue medications. This is a cross-over designed study, the outcomes by single dose, two doses and control cycles were evaluated by combining the results from both cycle 1 and cycle 2 according to the treatment received. (NCT01490060)
Timeframe: From Day 1 to Day 5 in two 21-days cycles (Cycle 1 and Cycle 2).

Interventionpercentage of participants (Number)
Control Cycle (Arm A/Arm B)17
Arm A: Single Dose, Day 110
Arm B: Two Doses, Day 1 + Day 450

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Estimation of the PFS Distribution of Patients With NGGCT Treated With Involved-field Radiation Therapy (IFR)

Kaplan Meier estimate of the 3-year PFS is provided. PFS is the time interval measured from enrollment until progression or death from any cause or until last follow-up for those who were event free at the time of analysis. Patients who were lost to follow-up or withdrew consent were censored in this analysis. Progression was determined by MRI using the COG Guidelines for Measurement of Tumor Size (>25% increase in 2D or >40% in 3D of the product of perpendicular diameters of the target lesion) as well as by tumor marker assessments which were mandatory for this study. (NCT01602666)
Timeframe: Up to 3 years

Interventionpercentage of patients (Number)
Stratum 1 Localized Non-Germinomatous Germ Cell Tumors (NGGCT)87.88

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Estimation of the PFS Distribution of Patients With Localized Germinoma Patients and Cerebrospinal Fluid (CSF) Serum hCGbeta of 50 mIU/mL or Less or CSF Serum hCGbeta Greater Than 50 mIU/mL and Less Than or Equal to 100 mIU/mL

Kaplan Meier estimate of the 3-year PFS rate is provided. PFS is the time interval measured from initiation of treatment until progression or death from any cause or until last follow-up for those who were event free at the time of analysis. Patients who were lost to follow-up or withdrew consent were censored in this analysis. Progression was determined by MRI using the COG Guidelines for Measurement of Tumor Size (>25% increase in 2D or >40% in 3D of the product of perpendicular diameters of the target lesion) as well as by tumor marker assessments which were mandatory for this study. (NCT01602666)
Timeframe: Up to 3 years

Interventionpercentage of patients (Number)
hCGbeta <= 50 mIU/mL93.26
50 mIU/mL < hCGbeta <= 100 mIU/mL80.00

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Estimation of the OS Distribution of Patients With Localized Germinoma Patients and CSF Serum hCGbeta of 50 mIU/mL or Less or CSF Serum hCGbeta Greater Than 50 mIU/mL and Less Than or Equal to 100 mIU/mL

Kaplan Meier estimate of the 3-year overall survival (OS) is provided for each group. OS is the time interval measured from enrollment until death from any cause or until last follow-up for those who were alive at the time of analysis. Patients who were lost to follow-up or withdrew consent were censored in this analysis. (NCT01602666)
Timeframe: Up to 3 years

Interventionpercentage of patients (Number)
hCGbeta <= 50 mIU/mL98.38
50 mIU/mL < hCGbeta <= 100 mIU/mL100

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Estimation of the Overall Survival (OS) Distribution of Patients With NGGCT Treated With IFR Assessed

Kaplan Meier estimate of the 3-year overall survival (OS) is provided. OS is the time interval measured from enrollment until death from any cause or until last follow-up for those who were alive at the time of analysis. Patients who were lost to follow-up or withdrew consent were censored in this analysis. (NCT01602666)
Timeframe: Up to 3 years

Interventionpercentage of patients (Number)
Stratum 1 Localized Non-Germinomatous Germ Cell Tumors (NGGCT)92.42

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3-year Progression-free Survival (PFS) Rate of Patients With Nongerminomatous Germ Cell Tumor (NGGCT) Who Were Treated With Reduced Dose Whole Ventricular-field Irradiation

"Binomial estimate of the 3-year PFS rate defined as Yes for patients who were followed up per protocol and were progression free at 3-years, and No for those who either experienced a progression or were lost to follow-up/withdrew from the trial within 3 years from enrollment. Progression was determined by MRI using the COG Guidelines for Measurement of Tumor Size (>25% increase in 2D or >40% in 3D of the product of perpendicular diameters of the target lesion) as well as by tumor marker assessments which were mandatory for this study." (NCT01602666)
Timeframe: 3 years

Interventionpercentage of patients (Number)
Stratum 1 Localized Non-Germinomatous Germ Cell Tumors (NGGCT)83.33

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3-year PFS Rate of Patients With Localized CNS Germinoma Who Were Treated With Reduced Dose Radiation Therapy

"Binomial estimate of the 3-year PFS rate defined as Yes for patients who were followed up per protocol and were progression free at 3-years, and No for those who either experienced a progression or were lost to follow-up/withdrew from the trial within 3 years from initiation of treatment. Progression was determined by MRI using the COG Guidelines for Measurement of Tumor Size (>25% increase in 2D or >40% in 3D of the product of perpendicular diameters of the target lesion) as well as by tumor marker assessments which were mandatory for this study." (NCT01602666)
Timeframe: 3 years

Interventionpercentage of patients (Number)
Stratum 2 Localized Germinoma86.49

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Progression Free Survival (PFS)

Summarized by Kaplan-Meier methods including 90% confidence intervals for the median using method of Brookmeyer and Crowley. Time until progression, death or last evaluation will be calculated. If a patient did not progress or die, they will be censored at their last evaluation in the analysis. (NCT01808534)
Timeframe: Up to 2 years

Interventionmonths (Median)
Treatment (Palifosfamide)0.69

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Duration of Remission in Patients Who Achieve a Partial or Complete Response

The duration of remission is from the time of confirmed partial or complete response until progression or death. Patients continuing in remission at the end of the study will be treated as censored. Summarized by Kaplan-Meier methods including 90% confidence intervals for the median using method of Brookmeyer and Crowley. Note: There were no patients who achieved partial or complete response. (NCT01808534)
Timeframe: Up to 2 years

Interventionmonths (Median)
Treatment (Palifosfamide)0

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Overall Response Rate (Defined as Partial Response or Complete Response)

The percent of patients who were shown as having a partial remission or better based on definitions of response in RECIST 1.1. At least a 30% decrease in the sum of the diameters of target lesions, in reference to baseline sum diameters, needs to be confirmed to be considered as partial response or better. Note: There were no patients with a partial or complete response. (NCT01808534)
Timeframe: Up to 2 years

Interventionpercentage of participants (Number)
Treatment (Palifosfamide)0

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Overall Survival

Summarized by Kaplan-Meier methods including 90% confidence intervals for the median using method of Brookmeyer and Crowley. Time until death or last evaluation will be calculated. If a patient did not die, they will be censored in the analysis at their last known alive date. (NCT01808534)
Timeframe: Up to 2 years

Interventionmonths (Median)
Treatment (Palifosfamide)0.95

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Response to Window Therapy (2 Courses) for Group B (High-risk) - ESFT Participants

Response rate will be defined as the proportion of patients who achieved complete response or partial response (CR+PR) using the World Health Organization (WHO) criteria evaluated after two initial courses of temsirolimus, temozolomide and irinotecan in previously untreated patients with high risk Ewing Sarcoma Family of Tumor (ESFT). Participants who are treated in Group B with Desmoplastic Small Round Cell Tumor (DSRCT) or those who do not receive window therapy will not be included in this analysis. (NCT01946529)
Timeframe: at 6 weeks after start of therapy (after 2 initial courses)

Interventionparticipants (Number)
Partial Response (PR)Stable disease (no response) (NR)Progressive Disease (PD)
Group B (High Risk) - ESFT381

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Overall Survival

The estimated distributions of overall survival will be obtained using the Kaplan-Meier method. Corresponding confidence intervals using the methodology of Brookmeyer and Crowley will be computed. It is assumed a priori that any drop out times will be non-informative in terms of the censoring mechanism. Groups defined by levels of categorical or dichotomized numeric demographic/baseline variables will be compared in regards to time-to-event distributions using the log-rank test. Cox proportional hazards model regression will be utilized for multivariate analyses. (NCT01959698)
Timeframe: From the start of treatment until death for any reason, assessed up to 5 years

Interventionmonths (Median)
Treatment (Carfilzomib, Rituximab, Chemotherapy)22.6

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Complete Response Rate According to the International Working Group Response Criteria as Reported by the Revised Cheson Criteria

Efficacy rates were estimated using simple relative frequencies. Complete response rate after 3 cycles of C R ICE in patients age of 18 to 75 with relapsed/refractory CD20-positive DLBCL treated with rituximab-based immunochemotherapy (e.g., R-CHOP, R-EPOCH, R-HyperCVAD, etc.) induction. Response was based on a Modified Cheson Criteria with Complete response (CR): All lesions with a longest diameter ≤ 15 mm or short axis ≤ 10 mm (Not palpable during the clinical examination, No visible nodule on imaging, And disappearance of all non-nodal target lesions Or in case of hypermetabolic disease on the baseline PET scan, negative PET scan whatever the appearance of lesions on CT) and Partial Response (PR): ≥ 50 % of sum of the products of the diameters (SPD) of target lesions or in the case of hypermetabolic lesions on the baseline PET scan, persistence of at least one PET-positive site without progression of other lesions on CT (≥ 50 % of SPD of target lesions (or longest diameter if a si (NCT01959698)
Timeframe: Up to 5 years

Interventionpercentage of participants (Number)
Treatment (Carfilzomib, Rituximab, Chemotherapy)48

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MTD Defined as the Dose of Carfilzomib Added to Standard R-ICE Chemotherapy Which, if Exceeded, Would Put the Patient at an Undesirable Risk of Medically Unacceptable Dose-limiting Toxicities (Phase I)

(NCT01959698)
Timeframe: 28 days

Interventionmg/m2 (Number)
Dose Level 1: Carfilzomib 10mg/m2(d1-2; d8-9)NA
Dose Level 2: Carfilzomib 15mg/m2(d1-2; d8-9)NA
Dose Level 3: Carfilzomib 20mg/m2(d1-2; d8-9)NA
Dose Level 4: Carfilzomib 20mg/m2(d1-2); 27mg/m2(d8-9)NA
Dose Level 5: Carfilzomib 20mg/m2(d1-2); 36mg/m2(d8-9)NA
Dose Level 6: Carfilzomib 20mg/m2(d1-2); 45mg/m2(d8-9)NA
Expansion Cohort: Carfilzomib 20mg/m2(d1-2); 45mg/m2(d8-9)NA

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Overall Response Rate (PR + CR)

Overall response rate (CR and PR) after 3 cycles of C R ICE in patients age of 18 to 75 with relapsed/refractory CD20-positive DLBCL treated with rituximab-based immunochemotherapy (e.g., R-CHOP, R-EPOCH, R-HyperCVAD, etc.) induction. Response was based on a Modified Cheson Criteria with Complete response (CR): All lesions with a longest diameter ≤ 15 mm or short axis ≤ 10 mm (Not palpable during the clinical examination, No visible nodule on imaging, And disappearance of all non-nodal target lesions Or in case of hypermetabolic disease on the baseline PET scan, negative PET scan whatever the appearance of lesions on CT) and Partial Response (PR): ≥ 50 % of sum of the products of the diameters (SPD) of target lesions or in the case of hypermetabolic lesions on the baseline PET scan, persistence of at least one PET-positive site without progression of other lesions on CT (≥ 50 % of SPD of target lesions (or longest diameter if a single nodule) No clinically enlarged liver or spleen) (NCT01959698)
Timeframe: The time measurement criteria are first met for CR until the first date that recurrent disease is objectively documented, assessed up to 12 weeks

Interventionpercentage of participants (Number)
Treatment (Carfilzomib, Rituximab, Chemotherapy)66

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Progression-free Survival

The estimated distributions of progression-free survival will be obtained using the Kaplan-Meier method. Corresponding confidence intervals using the methodology of Brookmeyer and Crowley will be computed. It is assumed a priori that any drop out times will be non-informative in terms of the censoring mechanism. Groups defined by levels of categorical or dichotomized numeric demographic/baseline variables will be compared in regards to time-to-event distributions using the log-rank test. Cox proportional hazards model regression will be utilized for multivariate analyses. (NCT01959698)
Timeframe: Up to 5 years

Interventionmonths (Median)
Treatment (Carfilzomib, Rituximab, Chemotherapy)15.2

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Toxicity of the Addition of Carfilzomib to R-ICE at the MTD, Assessed by the CTEP Version 4.0 of the NCI CTCAE

Count of participants that experienced serious adverse events assessed by the CTEP version 4.0 of the NCI CTCAE (NCT01959698)
Timeframe: Up to 5 years

InterventionParticipants (Count of Participants)
Dose Level 1: Carfilzomib 10mg/m2(d1-2; d8-9)2
Dose Level 2: Carfilzomib 15mg/m2(d1-2; d8-9)0
Dose Level 3: Carfilzomib 20mg/m2(d1-2; d8-9)0
Dose Level 4: Carfilzomib 20mg/m2(d1-2); 27mg/m2(d8-9)1
Dose Level 5: Carfilzomib 20mg/m2(d1-2); 36mg/m2(d8-9)1
Dose Level 6: Carfilzomib 20mg/m2(d1-2); 45mg/m2(d8-9)3
Expansion Cohort: Carfilzomib 20mg/m2(d1-2); 45mg/m2(d8-9)4

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Prognostic Significance of Minimal Residual Disease

Analyzed by estimating the 2-year EFS of negative MRD and positive MRD by arm. Minimal disease was performed using serial assessments of the t(2;5)(p23;q35) NPM-ALK fusion transcript using quantitative RT-PCR. Quantitative RT-PCR was performed by extracting total RNA from peripheral blood specimens. Peripheral blood samples were obtained at baseline, on day 1 of cycle 1, and on day 1 of cycle 2. The normalized copy numbers (NCN) were expressed as copy numbers of NPM-ALK per 104 copies of ABL. Minimal disease (MDD) was defined as >10 NCN at baseline. (NCT01979536)
Timeframe: Baseline up to progressive disease, relapse, or death, assessed up to 2 years

InterventionPercentage of patients (Number)
MRD Negative Arm BV (Brentuximab Vedotin, Combination Chemotherapy)89
MRD Positive Arm BV (Brentuximab Vedotin, Combination Chemotherapy)52.6
MRD Negative Arm CZ (Crizotinib, Combination Chemotherapy)85.6
MRD Positive Arm CZ (Crizotinib, Combination Chemotherapy)58.1

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Occurrence of Grade 3+ Non-hematologic Adverse Events

Will be assessed using the National Cancer Institute Common Terminology Criteria for Adverse Events version 5.0. Toxicities will be summarized by individual toxicity counts separated by arm. (NCT01979536)
Timeframe: Up to 60 months

InterventionPercentage of patients (Number)
Arm BV (Brentuximab Vedotin, Combination Chemotherapy)80.6
Arm CZ (Crizotinib, Combination Chemotherapy)87.9

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Event Free Survival (EFS)

The Kaplan-Meier method will be used to estimate the 2-year EFS for each of the treatment regimens. (NCT01979536)
Timeframe: Time from study entry until progressive disease, relapse, or death, assessed up to 2 years

InterventionPercentage of patients (Number)
Arm BV (Brentuximab Vedotin, Combination Chemotherapy)78.8
Arm CZ (Crizotinib, Combination Chemotherapy)76.8

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Highest FEV1 After Methacholine Challenge

Serial FEV1 was measured post inhalation of methacholine challenges for 90 minutes. The highest FEV1 at 5, 15, 30, 45, 60, and 90 minutes following methacholine challenge were evaluated for each subject. The minimum highest FEV1 was derived using the first three available measures that cover the first 30 minutes after the challenge. (NCT01993329)
Timeframe: Screening (Day -21 to Day -1) and Day 3

,,,
InterventionLiters (Mean)
+ 5 minutes+15 minutes+30 minutes+45 minutes+60 minutes+90 minutesMinimum Highest FEV1
Gefapixant 3002.432.672.832.993.063.122.43
Gefapixant 502.532.722.933.023.113.152.53
Placebo2.542.772.943.033.143.182.54
Screening2.442.692.862.932.993.102.44

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Provocative Concentration (PC20) After Methacholine Challenge

The provocative concentration (PC) of inhaled methacholine required to reduce forced expiratory volume in 1 second (FEV1) by 20% (PC20) was calculated from the methacholine challenge at screening and 2 hours (+15 minutes) post dose on Day 3 of each Treatment Period using a five-breath dosimeter method. The primary endpoint was the methacholine PC20 value normalized by means of a log (base 2) transformation, at 2 dose levels compared with placebo in participants with asthma following provocation with methacholine. (NCT01993329)
Timeframe: Screening (Day -21 to Day -1) and Day 3

Interventionlog [mg/mL] (Geometric Mean)
Gefapixant 500.91
Gefapixant 3000.84
Placebo0.82

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Tmax of Itacitinib in Combination With Parsaclisib

tmax is defined as the time to the maximum concentration of itacitinib. (NCT02018861)
Timeframe: Cycle 1 Day 15; pre-dose and 0.5, 1, 2, 4, 6, 8, and 12 hours post-dose

Interventionhours (Median)
Parsaclisib 20/30 mg + Itacitinib 300 mg2.0

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Parts 1 and 2: Cmax of Parsaclisib as Monotherapy and in Combination With Itacitinib

Cmax is defined as the maximum observed plasma or serum concentration of parsaclisib. PK samples collected in Part 2, the combination dose escalation study, and in Part 3, Cohort E expansion group, were analyzed for both parsaclisib and itacitinib. (NCT02018861)
Timeframe: Cycle 1 Days 1 and 15; pre-dose and 0.5, 1, 2, 4, 6, 8, and 12 hours post-dose

,,,,,,,
Interventionnmol (Mean)
Cycle 1 Day 1Cycle 1 Day 15
Parsaclisib 10 mg QD791856
Parsaclisib 15 mg QD8081310
Parsaclisib 20 mg + Itacitinib 300 mg17402390
Parsaclisib 20 mg QD12701280
Parsaclisib 30 mg + Itacitinib 300 mg20402500
Parsaclisib 30 mg QD32703310
Parsaclisib 45 mg QD40105530
Parsaclisib 5 mg QD354690

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Parts 1 and 2: Cmin of Parsaclisib as Monotherapy and in Combination With Itacitinib

Cmin is defined as the minimum observed plasma or serum concentration over the dose interval of parsaclisib. PK samples collected in Part 2, the combination dose escalation study, and in Part 3, Cohort E expansion group, were analyzed for both parsaclisib and itacitinib. (NCT02018861)
Timeframe: Cycle 1 Days 1 and 15; pre-dose and 0.5, 1, 2, 4, 6, 8, and 12 hours post-dose

,,,,,,,
Interventionnmol (Mean)
Cycle 1 Day 15
Parsaclisib 10 mg QD104
Parsaclisib 15 mg QD156
Parsaclisib 20 mg + Itacitinib 300 mg515
Parsaclisib 20 mg QD178
Parsaclisib 30 mg + Itacitinib 300 mg341
Parsaclisib 30 mg QD295
Parsaclisib 45 mg QD864
Parsaclisib 5 mg QD127

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Parts 1 and 2: Tmax of Parsaclisib as Monotherapy and in Combination With Itacitinib

tmax is defined as the time to the maximum concentration of parsaclisib. PK samples collected in Part 2, the combination dose escalation study, and in Part 3, Cohort E expansion group, were analyzed for both parsaclisib and itacitinib. (NCT02018861)
Timeframe: Cycle 1 Days 1 and 15; pre-dose and 0.5, 1, 2, 4, 6, 8, and 12 hours post-dose

,,,,,,,
Interventionhours (Median)
Cycle 1 Day 1Cycle 1 Day 15
Parsaclisib 10 mg QD1.01.0
Parsaclisib 15 mg QD1.01.0
Parsaclisib 20 mg + Itacitinib 300 mg1.01.0
Parsaclisib 20 mg QD1.01.0
Parsaclisib 30 mg + Itacitinib 300 mg1.01.0
Parsaclisib 30 mg QD0.50.5
Parsaclisib 45 mg QD1.00.5
Parsaclisib 5 mg QD2.00.5

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Parts 1 and 2: AUC0-τ of Parsaclisib as Monotherapy and in Combination With Itacitinib

AUC0-τ is defined as the area under the steady-state plasma or serum concentration-time curve over 1 dose interval (i.e., from hour 0 to 12 for q12h administration or from hour 0 to 24 for q24h administration) of parsaclisib. PK samples collected in Part 2, the combination dose escalation study, and in Part 3, Cohort E expansion group, were analyzed for both parsaclisib and itacitinib. (NCT02018861)
Timeframe: Cycle 1 Days 1 and 15; pre-dose and 0.5, 1, 2, 4, 6, 8, and 12 hours post-dose

,,,,,,,
Interventionhr*nmol/L (Mean)
Cycle 1 Day 15
Parsaclisib 10 mg QD6910
Parsaclisib 15 mg QD11100
Parsaclisib 20 mg + Itacitinib 300 mg22400
Parsaclisib 20 mg QD11900
Parsaclisib 30 mg + Itacitinib 300 mg22900
Parsaclisib 30 mg QD24800
Parsaclisib 45 mg QD47700
Parsaclisib 5 mg QD7130

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Parts 1 and 2: AUC0-t of Parsaclisib as Monotherapy and in Combination With Itacitinib

AUC0-t is defined as the area under the plasma or serum concentration-time curve from time = 0 to the last measurable concentration at time = t of parsaclisib. PK samples collected in Part 2, the combination dose escalation study, and in Part 3, Cohort E expansion group, were analyzed for both parsaclisib and itacitinib. (NCT02018861)
Timeframe: Cycle 1 Days 1 and 15; pre-dose and 0.5, 1, 2, 4, 6, 8, and 12 hours post-dose

,,,,,,,
Interventionhr*nmol/L (Mean)
Cycle 1 Day 1
Parsaclisib 10 mg QD3260
Parsaclisib 15 mg QD3730
Parsaclisib 20 mg + Itacitinib 300 mg7540
Parsaclisib 20 mg QD5990
Parsaclisib 30 mg + Itacitinib 300 mg10400
Parsaclisib 30 mg QD13300
Parsaclisib 45 mg QD16800
Parsaclisib 5 mg QD2110

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Part 6: ORR (Sum of Participants With CR and PR) Based on the Revised Response Criteria for HL and NHL, Using PET-CT and CT

CR, PET-CT: (a) complete MR; (b) LNs/ELSs: score 1, 2, or 3, with/without residual mass; (c) NNLs; (d) no evidence of fluorodeoxyglucose-avid disease in marrow. CT: complete radiologic response: (a) regression of target nodes/nodal masses to ≤ 1.5 cm in longest transverse lesion diameter; (b) no ELSs of disease; (c) absence of nonmeasured lesions; (d) regression to normal organ size; (e) NNLs; (f) normal morphological bone marrow. PR, PET-CT: (a) partial MR; (b) LNs/ELSs: score 4 or 5, with reduced uptake compared with Baseline and residual mass of any size; (c) NNLs; (d) residual uptake higher than uptake in normal marrow but reduced compared with Baseline. CT: partial remission: (a) LNs/ELSs: ≥ 50% decrease in the sum of the product of the perpendicular diameters for multiple lesions of up to 6 target measurable sites; (b) spleen must have regressed by > 50% in length beyond normal; (c) NNLs. (NCT02018861)
Timeframe: Up to approximately 4 months

,
Interventionpercentage of participants (Number)
Diffuse large B-cell lymphoma
Parsaclisib 15 mg QD + R-ICE50.0
Parsaclisib 20 mg QD + R-ICE100.0

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Part 1: ORR (Sum of Participants With CR and PR) Based on the Revised Response Criteria for Hodgkin's Lymphoma (HL) and Non-Hodgkin's Lymphoma (NHL), Using Positron Emission Tomography-computed Tomography (PET-CT) and CT

CR, PET-CT: (a) complete metabolic response (MR); (b) lymph nodes and extralymphatic sites (LNs/ELSs): score 1, 2, or 3, with/without residual mass; (c) no new lesions (NNLs); (d) no evidence of fluorodeoxyglucose-avid disease in marrow. CT: complete radiologic response: (a) regression of target nodes/nodal masses to ≤ 1.5 cm in longest transverse lesion diameter; (b) no ELSs of disease; (c) absence of nonmeasured lesions; (d) regression to normal organ size; (e) NNLs; (f) normal morphological bone marrow. PR, PET-CT: (a) partial MR; (b) LNs/ELSs: score 4 or 5, with reduced uptake compared with Baseline and residual mass of any size; (c) NNLs; (d) residual uptake higher than uptake in normal marrow but reduced compared with Baseline. CT: partial remission: (a) LNs/ELSs: ≥ 50% decrease in the sum of the product of the perpendicular diameters for multiple lesions of up to 6 target measurable sites; (b) spleen must have regressed by > 50% in length beyond normal; (c) NNLs. (NCT02018861)
Timeframe: Up to approximately 53 months (4.4 years)

Interventionpercentage of participants (Number)
Diffuse large B-cell lymphoma
Parsaclisib 5 mg QD0.0

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Cmin of Itacitinib in Combination With Parsaclisib

Cmin is defined as the minimum observed plasma or serum concentration over the dose interval of itacitinib. (NCT02018861)
Timeframe: Cycle 1 Day 15; pre-dose and 0.5, 1, 2, 4, 6, 8, and 12 hours post-dose

Interventionnmol (Mean)
Parsaclisib 20/30 mg + Itacitinib 300 mg32.8

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Number of Participants With Treatment-emergent Adverse Events (TEAEs)

An adverse event (AE) is defined as the appearance of (or worsening of any pre-existing) undesirable sign(s), symptom(s), or medical condition(s) that occur after a participant provides informed consent. Abnormal laboratory values or test results occurring after informed consent constitute AEs only if they induce clinical signs or symptoms, are considered clinically meaningful, require therapy (e.g., hematologic abnormality that requires transfusion), or require changes in the study drug(s). A TEAE is defined as an event that was reported for the first time, or the worsening of a pre-existing event, after the first dose of study drug. (NCT02018861)
Timeframe: Up to approximately 53 months (4.4 years)

InterventionParticipants (Count of Participants)
Parsaclisib 5 mg QD1
Parsaclisib 10 mg QD3
Parsaclisib 15 mg QD3
Parsaclisib 20 mg QD32
Parsaclisib 30 mg QD25
Parsaclisib 45 mg QD4
Parsaclisib 20 mg + Itacitinib 300 mg6
Parsaclisib 30 mg + Itacitinib 300 mg3
Parsaclisib 15 mg QD + R-ICE4
Parsaclisib 20 mg QD + R-ICE1

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Part 1: ORR Based on the VIth International Workshop on Waldenström Macroglobulinemia (WM) Response Assessment for Participants With WM

ORR: sum of participants achieving minor response (MR), PR, very good partial response (VGPR), and CR. CR: (a) no serum monoclonal IgM protein by immunofixation; (b) normal serum IgM level; (c) complete resolution of extramedullary disease, i.e., lymphadenopathy/splenomegaly if present at Baseline (BL); (d) morphologically normal bone marrow aspirate and trephine biopsy. VGPR: (a) detectable monoclonal IgM protein; (b) ≥90% reduction in serum IgM level from BL; (c) complete resolution of extramedullary disease, i.e., lymphadenopathy/splenomegaly if present at BL; (d) no new signs/symptoms of active disease. PR: (a) detectable monoclonal IgM protein; (b) ≥50% but <90% reduction in serum IgM level from BL; (c) reduction in extramedullary disease, i.e., lymphadenopathy/splenomegaly if present at BL; (d) no new signs/symptoms of active disease. MR: (a) detectable monoclonal IgM protein; (b) ≥25% but <50% reduction in serum IgM level from BL; (d) no new signs/symptoms of active disease. (NCT02018861)
Timeframe: Up to approximately 53 months (4.4 years)

Interventionpercentage of participants (Number)
Parsaclisib 20 mg QD100.0

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Part 1: Overall Response Rate (Percentage of Participants With Complete Response [CR] and Partial Response [PR]) Based on International Workshop on Chronic Lymphocytic Leukemia (IWCLL) Criteria for Chronic Lymphocytic Leukemia (CLL) for CLL Participants

CR: (a) peripheral blood lymphocytes <4 x 10^9/Liter (L); (b) no significant lymphadenopathy and lymph nodes <1.5 centimeters (cm) in longest diameter; (c) no splenomegaly/hepatomegaly; (d) no disease-related constitutional symptoms; (e) neutrophils ≥1.5 x 10^9/L; (f) platelets ≥100 x 10^9/L; (g) hemoglobin ≥11.0 grams/deciliter (g/dL) (without transfusion); (h) minimal residual disease assessment; (i) normocellular marrow, with no CLL cells/no B-lymphoid nodules. PR (improvement in ≥2 Group A parameters and ≥1 Group B parameter if previously abnormal. If only 1 parameter of both Groups A and B was abnormal before therapy, only 1 needs to improve): Group A: (a) decrease of ≥50% (from Baseline) in lymph nodes, liver/spleen size, and circulating lymphocyte count; (b) any constitutional symptoms. Group B: (a) platelets ≥100 x 10^9/L or increase ≥50% over Baseline; (b) hemoglobin ≥11 g/dL or increase ≥50% over Baseline; (c) presence of CLL cells or B-lymphoid nodules. (NCT02018861)
Timeframe: Up to approximately 53 months (4.4 years)

Interventionpercentage of participants (Number)
Parsaclisib 10 mg QD0.0
Parsaclisib 20 mg QD0.0
Parsaclisib 30 mg QD66.7
Parsaclisib 45 mg QD0.0

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Part 3: Tmax of Parsaclisib Monotherapy

tmax is defined as the time to the maximum concentration of parsaclisib. PK samples for parsaclisib monotherapy were collected and analyzed from the Part 3 dose expansion (different participant populations). Cohort A: B-cell malignancies; Cohort B: Hodgkin's lymphoma; Cohort C: diffuse large B-cell lymphoma; Cohort D: indolent lymphoma. (NCT02018861)
Timeframe: Cycle 1 Days 1 and 15; pre-dose and 0.5, 1, 2, 4, 6, 8, and 12 hours post-dose

,
Interventionhours (Median)
Cycle 1 Day 1, Cohort ACycle 1 Day 15, Cohort ACycle 1 Day 1, Cohort BCycle 1 Day 15, Cohort BCycle 1 Day 1, Cohort CCycle 1 Day 15, Cohort CCycle 1 Day 1, Cohort DCycle 1 Day 15, Cohort D
Parsaclisib 20 mg QD0.51.02.00.50.51.01.00.5
Parsaclisib 30 mg QD1.01.01.50.751.00.50.751.0

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Part 3: Cmin of Parsaclisib Monotherapy

Cmin is defined as the minimum observed plasma or serum concentration over the dose interval of parsaclisib. PK samples for parsaclisib monotherapy were collected and analyzed from the Part 3 dose expansion (different participant populations). Cohort A: B-cell malignancies; Cohort B: Hodgkin's lymphoma; Cohort C: diffuse large B-cell lymphoma; Cohort D: indolent lymphoma. (NCT02018861)
Timeframe: Cycle 1 Days 1 and 15; pre-dose and 0.5, 1, 2, 4, 6, 8, and 12 hours post-dose

,
Interventionnmol (Mean)
Cycle 1 Day 15, Cohort ACycle 1 Day 15, Cohort BCycle 1 Day 15, Cohort CCycle 1 Day 15, Cohort D
Parsaclisib 20 mg QD214395197202
Parsaclisib 30 mg QD281296477421

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Part 3: Cmax of Parsaclisib Monotherapy

Cmax is defined as the maximum observed plasma or serum concentration of parsaclisib. PK samples for parsaclisib monotherapy were collected and analyzed from the Part 3 dose expansion (different participant populations). Cohort A: B-cell malignancies; Cohort B: Hodgkin's lymphoma; Cohort C: diffuse large B-cell lymphoma; Cohort D: indolent lymphoma. (NCT02018861)
Timeframe: Cycle 1 Days 1 and 15; pre-dose and 0.5, 1, 2, 4, 6, 8, and 12 hours post-dose

,
Interventionnmol (Mean)
Cycle 1 Day 1, Cohort ACycle 1 Day 15, Cohort ACycle 1 Day 1, Cohort BCycle 1 Day 15, Cohort BCycle 1 Day 1, Cohort CCycle 1 Day 15, Cohort CCycle 1 Day 1, Cohort DCycle 1 Day 15, Cohort D
Parsaclisib 20 mg QD15501720120019301760206017601600
Parsaclisib 30 mg QD23502390172022601760392025002990

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Part 3: AUC0-τ of Parsaclisib Monotherapy

AUC0-τ is defined as the area under the steady-state plasma or serum concentration-time curve over 1 dose interval (i.e., from hour 0 to 12 for once every 12 hours [q12h] administration or from hour 0 to 24 for once every 24 hours [q24h] administration) of parsaclisib. PK samples for parsaclisib monotherapy were collected and analyzed from the Part 3 dose expansion (different participant populations). Cohort A: B-cell malignancies; Cohort B: Hodgkin's lymphoma; Cohort C: diffuse large B-cell lymphoma; Cohort D: indolent lymphoma. (NCT02018861)
Timeframe: Cycle 1 Days 1 and 15; pre-dose and 0.5, 1, 2, 4, 6, 8, and 12 hours post-dose

,
Interventionhr*nmol/L (Mean)
Cycle 1 Day 15, Cohort ACycle 1 Day 15, Cohort BCycle 1 Day 15, Cohort CCycle 1 Day 15, Cohort D
Parsaclisib 20 mg QD12600179001420013600
Parsaclisib 30 mg QD19500201002800025200

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Part 2: Overall Response Rate (Percentage of Participants With CR and PR) Based on IWCLL Criteria for CLL for Participants With CLL

CR: (a) peripheral blood lymphocytes <4 x 10^9/L; (b) no significant lymphadenopathy and lymph nodes <1.5 cm in longest diameter; (c) no splenomegaly/hepatomegaly; (d) no disease-related constitutional symptoms; (e) neutrophils ≥1.5 x 10^9/L; (f) platelets ≥100 x 10^9/L; (g) hemoglobin ≥11.0 g/dL (without transfusion); (h) minimal residual disease assessment; (i) normocellular marrow, with no CLL cells/no B-lymphoid nodules. PR (improvement in ≥2 Group A parameters and ≥1 Group B parameter if previously abnormal. If only 1 parameter of both Groups A and B was abnormal before therapy, only 1 needs to improve): Group A: (a) decrease of ≥50% (from Baseline) in lymph nodes, liver/spleen size, and circulating lymphocyte count; (b) any constitutional symptoms. Group B: (a) platelets ≥100 x 10^9/L or increase ≥50% over Baseline; (b) ≥11 g/dL or increase ≥50% over Baseline; (c) presence of CLL cells or B-lymphoid nodules. (NCT02018861)
Timeframe: Up to approximately 44 months (3.7 years)

Interventionpercentage of participants (Number)
Parsaclisib 20 mg + Itacitinib 300 mg100.0

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AUC0-τ of Itacitinib in Combination With Parsaclisib

AUC0-τ is defined as the area under the steady-state plasma or serum concentration-time curve over 1 dose interval (i.e., from hour 0 to 12 for once every 12 hours [q12h] administration or from hour 0 to 24 for once every 24 hours [q24h] administration) of itacitinib. (NCT02018861)
Timeframe: Cycle 1 Day 15; pre-dose and 0.5, 1, 2, 4, 6, 8, and 12 hours post-dose

Interventionhr*nmol/L (Mean)
Parsaclisib 20/30 mg + Itacitinib 300 mg6450

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AUC0-t of Itacitinib in Combination With Parsaclisib

AUC0-t is defined as the area under the plasma or serum concentration-time curve from time = 0 to the last measurable concentration at time = t of itacitinib. (NCT02018861)
Timeframe: Cycle 1 Day 15; pre-dose and 0.5, 1, 2, 4, 6, 8, and 12 hours post-dose

Interventionhours (hr)*nmol/L (Mean)
Parsaclisib 20/30 mg + Itacitinib 300 mg6450

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Part 2: ORR (Sum of Participants With CR and PR) Based on the Revised Response Criteria for HL and NHL, Using PET-CT and CT

CR, PET-CT: (a) complete MR; (b) LNs/ELSs: score 1, 2, or 3, with/without residual mass; (c) NNLs; (d) no evidence of fluorodeoxyglucose-avid disease in marrow. CT: complete radiologic response: (a) regression of target nodes/nodal masses to ≤ 1.5 cm in longest transverse lesion diameter; (b) no ELSs of disease; (c) absence of nonmeasured lesions; (d) regression to normal organ size; (e) NNLs; (f) normal morphological bone marrow. PR, PET-CT: (a) partial MR; (b) LNs/ELSs: score 4 or 5, with reduced uptake compared with Baseline and residual mass of any size; (c) NNLs; (d) residual uptake higher than uptake in normal marrow but reduced compared with Baseline. CT: partial remission: (a) LNs/ELSs: ≥ 50% decrease in the sum of the product of the perpendicular diameters for multiple lesions of up to 6 target measurable sites; (b) spleen must have regressed by > 50% in length beyond normal; (c) NNLs. (NCT02018861)
Timeframe: Up to approximately 44 months (3.7 years)

Interventionpercentage of participants (Number)
Diffuse large B-cell lymphomaFollicular lymphomaMantle cell lymphomaClassical Hodgkin's lymphoma
Parsaclisib 20 mg + Itacitinib 300 mg0.00.0100.050.0

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Part 2: ORR (Sum of Participants With CR and PR) Based on the Revised Response Criteria for HL and NHL, Using PET-CT and CT

CR, PET-CT: (a) complete MR; (b) LNs/ELSs: score 1, 2, or 3, with/without residual mass; (c) NNLs; (d) no evidence of fluorodeoxyglucose-avid disease in marrow. CT: complete radiologic response: (a) regression of target nodes/nodal masses to ≤ 1.5 cm in longest transverse lesion diameter; (b) no ELSs of disease; (c) absence of nonmeasured lesions; (d) regression to normal organ size; (e) NNLs; (f) normal morphological bone marrow. PR, PET-CT: (a) partial MR; (b) LNs/ELSs: score 4 or 5, with reduced uptake compared with Baseline and residual mass of any size; (c) NNLs; (d) residual uptake higher than uptake in normal marrow but reduced compared with Baseline. CT: partial remission: (a) LNs/ELSs: ≥ 50% decrease in the sum of the product of the perpendicular diameters for multiple lesions of up to 6 target measurable sites; (b) spleen must have regressed by > 50% in length beyond normal; (c) NNLs. (NCT02018861)
Timeframe: Up to approximately 44 months (3.7 years)

Interventionpercentage of participants (Number)
Diffuse large B-cell lymphoma
Parsaclisib 30 mg + Itacitinib 300 mg0.0

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Part 1: ORR (Sum of Participants With CR and PR) Based on the Revised Response Criteria for Hodgkin's Lymphoma (HL) and Non-Hodgkin's Lymphoma (NHL), Using Positron Emission Tomography-computed Tomography (PET-CT) and CT

CR, PET-CT: (a) complete metabolic response (MR); (b) lymph nodes and extralymphatic sites (LNs/ELSs): score 1, 2, or 3, with/without residual mass; (c) no new lesions (NNLs); (d) no evidence of fluorodeoxyglucose-avid disease in marrow. CT: complete radiologic response: (a) regression of target nodes/nodal masses to ≤ 1.5 cm in longest transverse lesion diameter; (b) no ELSs of disease; (c) absence of nonmeasured lesions; (d) regression to normal organ size; (e) NNLs; (f) normal morphological bone marrow. PR, PET-CT: (a) partial MR; (b) LNs/ELSs: score 4 or 5, with reduced uptake compared with Baseline and residual mass of any size; (c) NNLs; (d) residual uptake higher than uptake in normal marrow but reduced compared with Baseline. CT: partial remission: (a) LNs/ELSs: ≥ 50% decrease in the sum of the product of the perpendicular diameters for multiple lesions of up to 6 target measurable sites; (b) spleen must have regressed by > 50% in length beyond normal; (c) NNLs. (NCT02018861)
Timeframe: Up to approximately 53 months (4.4 years)

Interventionpercentage of participants (Number)
Diffuse large B-cell lymphomaFollicular lymphomaMantle cell lymphomaMarginal zone lymphomaNodal marginal zone B-cell lymphomaSplenic marginal zone lymphomaClassical Hodgkin's lymphomaNodular lymphocytic-predominant Hodgkin's lymphoma
Parsaclisib 30 mg QD16.740.0100.00.0100.0100.00.00.0

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Part 1: ORR (Sum of Participants With CR and PR) Based on the Revised Response Criteria for Hodgkin's Lymphoma (HL) and Non-Hodgkin's Lymphoma (NHL), Using Positron Emission Tomography-computed Tomography (PET-CT) and CT

CR, PET-CT: (a) complete metabolic response (MR); (b) lymph nodes and extralymphatic sites (LNs/ELSs): score 1, 2, or 3, with/without residual mass; (c) no new lesions (NNLs); (d) no evidence of fluorodeoxyglucose-avid disease in marrow. CT: complete radiologic response: (a) regression of target nodes/nodal masses to ≤ 1.5 cm in longest transverse lesion diameter; (b) no ELSs of disease; (c) absence of nonmeasured lesions; (d) regression to normal organ size; (e) NNLs; (f) normal morphological bone marrow. PR, PET-CT: (a) partial MR; (b) LNs/ELSs: score 4 or 5, with reduced uptake compared with Baseline and residual mass of any size; (c) NNLs; (d) residual uptake higher than uptake in normal marrow but reduced compared with Baseline. CT: partial remission: (a) LNs/ELSs: ≥ 50% decrease in the sum of the product of the perpendicular diameters for multiple lesions of up to 6 target measurable sites; (b) spleen must have regressed by > 50% in length beyond normal; (c) NNLs. (NCT02018861)
Timeframe: Up to approximately 53 months (4.4 years)

Interventionpercentage of participants (Number)
Diffuse large B-cell lymphomaFollicular lymphomaMantle cell lymphomaExtranodal marginal zone lymphoma of mucosa-associated lymphatic tissueNodal marginal zone B-cell lymphomaSplenic marginal zone lymphomaClassical Hodgkin's lymphoma
Parsaclisib 20 mg QD36.485.766.750.0100.0100.050.0

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Part 1: ORR (Sum of Participants With CR and PR) Based on the Revised Response Criteria for Hodgkin's Lymphoma (HL) and Non-Hodgkin's Lymphoma (NHL), Using Positron Emission Tomography-computed Tomography (PET-CT) and CT

CR, PET-CT: (a) complete metabolic response (MR); (b) lymph nodes and extralymphatic sites (LNs/ELSs): score 1, 2, or 3, with/without residual mass; (c) no new lesions (NNLs); (d) no evidence of fluorodeoxyglucose-avid disease in marrow. CT: complete radiologic response: (a) regression of target nodes/nodal masses to ≤ 1.5 cm in longest transverse lesion diameter; (b) no ELSs of disease; (c) absence of nonmeasured lesions; (d) regression to normal organ size; (e) NNLs; (f) normal morphological bone marrow. PR, PET-CT: (a) partial MR; (b) LNs/ELSs: score 4 or 5, with reduced uptake compared with Baseline and residual mass of any size; (c) NNLs; (d) residual uptake higher than uptake in normal marrow but reduced compared with Baseline. CT: partial remission: (a) LNs/ELSs: ≥ 50% decrease in the sum of the product of the perpendicular diameters for multiple lesions of up to 6 target measurable sites; (b) spleen must have regressed by > 50% in length beyond normal; (c) NNLs. (NCT02018861)
Timeframe: Up to approximately 53 months (4.4 years)

Interventionpercentage of participants (Number)
Diffuse large B-cell lymphomaMantle cell lymphoma
Parsaclisib 45 mg QD50.00.0

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Part 1: ORR (Sum of Participants With CR and PR) Based on the Revised Response Criteria for Hodgkin's Lymphoma (HL) and Non-Hodgkin's Lymphoma (NHL), Using Positron Emission Tomography-computed Tomography (PET-CT) and CT

CR, PET-CT: (a) complete metabolic response (MR); (b) lymph nodes and extralymphatic sites (LNs/ELSs): score 1, 2, or 3, with/without residual mass; (c) no new lesions (NNLs); (d) no evidence of fluorodeoxyglucose-avid disease in marrow. CT: complete radiologic response: (a) regression of target nodes/nodal masses to ≤ 1.5 cm in longest transverse lesion diameter; (b) no ELSs of disease; (c) absence of nonmeasured lesions; (d) regression to normal organ size; (e) NNLs; (f) normal morphological bone marrow. PR, PET-CT: (a) partial MR; (b) LNs/ELSs: score 4 or 5, with reduced uptake compared with Baseline and residual mass of any size; (c) NNLs; (d) residual uptake higher than uptake in normal marrow but reduced compared with Baseline. CT: partial remission: (a) LNs/ELSs: ≥ 50% decrease in the sum of the product of the perpendicular diameters for multiple lesions of up to 6 target measurable sites; (b) spleen must have regressed by > 50% in length beyond normal; (c) NNLs. (NCT02018861)
Timeframe: Up to approximately 53 months (4.4 years)

,
Interventionpercentage of participants (Number)
Diffuse large B-cell lymphomaFollicular lymphoma
Parsaclisib 10 mg QD0.0100.0
Parsaclisib 15 mg QD50.0100.0

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Part 3: AUC0-t of Parsaclisib Monotherapy

AUC0-t is defined as the area under the plasma or serum concentration-time curve from time = 0 to the last measurable concentration at time = t of of parsaclisib. PK samples for parsaclisib monotherapy were collected and analyzed from the Part 3 dose expansion (different participant populations). Cohort A: B-cell malignancies; Cohort B: Hodgkin's lymphoma; Cohort C: diffuse large B-cell lymphoma; Cohort D: indolent lymphoma. (NCT02018861)
Timeframe: Cycle 1 Days 1 and 15; pre-dose and 0.5, 1, 2, 4, 6, 8, and 12 hours post-dose

,
Interventionhr*nmol/L (Mean)
Cycle 1 Day 1, Cohort ACycle 1 Day 1, Cohort BCycle 1 Day 1, Cohort CCycle 1 Day 1, Cohort D
Parsaclisib 20 mg QD6530701071107230
Parsaclisib 30 mg QD107008430120009970

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Cmax of Itacitinib in Combination With Parsaclisib

Cmax is defined as the maximum observed plasma or serum concentration of itacitinib. (NCT02018861)
Timeframe: Cycle 1 Day 15; pre-dose and 0.5, 1, 2, 4, 6, 8, and 12 hours post-dose

Interventionnanomoles (nmol) (Mean)
Parsaclisib 20/30 mg + Itacitinib 300 mg887

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Pathologic Response Rate, Defined as the Percentage of Participants With Greater Than or Equal to 95% Necrosis.

Descriptive statistical analysis will be conducted. The proportion with 95% confidence interval will be summarized. (NCT02050919)
Timeframe: Assessed at surgical resection

Intervention% of participants (Number)
Treatment (Sorafenib, Chemotherapy, Radiation, Surgery)20

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Overall Survival at 2 Years

Percentage of patients alive at 2 years, Method of Kaplan-Meier used. (NCT02050919)
Timeframe: Time from registration until death from any cause

Interventionpercentage of patients (Number)
Treatment (Sorafenib, Chemotherapy, Radiation, Surgery)82

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Overall Disease-free Survival (Stage IIB-III Patients)

Time from surgical resection to local recurrence, distant metastatic disease or death, subjects with stage IV disease excluded. Method of Kaplan-Meier used. (NCT02050919)
Timeframe: Time from surgical resection to local recurrence, distant metastatic disease, or death, whichever occurs first, assessed up to 2 years

InterventionMonths (Median)
Treatment (Sorafenib, Chemotherapy, Radiation, Surgery)13.3

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Number of Participants With Wound Complications

Wound complication rate, including 1) any secondary operation for wound repair, or 2) wound management without secondary operation including invasive procedures without general or regional anesthesia, readmission for wound care, or persistent deep packing for 120 days or longer. (NCT02050919)
Timeframe: At least 120 days

InterventionParticipants (Count of Participants)
Treatment (Sorafenib, Chemotherapy, Radiation, Surgery)10

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Number of Participants With Local Recurrence

Number of patients with local recurrence after surgical resection of the primary tumor (NCT02050919)
Timeframe: Time from surgical resection until primary analysis ( Median follow-up for local recurrence 17.11 months, range 6.18 - 42.8 months)

InterventionParticipants (Count of Participants)
Treatment (Sorafenib, Chemotherapy, Radiation, Surgery)0

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Number of Grade 3-4 Adverse Events

Measured as the number of Grade 3-4 Adverse Events, graded according to National Cancer Institute Common Terminology Criteria for Adverse Events (NCI CTCAE) version 4.0 (NCT02050919)
Timeframe: Up to 5 years

InterventionGrade 3-4 Adverse Events (Number)
Treatment (Sorafenib, Chemotherapy, Radiation, Surgery)86

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Distant Disease-free Survival (Stage IIB-III Patients)

Time from registration to development of distant metastatic disease or death, subjects with stage IV disease excluded. Method of Kaplan-Meier used. (NCT02050919)
Timeframe: Time from registration until development of distant metastatic disease or death, whichever occurs first, assessed up to 2 years

InterventionMonths (Median)
Treatment (Sorafenib, Chemotherapy, Radiation, Surgery)16.4

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Event-free Survival (EFS) for Modified Augmented Berlin-Frankfurt-Munster Backbone With or Without Bortezomib in All Randomized Patients

EFS is calculated as time from randomization at study entry to first event (induction failure, induction death, relapse, second malignancy, remission death) or date of last contact. Three-year EFS rates will be calculated for both groups. (NCT02112916)
Timeframe: 3 years

InterventionPercentage of participants (Number)
Arm A (Combination Chemotherapy)81.7
Arm B (Combination Chemotherapy, Bortezomib)85.1

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Cumulative Incidence Rates of Isolated Central Nervous System (CNS) Relapse for SR and IR T-ALL Patients on the Non-bortezomib Containing Arm on This Study (no CRT) and Similar Patients on AALL0434 (Receive CRT)

Cumulative incidence of isolated CNS relapse adjusting for competing risks using the method of: Gray R, A class of K-sample tests for comparing the cumulative incidence of a competing risk. Ann Stat 1141:1154, 1988 (NCT02112916)
Timeframe: 3 years

,
InterventionPercentage of participants (Number)
Isolated CNS RelapseIsolated Bone Marrow RelapseCombined Bone Marrow Relapse
AALL0434 T-ALL Patients2.23.01.8
AALL1231 T-ALL Patients3.61.41.3

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Toxicity Rates Associated With Modified Standard Therapy, Including Dexamethasone and Additional Pegaspargase

Percentage of patients who experienced Grade 3 or higher Toxicity Assessed by the National Cancer Institute (NCI) Common Terminology Criteria for Adverse Events (CTCAE) Version 4.0 (NCT02112916)
Timeframe: 3 years from start of therapy by patient

InterventionPercentage of participants (Number)
Total Patients78.0

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EFS for Standard (SR) and Intermediate Risk (IR) T-ALL Patients on the Non-bortezomib Containing Arm on This Study (no Cranial Radiation Therapy [CRT]) and Similar Patients on AALL0434 (Received CRT)

EFS is calculated as time from randomization at study entry to first event (induction failure, induction death, relapse, second malignancy, remission death) or date of last contact. (NCT02112916)
Timeframe: 3 years

InterventionPercentage of participants (Number)
AALL1231 T-ALL Patients88.3
AALL0434 T-ALL Patients88.8

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EFS for Very High Risk (VHR) T-ALL Patients Treated With High Risk (HR) Berlin-Frankfurt-Munster (BFM) Intensification Blocks Who Become Minimal Residual Disease (MRD) Negative and Those Who Remain MRD Positive at the End of HR Block 3

EFS will be calculated as time from the end of the three high-risk blocks of therapy to first event (relapse, second malignancy, remission death) or date of last contact. (NCT02112916)
Timeframe: 3 years

InterventionPercentage of participants (Number)
VHR T-ALL MRD Undetectable25.0
VHR T-ALL MRD Detectable88.9

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EFS for Very High Risk (VHR) T-LLy Patients Treated With HR Berlin-Frankfurt-Munster (BFM) Intensification Blocks Who Have Complete or Partial Remission and Those Who do Not Respond

EFS for very high risk (VHR) T-LLy patients treated with HR Berlin-Frankfurt-Munster (BFM) intensification blocks who have complete or partial remission and those who do not respond (NCT02112916)
Timeframe: 3 years

InterventionPercentage of participants (Number)
VHR T-LLy (CR/PR)0

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Percentage of Radiotherapy Patients With Positive Pathologic Response at Week 10

A responder is defined by more than 90% tumor necrosis at week 10. A non-responder has less than 90% necrosis or progressive disease before week 10. (NCT02180867)
Timeframe: Week 10 after induction

InterventionPercentage of patients (Number)
Dose-Finding Level 1 RT0
Dose-Finding Level 2 RT40
Regimen C0
Regimen D0

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Percentage of Chemoradiotherapy Patients With Positive Pathologic Response at Week 13

A responder is defined by more than (90% tumor necrosis at week 13). A non-responder has less than 90% necrosis or progressive disease before week 13. (NCT02180867)
Timeframe: Week 13 after induction

InterventionPercentage of patients (Number)
Dose-Finding Level 1 CR66.67
Regimen A46.67
Regimen B24

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Percentage of Patients Who Experienced Grade 3 or Higher Toxicity Assessed by the National Cancer Institute (NCI) Common Terminology Criteria for Adverse Events (CTCAE)

Participants who experienced Grade 3 or higher toxicity was assessed by the National Cancer Institute (NCI) Common Terminology Criteria for Adverse Events (CTCAE). (NCT02180867)
Timeframe: Reporting of adverse events was required from the start of protocol therapy and until 30 days from the last administration of study drugs; up to 1 year

InterventionPercentage of patients (Number)
Adult Patients
Regimen D0

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Percentage of Patients Who Experienced Grade 3 or Higher Toxicity Assessed by the National Cancer Institute (NCI) Common Terminology Criteria for Adverse Events (CTCAE)

Participants who experienced Grade 3 or higher toxicity was assessed by the National Cancer Institute (NCI) Common Terminology Criteria for Adverse Events (CTCAE). (NCT02180867)
Timeframe: Reporting of adverse events was required from the start of protocol therapy and until 30 days from the last administration of study drugs; up to 1 year

,,,,,
InterventionPercentage of patients (Number)
Pediatric PatientsAdult Patients
Dose-Finding Level 1 CR6075
Dose-Finding Level 1 RT66.6766.67
Dose-Finding Level 2 RT33.3357.14
Regimen A7586.67
Regimen B33.3336
Regimen C040

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Feasible Dose: Pediatric

The dose of pazopanib that is feasible when given in combination with radiation or chemoradiation in pediatric unresected intermediate- and high-risk NRSTS patients. Initially, up to 10 patients (minimum of 3 patients ≥ 2 and < 18 years of age and 3 patients ≥ 18 years of age) eligible for each of the two study cohorts were non-randomly assigned (to generate 8 patients evaluable for toxicity) to receive treatment with pazopanib at dose level 1. A protocol-defined list of pazopanib-associated adverse events were defined as dose-limiting toxicities. The pazopanib dose determined to be feasible was based on the number of patient-reported dose-limiting toxicities encountered. (NCT02180867)
Timeframe: After the first 6 weeks of Induction

Interventionmilligram per square meter (Number)
All Pediatric Dose Finding CR Cohorts350
All Pediatric Dose Finding RT Cohorts450

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Feasible Dose: Adult

The dose of pazopanib that is feasible when given in combination with radiation or chemoradiation in adult unresected intermediate- and high-risk NRSTS patients. Initially, up to 10 patients (minimum of 3 patients ≥ 2 and < 18 years of age and 3 patients ≥ 18 years of age) eligible for each of the two study cohorts were non-randomly assigned (to generate 8 patients evaluable for toxicity) to receive treatment with pazopanib at dose level 1. A protocol-defined list of pazopanib-associated adverse events were defined as dose-limiting toxicities. The pazopanib dose determined to be feasible was based on the number of patient-reported dose-limiting toxicities encountered. (NCT02180867)
Timeframe: After the first 6 weeks of Induction

Interventionmilligram (Number)
All Adult Dose Finding CR Cohorts600
All Adult Dose Finding RT Cohorts800

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2 Year Progression-free Survival

(NCT02227199)
Timeframe: Up to 2 years from initiation of therapy.

InterventionParticipants (Count of Participants)
Phase I: Dose Escalation, Dose Level 1 (Brentuximab 1.2mg/kg, Ifosfamide, Carboplatin, Etoposide)2
Phase I: Dose Escalation, Dose Level 2 (Brentuximab 1.5mg/kg, Ifosfamide, Carboplatin, Etoposide)3
Phase II: Dose Expansion (Brentuximab 1.5mg/kg, Ifosfamide, Carboplatin, Etoposide)33

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Percentage of Patients That Achieve a Complete Remission Following Study Treatment

(NCT02227199)
Timeframe: 3 weeks following the completion of chemotherapy

InterventionParticipants (Count of Participants)
Phase I: Dose Escalation, Dose Level 1 (Brentuximab 1.2mg/kg, Ifosfamide, Carboplatin, Etoposide)3
Phase I: Dose Escalation, Dose Level 2 (Brentuximab 1.5mg/kg, Ifosfamide, Carboplatin, Etoposide)3
Phase II: Dose Expansion (Brentuximab 1.5mg/kg, Ifosfamide, Carboplatin, Etoposide)26

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2 Year Overall Survival

(NCT02227199)
Timeframe: Up to 2 years from initiation of study therapy.

InterventionParticipants (Count of Participants)
Phase I: Dose Escalation, Dose Level 1 (Brentuximab 1.2mg/kg, Ifosfamide, Carboplatin, Etoposide)3
Phase I: Dose Escalation, Dose Level 2 (Brentuximab 1.5mg/kg, Ifosfamide, Carboplatin, Etoposide)3
Phase II: Dose Expansion (Brentuximab 1.5mg/kg, Ifosfamide, Carboplatin, Etoposide)37

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Maximum Tolerated Dose of Brentuximab Vedotin That Can be Combined With Ifosfamide, Carboplatin, and Etoposide Chemotherapy

Will be defined as the dose at which =< 1 of 6 patients experience a dose-limiting toxicity. Dose-limiting toxicity will be graded according to National Cancer Institute Common Terminology Criteria for Adverse Events version 4.0. (NCT02227199)
Timeframe: Up to 28 days following the second course of chemotherapy, approximately 70 days

Interventionmg/kg (Number)
Treatment (Brentuximab, Ifosfamide, Carboplatin, Etoposide)1.5

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Overall Survival

Time from study enrollment to death or last patient contact. (NCT02306161)
Timeframe: 5 years after enrollment

InterventionPercent Probability (Number)
Regimen A (VDC/IE)44.93
Regimen B (VDC/IE + Ganitumab)48.19

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Frequency of Toxicity-events

The number of induction or consolidation reporting periods in which a CTC version 4 codeable grade 4 or greater non-hematological adverse event, grade 3 or greater left ventricular systolic dysfunction or the reporting period is terminated because of a CTC codeable event. (NCT02306161)
Timeframe: Up to 202 days

InterventionReporting Periods (Number)
Regimen A (VDC/IE)10
Regimen B (VDC/IE + Ganitumab)27

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Event-free Survival

Estimated 5-year EFS where EFS is calculated as the time from study enrollment to disease progression, disease relapse, occurrence of a second malignant neoplasm, death from any cause or last follow-up whichever occurs first. Kaplan-Meier method is used for estimation. Patients without an event are censored at last contact. (NCT02306161)
Timeframe: 5 years after enrollment

Interventionpercent probability of participants (Number)
Regimen A (VDC/IE)30.88
Regimen B (VDC/IE + Ganitumab)30.4

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Pharmacokinetics: Concentration at Steady State (Css) (Blinatumomab Arm Only)

(NCT02393859)
Timeframe: Day 1: at least 10 hours after infusion start and up to 24 hours; Day 15

Interventionpg/mL (Mean)
Blinatumomab884

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Kaplan Meier Estimate: Event-Free Survival (EFS; Primary Analysis)

"EFS is calculated from the time of randomization until the date of relapse or M2 marrow (representative bone marrow aspirate or biopsy with ≥ 5% and < 25% blasts) after having achieved a complete remission (CR), failure to achieve a CR at the end of treatment, second malignancy, or death due to any cause, whichever occurs first. Participants who failed to achieve a CR following treatment with investigational product (IP) or who died before the disease assessment at the end of treatment were considered treatment failures and assigned an EFS duration of 1 day. Participants still alive and event-free were censored on their last disease assessment date.~Participants were said to be in CR when they had the following:~M1 marrow~Peripheral blood without blasts~Absence of extramedullary leukemic involvement~Months are calculated as days from randomization date to event/censor date, divided by 30.5." (NCT02393859)
Timeframe: As of the primary analysis data cutoff date (17 July 2019), overall median follow-up time for EFS was 22.4 months.

Interventionmonths (Median)
HC3 Chemotherapy7.4
BlinatumomabNA

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Number of Participants With Anti-Blinatumomab Antibodies Postbaseline (Blinatumomab Arm Only)

"Participants receiving blinatumomab had blood samples analyzed for binding antibodies. Samples testing positive for binding antibodies were also tested for neutralizing antibodies.~Participants who were binding antibody-positive or neutralizing antibody-positive post-baseline with a negative or no result at baseline are presented." (NCT02393859)
Timeframe: Day 1 to Day 29.

Interventionparticipants (Number)
Binding Antibody PositiveNeutralizing Antibody Positive
Blinatumomab00

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Number of Participants With Shifts From Baseline Grade 0 or 1 to Worst Postbaseline Grade 3 or 4 Clinical Chemistry and Hematology Values

Severity was graded according to the CTCAE version 4.03: 1=mild, 2=moderate, 3=severe, 4=life-threatening, 5=death. Increases (↑) or decreases (↓) in laboratory value grades (Gr) from baseline (BL) to worst postbaseline (→ PB) grade are presented. NA=not available. (NCT02393859)
Timeframe: Up to Day 29 (± 2 days).

,
Interventionparticipants (Number)
Potassium ↑ BL Gr 0 → PB Gr 3Potassium ↓ BL Gr 0 → PB Gr 3Potassium ↓ BL Gr 0 → PB Gr 4Albumin ↓ BL Gr 0 → PB Gr 3Calcium ↓ BL Gr 0 → PB Gr 4Alanine Aminotransferase ↑ BL Gr 0 → PB Gr 3Alanine Aminotransferase ↑ BL Gr 1 → PB Gr 3Aspartate Aminotransferase ↑ BL Gr NA → PB Gr 3Aspartate Aminotransferase ↑ BL Gr 0 → PB Gr 3Aspartate Aminotransferase ↑ BL Gr 1 → PB Gr 3Aspartate Aminotransferase ↑ BL Gr 1 → PB Gr 4Gamma-Glutamyl Transferase ↑ BL Gr NA → PB Gr 3Gamma-Glutamyl Transferase ↑ BL Gr 0 → PB Gr 3Gamma-Glutamyl Transferase ↑ BL Gr 1 → PB Gr 3Gamma-Glutamyl Transferase ↑ BL Gr 1 → PB Gr 4Amylase ↑ BL Gr 0 → PB Gr 3Amylase ↑ BL Gr 0 → PB Gr 4Amylase ↑ BL Gr 1 → PB Gr 3Lipase ↑ BL Gr 0 → PB Gr 3Lipase ↑ BL Gr 0 → PB Gr 4Bilirubin ↑ BL Gr 0 → PB Gr 3Bilirubin ↑ BL Gr 0 → PB Gr 4Creatinine ↑ BL Gr NA → PB Gr 3Hemoglobin ↓ BL Gr 0 → PB Gr 3Hemoglobin ↓ BL Gr 1 → PB Gr 3Platelets ↓ BL Gr 0 → PB Gr 3Platelets ↓ BL Gr 0 → PB Gr 4Platelets ↓ BL Gr 1 → PB Gr 3Platelets ↓ BL Gr 1 → PB Gr 4Leukocytes ↓ BL Gr 0 → PB Gr 3Leukocytes ↓ BL Gr 0 → PB Gr 4Leukocytes ↓ BL Gr 1 → PB Gr 3Leukocytes ↓ BL Gr 1 → PB Gr 4Neutrophils ↓ BL Gr 0 → PB Gr 3Neutrophils ↓ BL Gr 0 → PB Gr 4Lymphocytes ↑ BL Gr 0 → PB Gr 3Lymphocytes ↓ BL Gr 0 → PB Gr 3Lymphocytes ↓ BL Gr 0 → PB Gr 4Lymphocytes ↓ BL Gr 1 → PB Gr 3Lymphocytes ↓ BL Gr 1 → PB Gr 4
Blinatumomab15111050010142310122102016622004111313112
HC3 Chemotherapy041011912510360110312101471318244742301101

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Number of Participants With TEAEs of Interest

TEAEs of interest included capillary leak syndrome (CLS), cytokine release syndrome (CRS), decreased immunoglobulins (DI), elevated liver enzymes (ELE), embolic and thrombotic events (ETE), infections (INF), infusion reactions without considering duration (IRWCD), medication errors (ME), neurologic events (NE), neutropenia and febrile neutropenia (NFN), pancreatitis (PNC), tumor lysis syndrome, leukoencephalopathy, immunogenicity. Severity was graded according to the CTCAE version 4.03: 1=mild, 2=moderate, 3=severe, 4=life-threatening, 5=death. (NCT02393859)
Timeframe: From first dose of IP through the last dose of IP (up to Day 29) plus 30 days.

,
Interventionparticipants (Number)
CLS EventsCLS Events Grade ≥ 3Serious CLS EventsFatal CLS EventsCLS Events Leading to Discontinuation of IPCLS Events Leading to Interruption of IPCRS EventsCRS Events Grade ≥ 3Serious CRS EventsFatal CRS EventsCRS Events Leading to Discontinuation of IPCRS Events Leading to Interruption of IPDI EventsDI Events Grade ≥ 3Serious DI EventsFatal DI EventsDI Events Leading to Discontinuation of IPDI Events Leading to Interruption of IPELE EventsELE Events Grade ≥ 3Serious ELE EventsFatal ELE EventsELE Events Leading to Discontinuation of IPELE Events Leading to Interruption of IPETE EventsETE Events Grade ≥ 3Serious ETE EventsFatal ETE EventsETE Events Leading to Discontinuation of IPETE Events Leading to Interruption of IPINF EventsINF Events Grade ≥ 3Serious INF EventsFatal INF EventsIFN Events Leading to Discontinuation of IPIFN Events Leading to Interruption of IPIRWCD EventsIRWCD Events Grade ≥ 3Serious IRWCD EventsFatal IRWCD EventsIRWCD Events Leading to Discontinuation of IPIRWCD Events Leading to Interruption of IPME EventsME Events Grade ≥ 3Serious ME EventsFatal ME EventsME Events Leading to Discontinuation of IPME Events Leading to Interruption of IPNE EventsNE Events Grade ≥ 3Serious NE EventsFatal NE EventsNE Events Leading to Discontinuation of IPNE Events Leading to Interruption of IPNFN EventsNFN Events Grade ≥ 3Serious NFN EventsFatal NFN EventsNFN Events Leading to Discontinuation of IPNFN Events Leading to Interruption of IPPNC EventsPNC Events Grade ≥ 3Serious PNC EventsFatal PNC EventsPNC Events Leading to Discontinuation of IPPNC Events Leading to Interruption of IPTumour Lysis Syndrome EventsLeukoencephalopathy EventsImmunogenicity Events
Blinatumomab000000200000911000730000420000251140003721000101001263502312110000000000000
HC3 Chemotherapy111000100000610000159100000000018660004000000000001511001282712000111000000

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Percentage of Participants With an MRD Response Within 29 Days of Treatment Initiation

"At the end of the first treatment cycle (Day 29) a bone marrow aspiration/biopsy was performed and evaluated by the central MRD laboratory.~MRD response was defined as MRD level < 10^-4, by polymerase chain reaction (PCR) or flow cytometry, at the end of treatment (Cycle 1 Day 29) with study drug. Participants who were part of the MRD Evaluable Set and were missing the end of treatment (Cycle 1 Day 29) assessment for a respective MRD assessment method were considered not to have achieved a response." (NCT02393859)
Timeframe: Up to End of Treatment (Cycle 1, Day 29)

,
Interventionpercentage of participants (Number)
MRD Response by PCRMRD Response by Flow Cytometry
Blinatumomab93.992.6
HC3 Chemotherapy53.160.0

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Pharmacokinetics: Clearance (CL) (Blinatumomab Arm Only)

(NCT02393859)
Timeframe: Day 1: at least 10 hours after infusion start and up to 24 hours; Day 15

InterventionL/hr/m^2 (Mean)
Blinatumomab1.14

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Kaplan-Meier Estimate of 100-Day Mortality After Allogeneic Hematopoietic Stem Cell Transplantation (alloHSCT)

"The analysis of 100-day mortality after alloHSCT was assessed for participants who received an alloHSCT while in remission and did not receive any additional anti-leukemic treatment. 100-day mortality after alloHSCT was calculated relative to the date of alloHSCT.~The 100-day mortality rate after alloHSCT was defined as the percentage of participants having died up to 100 days after alloHSCT, estimated using the estimated time to death in percent calculated by Kaplan-Meier methods. Participants still alive were censored at the date they were last known to be alive." (NCT02393859)
Timeframe: From the date of alloHSCT until death/censor date; median follow up time was 1742.0 days for blinatumomab and 1619.0 days for HC3.

Interventionpercentage of participants (Number)
HC3 Chemotherapy5.1
Blinatumomab3.9

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Kaplan Meier Estimate: Overall Survival (OS)

"OS was calculated from time of randomization until death due to any cause. Participants still alive were censored at the date they were last known to be alive.~Months were calculated as days from randomization date to event/censor date, divided by 30.5." (NCT02393859)
Timeframe: At final analysis, overall median follow-up time for OS was 55.2 months.

Interventionmonths (Median)
HC3 Chemotherapy25.6
BlinatumomabNA

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Kaplan Meier Estimate: EFS (Final Analysis)

"EFS is calculated from the time of randomization until the date of relapse or M2 marrow after having achieved a CR, failure to achieve a CR at the end of treatment, second malignancy, or death due to any cause, whichever occurs first. Participants who failed to achieve a CR following treatment with IP or who died before the disease assessment at the end of treatment were considered treatment failures and assigned an EFS duration of 1 day. Participants still alive and event-free were censored on their last disease assessment date.~Participants were said to be in CR when they had the following:~M1 marrow~Peripheral blood without blasts~Absence of extramedullary leukemic involvement~Months are calculated as days from randomization date to event/censor date, divided by 30.5." (NCT02393859)
Timeframe: At final analysis, overall median follow-up time for EFS was 51.9 months.

Interventionmonths (Median)
HC3 Chemotherapy7.8
BlinatumomabNA

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Cumulative Incidence of Relapse (CIR)

"CIR estimate, presented as median months to relapse, calculated from date of achievement of first CR, using the cumulative incidence method (Fine JP, Gray RJ:1999). Deaths prior to relapse not considered related to an otherwise undocumented relapse were treated as a competing risk. Participants still alive without a date of relapse were censored at the time of last follow-up.~Relapse=presence of ≥1 of the following:~isolated bone marrow relapse (M3 marrow [representative bone marrow aspirate or biopsy with ≥25% blasts] in the absence of extramedullary involvement)~combined bone marrow relapse (M2 [representative bone marrow aspirate or biopsy with ≥5% and <25% blasts] or M3 marrow and ≥1 extramedullary manifestation of acute lymphoblastic leukemia)~central nervous system extramedullary relapse~testicular extramedullary relapse~extramedullary relapse at other sites~Months were calculated as days from randomization to event/censor date, divided by 30.5." (NCT02393859)
Timeframe: At final analysis, the overall maximum follow-up time was 82.0 months.

Interventionmonths (Median)
HC3 Chemotherapy7.9
BlinatumomabNA

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Cohorts 1, 2A, 2B, 3A and 3B: Number of Participants With Treatment-emergent Adverse Events (TEAEs) and Serious Adverse Events (SAEs)

Number of participants with TEAEs (serious and non-serious adverse events) and SAEs were reported based on their safety assessments of hematology, clinical chemistry, proximal tibial growth, fecal occult blood, physical examinations, regular measurement of vital signs and electrocardiogram parameter values. (NCT02432274)
Timeframe: From the date of first dose of study drug up to 30 days after the last dose (up to approximately 7 years)

,,,,,,,
InterventionParticipants (Count of Participants)
TEAEsSAEs
Cohort 1, Single-agent Dose-finding: Lenvatinib 11 mg/m^253
Cohort 1, Single-agent Dose-finding: Lenvatinib 14 mg/m^2117
Cohort 1, Single-agent Dose-finding: Lenvatinib 17 mg/m^275
Cohort 2A, Single-agent Expansion, DTC: Lenvatinib 14 mg/m^211
Cohort 3A, Combination Dose-finding: Lenvatinib 11 mg/m^2117
Cohort 3A, Combination Dose-finding: Lenvatinib 14 mg/m^2119
Cohort 3B, Combination Expansion: Lenvatinib 14 mg/m^22016
Cohort2B,Single-agentExpansion,Osteosarcoma:Lenvatinib14mg/m^22921

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Cohorts 1, 2A, 2B, 3A, and 3B: Number of Participants With Shift From Baseline to Worst Post Baseline Measurements on Urine DipStick for Proteinuria

"An aliquot of the urine samples were collected to analyze protein by dipstick method, microscopic examination (if protein was abnormal). The dipstick test gives results in a semi-quantitative manner and results for urinalysis parameters of urine protein can be read as negative, Trace, plus (+) 1, +2, +3 and +4 indicating proportional concentrations in the urine sample. The plus sign increases with a higher level of proteins in the urine." (NCT02432274)
Timeframe: Baseline up to approximately 4 years 7 months

,,,,,,,
InterventionParticipants (Count of Participants)
Baseline: Trace, Worst Post baseline: NegativeBaseline: Trace, Worst Post baseline: TraceBaseline: +1, Worst Post baseline: NegativeBaseline: +1, Worst Post baseline: +1Baseline: Negative, Worst Post baseline: NegativeBaseline: +2, Worst Post baseline: NegativeBaseline: +3, Worst Post baseline: NegativeBaseline: +3, Worst Post baseline: +1Baseline: +3, Worst Post baseline: +2Baseline: +3, Worst Post baseline: TraceBaseline: +4, Worst Post baseline: TraceBaseline: +4, Worst Post baseline: +1Baseline: Negative, Worst Post baseline: TraceBaseline: Negative, Worst Post baseline: +1Baseline: Negative, Worst Post baseline: +2Baseline: Negative, Worst Post baseline: +3Baseline: Trace, Worst Post baseline: +1Baseline: Trace, Worst Post baseline: +2Baseline: Trace, Worst Post baseline: +3Baseline: +1, Worst Post baseline: TraceBaseline: +1, Worst Post baseline: +2Baseline: +1, Worst Post baseline: +3Baseline: Negative, Worst Post baseline: +4Baseline: +1, Worst Post baseline: +4
Cohort 1, Single-agent Dose-finding: Lenvatinib 11 mg/m^2212000000000000000000000
Cohort 1, Single-agent Dose-finding: Lenvatinib 14 mg/m^2203012111000000000000000
Cohort 1, Single-agent Dose-finding: Lenvatinib 17 mg/m^2001100110111000000000000
Cohort 2A, Single-agent Expansion, DTC: Lenvatinib 14 mg/m^2000010000000000000000000
Cohort 3A, Combination Dose-finding: Lenvatinib 11 mg/m^2000000000000071110000100
Cohort 3A, Combination Dose-finding: Lenvatinib 14 mg/m^2010040000000111200000010
Cohort 3B, Combination Expansion: Lenvatinib 14 mg/m^2010020000000316201101011
Cohort2B,Single-agentExpansion,Osteosarcoma:Lenvatinib14mg/m^2010041000001571121113100

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Cohorts 1, 2A, 2B, 3A, and 3B: Plasma Concentrations of Lenvatinib

Duration of each cycle for Cohorts 1, 2A, 2B is 28 days. Duration of each cycle for Cohorts 3A, 3B is 21 days. (NCT02432274)
Timeframe: Cohorts 1, 2A, 2B: Cycle(C)1 Day(D)1: 0.5-4 hours (h), 6-10 h post-dose, C1D15: pre-dose, 0.5-4 h, 6-10 h post-dose, C2D1: pre-dose, 2-12 h post-dose; Cohorts 3A, 3B: C1D1: 0.5-4 h, 6-10 h post-dose, C2D1: pre-dose, 2-12 h post-dose

,,
Interventionnanogram per milliliter (ng/mL) (Mean)
Cycle 1 Day 1: 0.5-4 hoursCycle 1 Day 1: 6-10 hoursCycle 2 Day 1: Pre-doseCycle 2 Day 1: 2-12 hours
Cohort 3A, Combination Dose-finding: Lenvatinib 11 mg/m^2105.2191.951.7205.6
Cohort 3A, Combination Dose-finding: Lenvatinib 14 mg/m^2111.4148.576.1237.4
Cohort 3B, Combination Expansion: Lenvatinib 14 mg/m^2209.7164.850.4275.3

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Cohorts 1, 2A, 2B, 3A, and 3B: Plasma Concentrations of Lenvatinib

Duration of each cycle for Cohorts 1, 2A, 2B is 28 days. Duration of each cycle for Cohorts 3A, 3B is 21 days. (NCT02432274)
Timeframe: Cohorts 1, 2A, 2B: Cycle(C)1 Day(D)1: 0.5-4 hours (h), 6-10 h post-dose, C1D15: pre-dose, 0.5-4 h, 6-10 h post-dose, C2D1: pre-dose, 2-12 h post-dose; Cohorts 3A, 3B: C1D1: 0.5-4 h, 6-10 h post-dose, C2D1: pre-dose, 2-12 h post-dose

,,,,
Interventionnanogram per milliliter (ng/mL) (Mean)
Cycle 1 Day 1: 0.5-4 hoursCycle 1 Day 1: 6-10 hoursCycle 1 Day 15: Pre-doseCycle 1 Day 15: 0.5-4 hoursCycle 1 Day 15: 6-10 hoursCycle 2 Day 1: Pre-doseCycle 2 Day 1: 2-12 hours
Cohort 1, Single-agent Dose-finding: Lenvatinib 11 mg/m^2295.6212.746.9133.4351.858.1502.4
Cohort 1, Single-agent Dose-finding: Lenvatinib 14 mg/m^2134.8281.959.1226.6375.861.6440.7
Cohort 1, Single-agent Dose-finding: Lenvatinib 17 mg/m^252.5238.096.9191.8413.097.9339.2
Cohort 2A, Single-agent Expansion, DTC: Lenvatinib 14 mg/m^211.118856.212424759.8102
Cohort2B,Single-agentExpansion,Osteosarcoma:Lenvatinib14mg/m^2177.4289.467.0168.3322.966.8382.4

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Cohorts 1, 2B, 3A, and 3B: Number of Participants With Best Overall Response (BOR)

BOR: best response of CR or PR for >4 weeks or SD for >=7 weeks from first dose, recorded from start of treatment until PD or death, whichever occurred first based on RECIST v1.1. CR: disappearance of all target and non-target lesions (non-lymph nodes). All pathological lymph nodes (whether target or non-target) must have reduction in their short axis <10 mm. PR: at least 30% decrease in SOD of target lesions, taking as reference the baseline sum diameters. SD: neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD, taking as reference the smallest SOD. PD was defined as: at least 20% increase (including an absolute increase of at least 5 mm) in the SOD of target lesions, taking as reference the smallest sum and/or unequivocal progression of existing non-target lesions and/or appearance of 1 or more new lesions. Not evaluable (NE) means BOR of NE or SD of <7 weeks duration. Unknown means no data were available on the case report form. (NCT02432274)
Timeframe: From date of first dose of study drug until PD or death, whichever occurred first (Cohort 1, Cohort 2B: until the data cut-off date, 31 May 2019; Cohort 3A, Cohort 3B: until the data cut-off date, 18 July 2019)

,,,,,,
InterventionParticipants (Count of Participants)
Complete ResponsePartial ResponseStable DiseaseProgressive DiseaseNot Evaluable or Unknown
Cohort 1, Single-agent Dose-finding: Lenvatinib 11 mg/m^200210
Cohort 1, Single-agent Dose-finding: Lenvatinib 14 mg/m^200522
Cohort 1, Single-agent Dose-finding: Lenvatinib 17 mg/m^200442
Cohort 3A, Combination Dose-finding: Lenvatinib 11 mg/m^202320
Cohort 3A, Combination Dose-finding: Lenvatinib 14 mg/m^2001022
Cohort 3B, Combination Expansion: Lenvatinib 14 mg/m^203942
Cohort2B,Single-agentExpansion,Osteosarcoma:Lenvatinib14mg/m^20213123

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Cohorts 1, 2A, 2B, 3A and 3B: Overall Survival (OS)

OS was defined as the time from the date of the first dose of study drug until the date of death from any cause. Participants who are lost to follow-up and those who are alive at the date of data cutoff were censored at the date the participant was last known to be alive (or the data cutoff date). 95% CI of median were calculated according to Brookmeyer and Crowley method. (NCT02432274)
Timeframe: From first dose of study drug until death (Cohort 1, Cohort 2A, Cohort 2B: until the data cut-off date, 31 May 2019; Cohort 3A, Cohort 3B: until the data cut-off date, 18 July 2019)

Interventionmonths (Median)
Cohort 1, Single-agent Dose-finding: Lenvatinib 11 mg/m^28.1
Cohort 1, Single-agent Dose-finding: Lenvatinib 14 mg/m^27.4
Cohort 1, Single-agent Dose-finding: Lenvatinib 17 mg/m^27.7
Cohort 2A, Single-agent Expansion, DTC: Lenvatinib 14 mg/m^26.1
Cohort2B,Single-agentExpansion,Osteosarcoma:Lenvatinib14mg/m^210.0
Cohort 3A, Combination Dose-finding: Lenvatinib 11 mg/m^213.6
Cohort 3A, Combination Dose-finding: Lenvatinib 14 mg/m^2NA
Cohort 3B, Combination Expansion: Lenvatinib 14 mg/m^2NA

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Cohort 2B, 3B: Percent Change From Baseline in Serum Biomarkers Level

"Serum biomarkers included Fibroblast Growth Factor (FGF) 19, FGF 21, Vascular Endothelial Growth Factor (VEGF). In this outcome measure, percent change from baseline in serum biomarkers level per PFS-4, Yes and PFS-4, No have been reported. As per assessment of investigator based on RECIST v1.1, PFS-4, Yes= participants evaluable for PFS-4 month and alive and without PD at 4 months from the first dose, PFS-4, No=participants evaluable for PFS-4 month and not alive or with PD at 4 months from the first dose." (NCT02432274)
Timeframe: Cohort 2B: Baseline, Cycle 2-3 Day 1 (Duration of each cycle=28 days); Cohort 3B: Baseline, Cycle 2 Day 1, Cycle 4 Day 1 (Duration of each cycle=21 days)

Interventionpercent change (Mean)
C2D1: FGF 19 (PFS-4, Yes)C2D1: FGF 19 (PFS-4, No)C3D1: FGF 19 (PFS-4, Yes)C3D1: FGF 19 (PFS-4, No)C2D1: FGF 21 (PFS-4, Yes)C2D1: FGF 21 (PFS-4, No)C3D1: FGF 21 (PFS-4, Yes)C3D1: FGF 21 (PFS-4, No)C2D1: VEGF (PFS-4, Yes)C2D1: VEGF (PFS-4, No)C3D1: VEGF (PFS-4, Yes)C3D1: VEGF (PFS-4, No)
Cohort2B,Single-agentExpansion,Osteosarcoma:Lenvatinib14mg/m^248.7109.947.3194.5-14.9134.355.017.0119.9124.264.323.2

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Cohorts 1, 2A, 2B, 3A and 3B: Number of Participants Who Experienced Disease Control

Participants were defined as having disease control if they had a BOR of CR or PR for >4 weeks, or SD (minimum duration from first dose to SD >=7 weeks) or if participants had a BOR of CR or Non-CR/Non-PD (minimum duration from first dose to Non-CR/Non-PD >=7 weeks) per RECIST v1.1, recorded from first dose until PD or death whichever occurred first. CR: disappearance of all target/non-target lesions (non-lymph nodes). All pathological lymph nodes (target/non-target) must have a reduction in their short axis <10 mm. PR: at least a 30% decrease in the SOD of target lesions, taking as reference the baseline sum diameters. SD: neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD, taking as reference smallest SOD. Non-CR/Non-PD: persistence of 1 or more non-target lesions, maintenance of tumor marker level above the normal limits. (NCT02432274)
Timeframe: From first dose of study drug until PD or death, whichever occurred first (Cohort 1, Cohort 2A, Cohort 2B: until the data cut-off date, 31 May 2019; Cohort 3A, Cohort 3B: until the data cut-off date, 18 July 2019)

InterventionParticipants (Count of Participants)
Cohort 1, Single-agent Dose-finding: Lenvatinib 11 mg/m^22
Cohort 1, Single-agent Dose-finding: Lenvatinib 14 mg/m^25
Cohort 1, Single-agent Dose-finding: Lenvatinib 17 mg/m^25
Cohort 2A, Single-agent Expansion, DTC: Lenvatinib 14 mg/m^21
Cohort2B,Single-agentExpansion,Osteosarcoma:Lenvatinib14mg/m^216
Cohort 3A, Combination Dose-finding: Lenvatinib 11 mg/m^25
Cohort 3A, Combination Dose-finding: Lenvatinib 14 mg/m^211
Cohort 3B, Combination Expansion: Lenvatinib 14 mg/m^214

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Cohorts 1, 2A, 2B, 3A and 3B: Number of Participants Experienced Clinical Benefit

Participants were defined as having clinical benefit if they had a BOR of CR or PR for >4 weeks or durable SD (lasting >=23 weeks) or if participants had a BOR of CR or durable Non-CR/Non-PD (lasting >=23 weeks) as per RECIST v1.1, recorded from first dose until PD or death whichever occurred first. CR: disappearance of all target/non-target lesions (non-lymph nodes). All pathological lymph nodes (whether target/non-target) must have a reduction in their short axis <10 mm. PR: at least a 30% decrease in the SOD of target lesions, taking as reference the baseline sum diameters. SD: neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD, taking as reference the smallest SOD. Non-CR/Non-PD:persistence of 1 or more non-target lesions and maintenance of tumor marker level above the normal limits. (NCT02432274)
Timeframe: From first dose of study drug until PD or death, whichever occurred first (Cohort 1, Cohort 2A, Cohort 2B: until the data cut-off date, 31 May 2019; Cohort 3A, Cohort 3B: until the data cut-off date, 18 July 2019)

InterventionParticipants (Count of Participants)
Cohort 1, Single-agent Dose-finding: Lenvatinib 11 mg/m^20
Cohort 1, Single-agent Dose-finding: Lenvatinib 14 mg/m^23
Cohort 1, Single-agent Dose-finding: Lenvatinib 17 mg/m^24
Cohort 2A, Single-agent Expansion, DTC: Lenvatinib 14 mg/m^21
Cohort2B,Single-agentExpansion,Osteosarcoma:Lenvatinib14mg/m^27
Cohort 3A, Combination Dose-finding: Lenvatinib 11 mg/m^24
Cohort 3A, Combination Dose-finding: Lenvatinib 14 mg/m^25
Cohort 3B, Combination Expansion: Lenvatinib 14 mg/m^28

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Cohorts 1, 2A, 2B, 3A and 3B: Duration of Response (DOR)

DOR was defined as time in months from the first documentation confirmed CR or PR until the first documentation of confirmed PD as assessed by investigator based on RECIST v1.1. CR: disappearance of all target and non-target lesions (non-lymph nodes). All pathological lymph nodes (whether target or non-target) must have a reduction in their short axis <10 mm. PR: at least a 30% decrease in the SOD of target lesions, taking as reference the baseline sum diameters. PD: at least 20% increase (including an absolute increase of at least 5 mm) in the SOD of target lesions, taking as reference the smallest sum and/or unequivocal progression of existing non-target lesions and/or appearance of 1 or more new lesions. 95% CI for the median were calculated according to Brookmeyer and Crowley method. (NCT02432274)
Timeframe: First documentation of CR/PR until first documentation of PD (Cohort 1, Cohort 2A, Cohort 2B: until the data cut-off date, 31 May 2019; Cohort 3A, Cohort 3B: until the data cut-off date, 18 July 2019)

Interventionmonths (Median)
Cohort 2A, Single-agent Expansion, DTC: Lenvatinib 14 mg/m^21.9
Cohort2B,Single-agentExpansion,Osteosarcoma:Lenvatinib14mg/m^24.6
Cohort 3A, Combination Dose-finding: Lenvatinib 11 mg/m^2NA
Cohort 3B, Combination Expansion: Lenvatinib 14 mg/m^2NA

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Cohort 2A: Number of Participants With Objective Response (OR) of Complete Response (CR) or Partial Response (PR)

OR was defined as participants with best overall response (BOR) of CR or PR as assessed by investigator based on response evaluation criteria in solid tumors (RECIST) version (v) 1.1. For OR, the BOR was defined as the best response (CR or PR for >4 weeks) recorded from the start of the treatment until PD or death whichever occurred first. CR was defined as the disappearance of all target and non-target lesions (non-lymph nodes). All pathological lymph nodes (whether target or non-target) must have a reduction in their short axis <10 millimeters (mm). PR was defined as at least a 30% decrease in the sum of diameter (SOD) of target lesions, taking as reference the baseline sum diameters. PD was defined as at least 20% increase (including an absolute increase of at least 5 mm) in the SOD of target lesions, taking as reference the smallest sum and/or unequivocal progression of existing non-target lesions and/or appearance of 1 or more new lesions. (NCT02432274)
Timeframe: From date of first dose of study drug until first documentation of PD or death, whichever occurred first (until the data cut-off date, 31 May 2019)

InterventionParticipants (Count of Participants)
Cohort 2A, Single-agent Expansion, DTC: Lenvatinib 14 mg/m^21

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Cohorts 1, 2A, 2B, 3A and 3B: Progression-free Survival (PFS)

PFS was defined as the time (in months) from the date of first dose of study drug to the date of first documentation of PD or date of death, whichever occurred first, based on RECIST v1.1. PD was defined as at least a 20% increase in the SOD of target lesions, taking as reference the baseline SOD of target lesions. 95% CI of median were calculated according to Brookmeyer and Crowley method. (NCT02432274)
Timeframe: From first dose of study drug until PD or death, whichever occurred first (Cohort 1, Cohort 2A, Cohort 2B: until the data cut-off date, 31 May 2019; Cohort 3A, Cohort 3B: until the data cut-off date, 18 July 2019)

Interventionmonths (Median)
Cohort 1, Single-agent Dose-finding: Lenvatinib 11 mg/m^23.7
Cohort 1, Single-agent Dose-finding: Lenvatinib 14 mg/m^26.3
Cohort 1, Single-agent Dose-finding: Lenvatinib 17 mg/m^25.5
Cohort 2A, Single-agent Expansion, DTC: Lenvatinib 14 mg/m^25.5
Cohort2B,Single-agentExpansion,Osteosarcoma:Lenvatinib14mg/m^23.0
Cohort 3A, Combination Dose-finding: Lenvatinib 11 mg/m^27.1
Cohort 3A, Combination Dose-finding: Lenvatinib 14 mg/m^212.0
Cohort 3B, Combination Expansion: Lenvatinib 14 mg/m^26.9

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Cohorts 1, 2A, 2B, 3A and 3B: Time to Progression (TTP)

TTP was defined as the time from the date of first dose of study drug to the date of first documentation of PD based on RECIST 1.1. PD was defined as at least a 20% increase (including an absolute increase of at least 5 mm) in the SOD of target lesions, taking as reference the baseline SOD of target lesions. 95% CI of median were calculated according to Brookmeyer and Crowley method. (NCT02432274)
Timeframe: From first dose of study drug until PD (Cohort 1, Cohort 2A, Cohort 2B: until the data cut-off date, 31 May 2019; Cohort 3A, Cohort 3B: until the data cut-off date, 18 July 2019)

Interventionmonths (Median)
Cohort 1, Single-agent Dose-finding: Lenvatinib 11 mg/m^23.7
Cohort 1, Single-agent Dose-finding: Lenvatinib 14 mg/m^26.3
Cohort 1, Single-agent Dose-finding: Lenvatinib 17 mg/m^25.5
Cohort 2A, Single-agent Expansion, DTC: Lenvatinib 14 mg/m^25.5
Cohort2B,Single-agentExpansion,Osteosarcoma:Lenvatinib14mg/m^23.0
Cohort 3A, Combination Dose-finding: Lenvatinib 11 mg/m^27.1
Cohort 3A, Combination Dose-finding: Lenvatinib 14 mg/m^212.0
Cohort 3B, Combination Expansion: Lenvatinib 14 mg/m^26.9

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Cohorts 1, 2B, 3A, and 3B: Objective Response Rate (ORR)

ORR was defined as the percentage of participants with a BOR of CR or PR for >4 weeks or SD for >=7 weeks as assessed by investigator based on RECIST v1.1, recorded from start of study treatment until PD or death whichever occurred first. CR was defined as the disappearance of all target and non-target lesions (non-lymph nodes). All pathological lymph nodes (whether target or non-target) must have a reduction in their short axis <10 mm. PR was defined as at least a 30% decrease in the SOD of target lesions, taking as reference the baseline sum diameters. 95% CI of the ORR were calculated according to Clopper and Pearson method. (NCT02432274)
Timeframe: From date of first dose of study drug until PD or death, whichever occurred first (Cohort 1, Cohort 2B: until the data cut-off date, 31 May 2019; Cohort 3A, Cohort 3B: until the data cut-off date, 18 July 2019)

Interventionpercentage of participants (Number)
Cohort 1, Single-agent Dose-finding: Lenvatinib 11 mg/m^20
Cohort 1, Single-agent Dose-finding: Lenvatinib 14 mg/m^20
Cohort 1, Single-agent Dose-finding: Lenvatinib 17 mg/m^20
Cohort2B,Single-agentExpansion,Osteosarcoma:Lenvatinib14mg/m^26.7
Cohort 3A, Combination Dose-finding: Lenvatinib 11 mg/m^228.6
Cohort 3A, Combination Dose-finding: Lenvatinib 14 mg/m^20
Cohort 3B, Combination Expansion: Lenvatinib 14 mg/m^216.7

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Cohorts 2B and 3B: Progression-free Survival (PFS) Rate at Month 4

Progression free survival at Month 4 (PFS-4) rate was defined as the percentage of participants who were alive and without PD at Month 4 after the first dose of study drug, based on RECIST v1.1, using a binomial proportion with corresponding 95% confidence interval (CI). PD: >= 20% increase in sum of diameters of target lesions, reference-smallest sum recorded in study (sum at baseline if that was smallest). Sum of diameters must have absolute increase of >=5 mm. Appearance of >=1 new lesions also considered PD. (NCT02432274)
Timeframe: At Month 4

Interventionpercentage of participants (Number)
Cohort2B,Single-agentExpansion,Osteosarcoma:Lenvatinib14mg/m^232.1
Cohort 3B, Combination Expansion: Lenvatinib 14 mg/m^266.7

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Cohort 2A: Number of Participants With Best Overall Response (BOR)

BOR was defined as the best response of CR or PR for >4 weeks or SD for >=7 weeks recorded from the start of the treatment until PD or death, whichever occurred first based on RECIST v1.1. CR: disappearance of all target and non-target lesions (non-lymph nodes). All pathological lymph nodes (whether target or non-target) must have a reduction in their short axis <10 mm. PR: at least a 30% decrease in the SOD of target lesions, taking as reference the baseline sum diameters. SD: neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD, taking as reference the smallest SOD. PD was defined as at least 20% increase (including an absolute increase of at least 5 mm) in the SOD of target lesions, taking as reference the smallest sum and/or unequivocal progression of existing non-target lesions and/or appearance of 1 or more new lesions. (NCT02432274)
Timeframe: From first dose of study drug until PD or death, whichever occurred first (until the data cut-off date, 31 May 2019)

InterventionParticipants (Count of Participants)
Complete ResponsePartial ResponseStable Disease
Cohort 2A, Single-agent Expansion, DTC: Lenvatinib 14 mg/m^2010

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Cohort 2B, 3B: Percent Change From Baseline in Serum Biomarkers Level

"Serum biomarkers included Fibroblast Growth Factor (FGF) 19, FGF 21, Vascular Endothelial Growth Factor (VEGF). In this outcome measure, percent change from baseline in serum biomarkers level per PFS-4, Yes and PFS-4, No have been reported. As per assessment of investigator based on RECIST v1.1, PFS-4, Yes= participants evaluable for PFS-4 month and alive and without PD at 4 months from the first dose, PFS-4, No=participants evaluable for PFS-4 month and not alive or with PD at 4 months from the first dose." (NCT02432274)
Timeframe: Cohort 2B: Baseline, Cycle 2-3 Day 1 (Duration of each cycle=28 days); Cohort 3B: Baseline, Cycle 2 Day 1, Cycle 4 Day 1 (Duration of each cycle=21 days)

Interventionpercent change (Mean)
C2D1: FGF 19 (PFS-4, Yes)C2D1: FGF 19 (PFS-4, No)C4D1: FGF 19 (PFS-4, Yes)C4D1: FGF 19 (PFS-4, No)C2D1: FGF 21 (PFS-4, Yes)C2D1: FGF 21 (PFS-4, No)C4D1: FGF 21 (PFS-4, Yes)C4D1: FGF 21 (PFS-4, No)C2D1: VEGF (PFS-4, Yes)C2D1: VEGF (PFS-4, No)C4D1: VEGF (PFS-4, Yes)
Cohort 3B, Combination Expansion: Lenvatinib 14 mg/m^2172.178.3237.791.970.27.2256.2-1.587.995.884.3

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Cohorts 1, 2A, 2B, 3A and 3B: Number of Participants Categorized Based on Overall Acceptability Questionnaire Responses for Suspension of Lenvatinib

In acceptability questionnaire, participants were asked to answer the overall acceptability of lenvatinib suspension considering the following elements: taste, appearance, smell and how does it feel in the mouth. Overall acceptability was answered in terms of 7 responses: Super good, really good, good, may be good or may be bad, bad, really bad, super bad. Overall acceptability was the overall acceptance for taste, appearance, smell, and the feeling in mouth. In this measure, number of participants have been reported per their overall acceptability responses. (NCT02432274)
Timeframe: Cycle 1 Day 1 (Cycle length=28 days for Cohorts 1, 2A, 2B; Cycle length=21 days for Cohorts 3A, 3B)

,,,,,,,
InterventionParticipants (Count of Participants)
Super GoodReally GoodGoodMay be Good or May be BadBadReally BadSuper Bad
Cohort 1, Single-agent Dose-finding: Lenvatinib 11 mg/m^20000000
Cohort 1, Single-agent Dose-finding: Lenvatinib 14 mg/m^20010010
Cohort 1, Single-agent Dose-finding: Lenvatinib 17 mg/m^20000001
Cohort 2A, Single-agent Expansion, DTC: Lenvatinib 14 mg/m^20000000
Cohort 3A, Combination Dose-finding: Lenvatinib 11 mg/m^20000000
Cohort 3A, Combination Dose-finding: Lenvatinib 14 mg/m^20010000
Cohort 3B, Combination Expansion: Lenvatinib 14 mg/m^20011110
Cohort2B,Single-agentExpansion,Osteosarcoma:Lenvatinib14mg/m^20010000

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Cohorts 1, 2A, 2B, 3A and 3B: Number of Participants With Shift From Baseline to Worst Post Baseline Score in Karnofsky Performance Status (KPS) Scores

KPS: compare effectiveness of medicine for disease and assess outcomes in participants. KPS Scores: recorded on 11 point scale (0, 10, 20, 30, 40, 50, 60, 70, 80, 90 and 100%), where 0=Dead; 10=moribund, fatal processes progressing rapidly; 20=very sick, hospital admission necessary, active supportive treatment necessary; 30=severely disabled, hospital admission is indicated although death not imminent; 40=disabled, requires special care/assistance; 50=requires considerable assistance/frequent medical care; 60=requires occasional assistance, but is able to care for personal needs; 70=cares for self, unable to carry normal activity or active work; 80=normal activity with effort, some signs of disease; 90=able to carry on normal activity, minor signs of disease; 100=normal no complaints, no evidence of disease. Lower score, worse survival for most serious illnesses. (NCT02432274)
Timeframe: Baseline up to approximately 4 years 7 months

,,,,,,,
InterventionParticipants (Count of Participants)
Baseline score: 100%, Worst Postbaseline score:80%Baseline score: 100%, Worst Postbaseline score:90%Baseline score: 70%, Worst Postbaseline score: 70%Baseline score: 90%, Worst Postbaseline score: 70%Baseline score: 80%, Worst Postbaseline score: 80%Baseline score: 90%, Worst Postbaseline score: 60%Baseline score:100%, Worst Postbaseline score:100%Baseline score: 100%, Worst Postbaseline score:70%Baseline score: 90%, Worst Postbaseline score: 80%Baseline score: 90%, Worst Postbaseline score: 90%
Cohort 1, Single-agent Dose-finding: Lenvatinib 11 mg/m^21000000000
Cohort 1, Single-agent Dose-finding: Lenvatinib 14 mg/m^20100000000
Cohort 1, Single-agent Dose-finding: Lenvatinib 17 mg/m^20000000000
Cohort 2A, Single-agent Expansion, DTC: Lenvatinib 14 mg/m^20000001000
Cohort 3A, Combination Dose-finding: Lenvatinib 11 mg/m^20100011000
Cohort 3A, Combination Dose-finding: Lenvatinib 14 mg/m^20010000000
Cohort 3B, Combination Expansion: Lenvatinib 14 mg/m^22200001211
Cohort2B,Single-agentExpansion,Osteosarcoma:Lenvatinib14mg/m^22211101013

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Cohorts 1, 2A, 2B, 3A and 3B: Number of Participants With Shift From Baseline to Worst Post Baseline Score in Lansky Performance Play Score

Lansky Performance Play Scale rates a child's activity level for <16 years of age. Scores on scale range from 0 (unresponsive) to 100 ( fully active, normal), where 100=fully active, normal; 90=minor restrictions in physically strenuous activity; 80=active, but tires more quickly; 70=both greater restriction of and less time spent in play activity; 60=up and around, but minimal active play, keeps busy with quieter activities; 50=gets dressed, but lies around much of day, no active play, able to participant in quiet play and activities; 40=mostly in bed, participates in quiet activities; 30=in bed, needs assistance even for quiet play; 20=often sleeping, play entirely limited to very passive activities; 10=no play, does not get out of bed; 0=unresponsive. Higher score indicates more activity and lower indicates less or no activity. (NCT02432274)
Timeframe: Baseline up to approximately 4 years 7 months

,,,,,,,
InterventionParticipants (Count of Participants)
Baseline score:100%, Worst Postbaseline score:90%Baseline score: 70%, Worst Postbaseline score: 60%Baseline score: 80%, Worst Postbaseline score: 60%Baseline score: 100%, Worst Postbaseline score:60%Baseline score: 80%, Worst Postbaseline score: 70%Baseline score: 90%, Worst Postbaseline score: 70%Baseline score: 90%, Worst Postbaseline score: 80%Baseline score:100%, Worst Postbaseline score:100%Baseline score: 80%, Worst Postbaseline score: 40%Baseline score: 70%, Worst Postbaseline score: 80%Baseline score: 80%, Worst Postbaseline score: 80%Baseline score: 100%, Worst Postbaseline score:80%Baseline score: 90%, Worst Postbaseline score: 90%Baseline score: 60%, Worst Postbaseline score: 60%Baseline score: 90%, Worst Postbaseline score: 60%Baseline score: 70%, Worst Postbaseline score: 70%Baseline score: 90%, Worst Postbaseline score:100%Baseline score: 100%, Worst Postbaseline score:70%Baseline score: 80%, Worst Postbaseline score: 50%
Cohort 1, Single-agent Dose-finding: Lenvatinib 11 mg/m^23000000000000000000
Cohort 1, Single-agent Dose-finding: Lenvatinib 14 mg/m^20111111100000000000
Cohort 1, Single-agent Dose-finding: Lenvatinib 17 mg/m^20010001011110100000
Cohort 2A, Single-agent Expansion, DTC: Lenvatinib 14 mg/m^20000000100000000000
Cohort 3A, Combination Dose-finding: Lenvatinib 11 mg/m^21010000000210000010
Cohort 3A, Combination Dose-finding: Lenvatinib 14 mg/m^21000300001001001000
Cohort 3B, Combination Expansion: Lenvatinib 14 mg/m^20000000500202000000
Cohort2B,Single-agentExpansion,Osteosarcoma:Lenvatinib14mg/m^21010011000204111101

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Number of Patients Experiencing a Laboratory Abnormality (Grade 3-4)

"A laboratory abnormality is defined as an adverse event of grade 3 or 4 identified by a laboratory test of participant blood samples.~Adverse events were graded according to Common Terminology Criteria for Adverse Events v4.0 (CTCAE)." (NCT02441309)
Timeframe: Up to 42 weeks

InterventionParticipants (Count of Participants)
A. Mifamurtide Only0
B. Ifosfamide (Followed by Mifamurtide)0
C. Ifosfamide + Mifamurtide0

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Number of Patients Experiencing a Grade 3 or More Severe Adverse Event (Graded According to CTCAE Criteria v4.0)

"Toxicity measured and graded according to Common Terminology Criteria for Adverse Events v4.0 (CTCAE)~Grade refers to the severity of the adverse event. The CTCAE displays Grades 1 through 5 with unique clinical descriptions of severity for each AE based on this general guideline:~Grade 1 Mild; asymptomatic or mild symptoms; clinical or diagnostic observations only; intervention not indicated.~Grade 2 Moderate; minimal, local or noninvasive intervention indicated; limiting age-appropriate instrumental activities of daily living.~Grade 3 Severe; medically significant but not immediately life-threatening; hospitalisation or prolongation of hospitalisation indicated; disabling or limiting self care activities of daily living.~Grade 4 Life-threatening consequences; urgent intervention indicated. Grade 5 Death related to AE." (NCT02441309)
Timeframe: Up to 42 weeks

InterventionParticipants (Count of Participants)
A. Mifamurtide Only1
B. Ifosfamide (Followed by Mifamurtide)2
C. Ifosfamide + Mifamurtide2

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Disease Specific Overall Survival

Median time from death attributed to the disease. Censored at last known time alive or death from other causes. (NCT02441309)
Timeframe: Up to 42 weeks

Interventionmonths (Median)
A. Mifamurtide Only0.7
B. Ifosfamide (Followed by Mifamurtide)9.2
C. Ifosfamide + Mifamurtide2.8

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Progression Free Survival

"Time from randomisation for deemed non-resectable groups, or time from registration for deemed resectable group to first event, where an event is Progressive Disease as (defined by RECIST criterion v1.1) or death due to any cause. Patients who have not had an event will be censored at their last follow-up date. Patients lost to follow-up without an event will be censored at the date of their last consultation.~Progressive disease according to RECIST v1.1 is defined as a >=20% increase in the sum of long diameters of target lesions, OR progression of non-target lesions, OR evidence of new lesions." (NCT02441309)
Timeframe: Up to 42 weeks

Interventionmonths (Median)
A. Mifamurtide OnlyNA
B. Ifosfamide (Followed by Mifamurtide)NA
C. Ifosfamide + Mifamurtide7.0

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Objective Radiological Response Based on RECIST v1.1

"Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.1) assessed by CT or MRI:~Complete Response (CR): Disappearance of all target and non-target lesions Partial Response (PR): >=30% decrease in the sum of the longest diameter of target lesions, AND no evidence of progression in non-target lesions, AND no new lesions Stable Disease (SD): sum of longest diameter of target lesions between PR and PD values, AND no evidence of progression in non-target lesions, AND no new lesions Progressive Disease (PD): >20% increase in the sum of the longest diameter of target lesions, OR evidence of progression in non-target lesions, OR evidence of new lesions" (NCT02441309)
Timeframe: Change from Baseline to after 12, 18, 24 & 36 weeks and end of treatment visit

InterventionParticipants (Count of Participants)
Week 1271950191Week 1271950192Week 1271950193Week 1871950192Week 1871950193Week 1871950191Week 2471950191Week 2471950192Week 2471950193Week 3671950191Week 3671950192Week 3671950193End of Treatment visit (prior to week 6)71950191End of Treatment visit (prior to week 6)71950192End of Treatment visit (prior to week 6)71950193
Stable Disease (SD)Progressive Disease (PD)Patient did not reach endpoint
B. Ifosfamide (Followed by Mifamurtide)1
C. Ifosfamide + Mifamurtide1
A. Mifamurtide Only3
C. Ifosfamide + Mifamurtide2
A. Mifamurtide Only0
C. Ifosfamide + Mifamurtide3
A. Mifamurtide Only2
B. Ifosfamide (Followed by Mifamurtide)0
C. Ifosfamide + Mifamurtide0

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Number of Participants With Laboratory Abnormalities

Number of participants who experienced a maximum post-baseline laboratory toxicity of Grade 3 or higher (per National Cancer Institute's Common Terminology Criteria for Adverse Events, version 4.03). (NCT02592876)
Timeframe: Up to 4 months

,
InterventionParticipants (Count of Participants)
Any Hematology TestHemoglobin LowLeukocytes HighLeukocytes LowLymphocytes HighLymphocytes LowNeutrophils LowPlatelets LowAny Chemistry TestAlanine Aminotransferase HighAspartate Aminotransferase HighCalcium HighCalcium LowCreatinine HighGlucose HighPhosphate LowPotassium LowSodium LowUrate High
19A+RICE37180240312235163202138530
RICE37191232342226183140049342

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Number of Patients Achieving Peripheral Blood Stem Cell (PBSC) Mobilization

Defined as the number of patients who are able to adequately mobilize PBSC per investigator assessment on or after completion of study treatment, prior to subsequent anticancer therapy. (NCT02592876)
Timeframe: Up to 30 months

,
InterventionParticipants (Count of Participants)
Patients with attempted stem cell collection(s)Patients with sufficient stem cell collection
19A+RICE2421
RICE2826

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Number of Patients Receiving Autologous Stem Cell Transplant (ASCT)

Number of patients receiving ASCT after completion of study treatment (EOT), prior to subsequent anticancer therapy. (NCT02592876)
Timeframe: Up to 30 months

,
InterventionParticipants (Count of Participants)
Patients planned to receive ASCT at EOTPatients who received ASCT at EOT
19A+RICE2522
RICE2825

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Objective Response Rate (ORR)

ORR is defined as the proportion of patients with complete remission (CR) or partial remission (PR) per independent review facility (IRF) at the end of treatment. (NCT02592876)
Timeframe: Up to 4 months

InterventionParticipants (Count of Participants)
RICE30
19A+RICE32

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Complete Remission Rate Per Independent Review Facility

Number of patients with complete metabolic response by PET (positive emission tomography) and CT (computed tomography) scans, or complete radiologic response by CT only. (NCT02592876)
Timeframe: Up to 4 months

InterventionParticipants (Count of Participants)
RICE18
19A+RICE25

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Duration of Complete Response (CR)

Defined as the time from the start of the first radiographic documentation of CR per investigator to the first documentation of progressive disease, death due to any cause, or receipt of subsequent anticancer therapy, whichever comes first. (NCT02592876)
Timeframe: Up to 27.9 months

Interventionmonths (Median)
RICENA
19A+RICENA

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Duration of Objective Response (OR)

Duration of OR is defined as the time from the start of the first radiographic documentation of OR per investigator to the first documentation of PD, death due to any cause, or receipt of subsequent anticancer therapy, whichever comes first. (NCT02592876)
Timeframe: Up to 27.9 months

Interventionmonths (Median)
RICENA
19A+RICENA

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Overall Survival (OS)

OS is defined as the time from date of randomization to date of death due to any cause. In the absence of confirmation of death, survival time will be censored at the last date the patient is known to be alive. (NCT02592876)
Timeframe: Up to 30 months

Interventionmonths (Median)
RICENA
19A+RICENA

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Progression-free Survival (PFS)

PFS is defined as the time from randomization to first documentation of disease progression per investigator, death due to any cause, or receipt of subsequent anticancer therapy, whichever comes first. (NCT02592876)
Timeframe: Up to 30 months

Interventionmonths (Median)
RICENA
19A+RICENA

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Number of Participants With Adverse Events (AEs)

Treatment-emergent adverse events (TEAEs) are presented and defined as newly occurring (not present at baseline) or worsening after first dose of investigational product. AE severity and seriousness are assessed independently. 'Severity' characterizes the intensity of an AE and is graded using the National Cancer Institute's Common Terminology Criteria for Adverse Events (NCI CTCAE), version 4.03. An AE is considered 'serious' if it is life-threatening, fatal, requires hospitalization, or is otherwise considered to be medically significant. (NCT02592876)
Timeframe: Up to 4 months

,
InterventionParticipants (Count of Participants)
Treatment-emergent AE (TEAE)Treatment-related AEsGrade 3 or Higher TEAEsSerious AEs (SAEs)Treatment-related SAEsAEs Leading to Dose DelayAEs Leading to Dose ReductionAEs Leading to Treatment Discontinuation
19A+RICE4040381913853
RICE393831139332

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PK: Maximum Concentration (Cmax) of Olaratumab Part B

PK: Maximum serum concentration (Cmax) data of Olaratumab was reported from available sample data. (NCT02677116)
Timeframe: Cycle 1, Day 8 and Cycle 2, Days 1 and 8: 1.25 hour (h), 2.5 h, 3.5h Postdose

Interventionmicrogram/milliliter (μg/mL) (Geometric Mean)
Cycle 1, Day 8
Olaratumab Alone (Part B)639

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PK: Maximum Concentration (Cmax) of Olaratumab Part B

PK: Maximum serum concentration (Cmax) data of Olaratumab was reported from available sample data. (NCT02677116)
Timeframe: Cycle 1, Day 8 and Cycle 2, Days 1 and 8: 1.25 hour (h), 2.5 h, 3.5h Postdose

,
Interventionmicrogram/milliliter (μg/mL) (Geometric Mean)
Cycle 2, Day 1Cycle 2, Day 8
Olaratumab +Vincristine + Irinotecan (Part B)585647
Olaratumab + Ifosfamide (Part B)629696

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PK: Maximum Concentration (Cmax) of Olaratumab Part C

Pharmacokinetics (PK): Maximum serum concentration (Cmax) data of Olaratumab was reported from available sample data. (NCT02677116)
Timeframe: Cycle 1, Days 1 and 8; Cycle 2, Days 1 and 8: 1.25 hour (h), 2.5 h, 3.5h Postdose

Interventionmicrogram/milliliter (μg/mL) (Geometric Mean)
Cycle 2, Day 8
Olaratumab + Doxorubicin (Part C)502

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PK: Maximum Concentration (Cmax) of Olaratumab Part C

Pharmacokinetics (PK): Maximum serum concentration (Cmax) data of Olaratumab was reported from available sample data. (NCT02677116)
Timeframe: Cycle 1, Days 1 and 8; Cycle 2, Days 1 and 8: 1.25 hour (h), 2.5 h, 3.5h Postdose

Interventionmicrogram/milliliter (μg/mL) (Geometric Mean)
Cycle 1, Day 1Cycle 1, Day 8
Olaratumab + Doxorubicin Cycle 1 (Part C)406493

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PK: Maximum Concentration (Cmax) of Olaratumab Part C

Pharmacokinetics (PK): Maximum serum concentration (Cmax) data of Olaratumab was reported from available sample data. (NCT02677116)
Timeframe: Cycle 1, Days 1 and 8; Cycle 2, Days 1 and 8: 1.25 hour (h), 2.5 h, 3.5h Postdose

,
Interventionmicrogram/milliliter (μg/mL) (Geometric Mean)
Cycle 1, Day 1Cycle 1, Day 8Cycle 2, Day 8
Olaratumab + Ifosfamide (Part C)363498567
Olaratumab + Vincristine + Irinotecan (Part C)548695707

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PK: Trough Serum Minimum Concentration (Cmin) of Olaratumab Part A

PK: Trough serum concentration (Cmin) of Olaratumab was reported. A sample was collected every other cycle from cycles 1, 2, 3-25. (NCT02677116)
Timeframe: Cycles 1, 2, 3-25; Day 8: 336 Hours Postdose

Interventionμg/mL (Geometric Mean)
Cycle 1, Day 8
Olaratumab Alone (Part A)73

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PK: Trough Serum Minimum Concentration (Cmin) of Olaratumab Part A

PK: Trough serum concentration (Cmin) of Olaratumab was reported. A sample was collected every other cycle from cycles 1, 2, 3-25. (NCT02677116)
Timeframe: Cycles 1, 2, 3-25; Day 8: 336 Hours Postdose

Interventionμg/mL (Geometric Mean)
Cycle 2, Day 8Cycle 3-25, Day 8
Olaratumab + Doxorubicin (Part A)38.594.4

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PK: Trough Serum Minimum Concentration (Cmin) of Olaratumab Part A

PK: Trough serum concentration (Cmin) of Olaratumab was reported. A sample was collected every other cycle from cycles 1, 2, 3-25. (NCT02677116)
Timeframe: Cycles 1, 2, 3-25; Day 8: 336 Hours Postdose

,
Interventionμg/mL (Geometric Mean)
Cycle 1, Day 8Cycle 2, Day 8Cycle 3-25, Day 8
Olaratumab + Ifosfamide (Part A)46.311488.2
Olaratumab + Vincristine + Irinotecan (Part A)97.837.795.1

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PK: Trough Serum Minimum Concentration (Cmin) of Olaratumab Part B

PK: Trough serum concentration (Cmin) of Olaratumab was reported. A sample was collected every other cycle from cycles 1, 2, 3-25. (NCT02677116)
Timeframe: Cycles 1, 2, 3-25; Day 8: 336 Hours Postdose

,
Interventionμg/mL (Geometric Mean)
Cycle 1, Day 8Cycle 2, Day 8Cycle 3-25, Day 8
Olaratumab + Ifosfamide (Part B)125199289
Olaratumab +Vincristine + Irinotecan (Part B)99.1230348

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Percentage of Participants With Treatment Emergent (TE) Positive Anti-Olaratumab Antibodies

Percentage of participants with a TE positive anti-olaratumab antibodies defined as a participant with a 4-fold (2 dilutions) increase over a positive baseline antibody titer. (NCT02677116)
Timeframe: From Baseline to Study Completion (Up to 33 Months)

Interventionpercentage of participants (Number)
Olaratumab + Vincristine + Irinotecan (Part A)0
Olaratumab + Ifosfamide (Part A)0
Olaratumab + Doxorubicin (Part A)0
Olaratumab + Vincristine + Irinotecan (Part B)0
Olaratumab + Ifosfamide (Part B)0
Olaratumab + Doxorubicin (Part B)0
Olaratumab + Vincristine + Irinotecan (Part C)0
Olaratumab + Ifosfamide (Part C)0
Olaratumab + Doxorubicin (Part C)0

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PK: Trough Serum Minimum Concentration (Cmin) of Olaratumab Part C

PK: Trough serum concentration (Cmin) of Olaratumab was reported. A sample was collected every other cycle from cycles 1, 2, 3-25. (NCT02677116)
Timeframe: Cycles 1, 2, 3-25; Day 8: 336 Hours Postdose

,,
Interventionμg/mL (Geometric Mean)
Cycle 1, Day 8Cycle 2, Day 8Cycle 3-25, Day 8
Olaratumab + Doxorubicin (Part C)90.3141156
Olaratumab + Ifosfamide (Part C)124NANA
Olaratumab + Vincristine + Irinotecan (Part C)83.713483.7

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Number of Participants With Olaratumab Dose Limiting Toxicities (DLTs)

A dose limiting toxicity (DLT) was defined as an adverse event (AE) during the first 21 days that was possibly related to the study drug and fulfilled any of the following criteria using the National Cancer Institute's (NCI) Common Terminology Criteria for Adverse Events (CTCAE), Version 4.0: CTCAE Grade 3 nonhematologic toxicity, grade 4 neutropenia that lasted longer than 2 weeks, grade ≥3 thrombocytopenia complicated by hemorrhage, and any hematologic toxicity that caused a cycle delay of >14 days. (NCT02677116)
Timeframe: Parts A and B: Cycle 1 through Cycle 2 in each arm (21-day cycle); Part C: Cycle 1 only (21-day cycle)

InterventionParticipants (Count of Participants)
Olaratumab + Vincristine + Irinotecan (Part A)0
Olaratumab + Ifosfamide (Part A)1
Olaratumab + Doxorubicin (Part A)0
Olaratumab + Vincristine + Irinotecan (Part B)1
Olaratumab + Ifosfamide (Part B)0
Olaratumab + Doxorubicin (Part B)1
Olaratumab + Vincristine + Irinotecan (Part C)1
Olaratumab + Ifosfamide (Part C)0
Olaratumab + Doxorubicin (Part C)0

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Percentage of Participants With a Complete Response (CR) or Partial Response (PR) (Objective Response Rate [ORR])

Objective Response Rate (ORR) is the percentage of participants achieving a confirmed best overall tumor response of CR or PR. According to RECIST v1.1, PR defined as a >30% decrease in the sum of the longest diameters (LD) of the target lesions, taking as reference the baseline sum of the LD; CR was defined as the disappearance of all target and non-target lesions. (NCT02677116)
Timeframe: Baseline to objective progression or start of new anti-cancer therapy (Up to 7 months)

Interventionpercentage of participants (Number)
Olaratumab + Vincristine + Irinotecan (Part A)0
Olaratumab + Ifosfamide (Part A)0
Olaratumab + Doxorubicin (Part A)9.1
Olaratumab + Vincristine + Irinotecan (Part B)20.0
Olaratumab + Ifosfamide (Part B)0
Olaratumab + Doxorubicin (Part B)0
Olaratumab + Vincristine + Irinotecan (Part C)0
Olaratumab + Ifosfamide (Part C)0
Olaratumab + Doxorubicin (Part C)25.0

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Progression Free Survival (PFS)

Progression-free survival (PFS) is defined as the time from baseline to the first date of radiological disease progression or death due to any cause. Progressive disease (PD) according to Response Evaluation Criteria in Solid Tumors (RECIST) v1.1 is defined as at least a 20% increase in the sum of the diameters of target lesions, taking as reference the smallest sum on study (including the baseline sum if that is the smallest). In addition to the relative increase of 20%, the sum must also demonstrate an absolute increase of at least 5 millimeters (mm). The appearance of one or more new lesions is also considered progression. If participant started new treatment before PD, the participant was censored at the date of last tumor assessment prior to new therapy. If treatment was discontinued for reasons other than PD and no further assessment, censoring occurred at last tumor assessment. (NCT02677116)
Timeframe: Baseline to radiological disease progression or death from any cause (Up to 2 Years)

InterventionMonths (Median)
Olaratumab + Vincristine + Irinotecan (Part A)1.54
Olaratumab + Ifosfamide (Part A)1.38
Olaratumab + Doxorubicin (Part A)1.26
Olaratumab + Vincristine + Irinotecan (Part B)1.28
Olaratumab + Ifosfamide (Part B)1.25
Olaratumab + Doxorubicin (Part B)NA
Olaratumab + Vincristine + Irinotecan (Part C)4.07
Olaratumab + Ifosfamide (Part C)4.88
Olaratumab + Doxorubicin (Part C)5.52

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Pharmacokinetics (PK): Maximum Concentration (Cmax) of Olaratumab Part A

Pharmacokinetics (PK): Maximum serum concentration (Cmax) data of Olaratumab was reported from available sample data. (NCT02677116)
Timeframe: Cycle 1, Day 8 and Cycle 2, Days 1 and 8: 1.25 hour (h), 2.5 h, 3.5h Postdose

Interventionmicrogram/milliliter (μg/mL) (Geometric Mean)
Cycle 1, Day 8
Olaratumab Alone (Part A)439

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Pharmacokinetics (PK): Maximum Concentration (Cmax) of Olaratumab Part A

Pharmacokinetics (PK): Maximum serum concentration (Cmax) data of Olaratumab was reported from available sample data. (NCT02677116)
Timeframe: Cycle 1, Day 8 and Cycle 2, Days 1 and 8: 1.25 hour (h), 2.5 h, 3.5h Postdose

,,
Interventionmicrogram/milliliter (μg/mL) (Geometric Mean)
Cycle 2, Day 1Cycle 2, Day 8
Olaratumab + Doxorubicin (Part A)406422
Olaratumab + Ifosfamide (Part A)396398
Olaratumab + Vincristine + Irinotecan (Part A)437523

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Part 1: Apparent (Oral) Plasma Clearance (CL/F) of Ibrutinib

CL/F is defined as apparent plasma clearance of ibrutinib. As per planned analyses, PK parameters for Part 1 were presented per dose group (240 mg/m^2, 329 mg/m^2 and 440 mg/m^2) and age group (1-5, 6-11, 12-17 and >18 years). As planned in protocol, the PK parameters were presented per dose group as dosing was dependent on age. (NCT02703272)
Timeframe: Up to Cycle 3 (each cycle of 21 or 28 days)

Interventionmilliliter per hour (mL/h) (Median)
1-5 years6-11 years
Part 1: Ibrutinib: 440 mg/m^212001300

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Part 1 and Part 2: Gene Expression Evaluated by Disease-specific Biomarkers at Baseline

"Tumor formalin-fixed paraffin-embedded (FFPE) samples were taken to evaluate the baseline gene expression by disease-specific biomarkers such as BCL-2L1 (BCL-xl), BIRC2 (cIAP1), Caspase 3 (CASP3), STAT3, and SYK. Transcripts per million (TPM) is a normalization method for RNA-sequencing, which means for every 1,000,000 RNA molecules in the RNA-sequencing tumor FFPE sample, x came from this gene/transcript." (NCT02703272)
Timeframe: Baseline

,
InterventionTranscripts per million (Mean)
BCL-2L1 (BCL-xl)BIRC2 (cIAP1)Caspase 3 (CASP3)STAT3SYK
Part 2: Chemoimmunotherapy74.3079040.0171647.61412526.35308618.36324
Part 2: Ibrutinib+CIT (RICE or RVICI)58.0934647.2078751.14711540.02256705.29909

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Part 2: Tumor Volume Reduction Rate at Day 14

The tumor volume reduction rate was defined as percent decrease in the sum of the products of the lesion diameters at Day 14. It was measured as the mean change in the sum of the products of the lesion diameters (SPD) at Day 14. (NCT02703272)
Timeframe: At Day 14

InterventionPercent change (Least Squares Mean)
Part 2: Ibrutinib+CIT (RICE or RVICI)-49.7
Part 2: Chemoimmunotherapy-58.60

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Part 2: Time to Response

Time to response was defined as the time interval from the first dose of ibrutinib to the first documented response for those participants who responded. Time to response was summarized for participants who achieved either CR (including CRb and CRu) or PR. CR=disappearance of all disease; CRb=residual mass has no morphologic evidence of disease from limited or core biopsy, with no new lesions by imaging examination; BM and CSF morphologically free of disease; no new or PD elsewhere, CRu=Residual mass is negative by FDG-PET; no new lesions by imaging examination; BM and CSF morphologically free of disease; no new or PD elsewhere, PR=50% decrease in SPD on CT or MRI; FDG-PET may be positive (deauville score or 4 or 5 with reduced lesional uptake compared with baseline); no new or PD; morphologic evidence of disease may be present in BM or CSF if present at diagnosis; however, there should be 50% reduction in percentage of lymphoma cells. (NCT02703272)
Timeframe: Up to 4 Years and 4 months

InterventionMonths (Median)
Part 2: Ibrutinib+CIT (RICE or RVICI)0.89
Part 2: Chemoimmunotherapy0.82

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Part 2: Percentage of Participants With EFS at 3 Years

EFS is the time interval from randomization to death, disease progression, or lack of complete response (CR) or partial response (PR) after 3 cycles of treatment, whichever occurs first based on blinded independent event review by the IRC. CR was defined as CT or MRI reveals no residual disease or new lesions, resected residual mass that is pathologically (morphologically) negative for disease, BM and CSF morphologically free of disease with no new lesions by imaging examination. PR was defined as 50% decrease in um of the products of the SPD on CT or MRI; FDG-PET may be positive, no new or PD; morphologic evidence of disease may be present in BM or CSF if present at diagnosis; however, there should be 50% reduction in percentage of lymphoma cells. (NCT02703272)
Timeframe: At 3 years

InterventionPercentage of participants (Number)
Part 2: Ibrutinib+CIT (RICE or RVICI)8.6
Part 2: Chemoimmunotherapy12.5

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Part 2: Percentage of Participants With EFS at 2 Years

EFS was the time interval from randomization to death, disease progression, or lack of complete response (CR) or partial response (PR) after 3 cycles of treatment, whichever occurred first based on blinded independent event review by the IRC. CR was defined as CT or MRI reveals no residual disease or new lesions, resected residual mass that is pathologically (morphologically) negative for disease, BM and CSF morphologically free of disease with no new lesions by imaging examination. PR was defined as 50% decrease in um of the products of the SPD on CT or MRI; FDG-PET may be positive, no new or PD; morphologic evidence of disease may be present in BM or CSF if present at diagnosis; however, there should be 50% reduction in percentage of lymphoma cells. (NCT02703272)
Timeframe: At 2 years

InterventionPercentage of participants (Number)
Part 2: Ibrutinib+CIT (RICE or RVICI)14.3
Part 2: Chemoimmunotherapy12.5

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Part 2: Percentage of Participants Who Achieved Partial Response (PR)

Percentage of participants who achieved PR were assessed. PR was defined as 50% decrease in SPD on computed tomography (CT) or magnetic resonance imaging (MRI); FDG-PET may be positive; no new or PD; morphologic evidence of disease may be present in BM or cerebrospinal fluid (CSF) if present at diagnosis; however, there should be 50% reduction in percentage of lymphoma cells. (NCT02703272)
Timeframe: Up to 4 year and 4 months

Interventionpercentage of participants (Number)
Part 2: Ibrutinib+CIT (RICE or RVICI)51.4
Part 2: Chemoimmunotherapy62.5

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Part 2: Percentage of Participants Who Achieved Complete Response (CR)

Complete response rate was defined as the percentage of participants who achieved complete response or complete response with an incomplete marrow recovery (CRi) on or prior to initiation of subsequent anti-leukemic therapy per the IRC assessment. (NCT02703272)
Timeframe: Up to 4 year and 4 months

InterventionPercentage of Participants (Number)
Part 2: Ibrutinib+CIT (RICE or RVICI)17.1
Part 2: Chemoimmunotherapy18.8

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Part 2: Overall Survival

Overall survival was defined as duration from the date of randomization to the date of the participant's death. (NCT02703272)
Timeframe: Up to 4 year and 4 months

InterventionMonths (Median)
Part 2: Ibrutinib+CIT (RICE or RVICI)14.13
Part 2: Chemoimmunotherapy11.07

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Part 2: Number of Participants With c-MYC Gene Rearrangement

Number of participants with c-MYC gene rearrangement were reported. Blood samples were taken to evaluate the levels of biomarker such as c-MYC Gene rearrangement. (NCT02703272)
Timeframe: At baseline (Cycle 1 Day 1)

InterventionParticipants (Count of Participants)
Part 2: Ibrutinib+CIT (RICE or RVICI)1
Part 2: Chemoimmunotherapy1

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Part 1: Apparent (Oral) Volume of Distribution (Vd/F) of Ibrutinib

Vd/F is defined as apparent (oral) volume of distribution of ibrutinib. As per planned analyses, pharmacokinetic (PK) parameters for Part 1 were presented per dose group (240 mg/m^2, 329 mg/m^2 and 440 mg/m^2) and age group (1-5, 6-11, 12-17 and >18 years). As planned in protocol, the PK parameters were presented per dose group as dosing was dependent on age. (NCT02703272)
Timeframe: Up to Cycle 3 (each cycle of 21 or 28 days)

,
Interventionliter(s) (Median)
1-5 years6-11 years12-17 years
Part 1: Ibrutinib: 240 mg/m^211.1183.63
Part 1: Ibrutinib: 329 mg/m^25.187.5511.3

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Part 1: Apparent (Oral) Volume of Distribution (Vd/F) of Ibrutinib

Vd/F is defined as apparent (oral) volume of distribution of ibrutinib. As per planned analyses, pharmacokinetic (PK) parameters for Part 1 were presented per dose group (240 mg/m^2, 329 mg/m^2 and 440 mg/m^2) and age group (1-5, 6-11, 12-17 and >18 years). As planned in protocol, the PK parameters were presented per dose group as dosing was dependent on age. (NCT02703272)
Timeframe: Up to Cycle 3 (each cycle of 21 or 28 days)

Interventionliter(s) (Median)
1-5 years6-11 years
Part 1: Ibrutinib: 440 mg/m^27.6319

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Part 1: Apparent (Oral) Plasma Clearance (CL/F) of Ibrutinib

CL/F is defined as apparent plasma clearance of ibrutinib. As per planned analyses, PK parameters for Part 1 were presented per dose group (240 mg/m^2, 329 mg/m^2 and 440 mg/m^2) and age group (1-5, 6-11, 12-17 and >18 years). As planned in protocol, the PK parameters were presented per dose group as dosing was dependent on age. (NCT02703272)
Timeframe: Up to Cycle 3 (each cycle of 21 or 28 days)

,
Interventionmilliliter per hour (mL/h) (Median)
1-5 years6-11 years12-17 years
Part 1: Ibrutinib: 240 mg/m^212201450348
Part 1: Ibrutinib: 329 mg/m^2508805729

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Part 2: Apparent (Oral) Plasma Clearance (CL/F) of Ibrutinib

CL/F is defined as apparent plasma clearance of ibrutinib. As per planned analyses, PK parameters for Part 2 were presented per dose group (240 mg/m^2, 329 mg/m^2 and 440 mg/m^2) and age group (1-5, 6-11, 12-17 and >18 years). As planned in protocol, the PK parameters were presented per dose group as dosing was dependent on age. (NCT02703272)
Timeframe: Up to Cycle 3 (each cycle of 21 or 28 days)

InterventionmL/h (Median)
1-5 years6-11 years
Part 2: Ibrutinib: 440 mg/m^21110856

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Part 1 and Part 2: Visual Analog Scale (VAS) Score for Palatability

Palatability of ibrutinib was measured by using a VAS. The scale is a 5-point visual analog scale incorporating a facial hedonic scale designed to span pediatric ages and levels of participant comprehension with a score range of 1 to 5, where 1 represents best score and 5 is worst palatability. (NCT02703272)
Timeframe: Day 1 of Cycle 1 and Cycle 3

,,
InterventionUnits on a scale (Mean)
Cycle 1 Day 1Cycle 3 Day 1
Part 1: Ibrutinib+RICE2.63.3
Part 1: Ibrutinib+RVICI3.22.3
Part 2: Ibrutinib+CIT (RICE or RVICI)2.42.6

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Part 1 and Part 2: Number of Participants With Adverse Events as Measure of Safety and Tolerability

An AE is any untoward medical event that occurs in a participant administered an investigational product, and it does not necessarily indicate only events with clear causal relationship with the relevant investigational product. (NCT02703272)
Timeframe: Up to 4 year and 4 months

InterventionParticipants (Count of Participants)
Part 1: Ibrutinib+RICE11
Part 1: Ibrutinib+RVICI10
Part 2: Ibrutinib+CIT (RICE or RVICI)35
Part 2: Chemoimmunotherapy15

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Part 2: Apparent (Oral) Plasma Clearance (CL/F) of Ibrutinib

CL/F is defined as apparent plasma clearance of ibrutinib. As per planned analyses, PK parameters for Part 2 were presented per dose group (240 mg/m^2, 329 mg/m^2 and 440 mg/m^2) and age group (1-5, 6-11, 12-17 and >18 years). As planned in protocol, the PK parameters were presented per dose group as dosing was dependent on age. (NCT02703272)
Timeframe: Up to Cycle 3 (each cycle of 21 or 28 days)

InterventionmL/h (Median)
12-17 years18+ years
Part 2: Ibrutinib: 329 mg/m^29821510

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Part 2: Number of Participants With CD79B, CARD11, and MYD Mutations

Number of participants with CD79B, CARD11, and MYD mutations were reported. Blood samples were taken to evaluate the levels of biomarkers such as CD79B, CARD11, and MYD mutations. (NCT02703272)
Timeframe: Up to 4 year and 4 months

,
InterventionParticipants (Count of Participants)
CD79BCARD11MYD mutation
Part 2: Chemoimmunotherapy000
Part 2: Ibrutinib+CIT (RICE or RVICI)110

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Part 2: Apparent (Oral) Volume of Distribution (Vd/F) of Ibrutinib

Vd/F is defined as apparent (oral) volume of distribution of ibrutinib. As per planned analyses, PK parameters for Part 2 were presented per dose group (240 mg/m^2, 329 mg/m^2 and 440 mg/m^2) and age group (1-5, 6-11, 12-17 and >18 years). As planned in protocol, the PK parameters were presented per dose group as dosing was dependent on age. (NCT02703272)
Timeframe: Up to Cycle 3 (each cycle of 21 or 28 days)

Interventionliter(s) (Median)
12-17 years
Part 2: Ibrutinib: 240 mg/m^29.9

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Part 2: Apparent (Oral) Volume of Distribution (Vd/F) of Ibrutinib

Vd/F is defined as apparent (oral) volume of distribution of ibrutinib. As per planned analyses, PK parameters for Part 2 were presented per dose group (240 mg/m^2, 329 mg/m^2 and 440 mg/m^2) and age group (1-5, 6-11, 12-17 and >18 years). As planned in protocol, the PK parameters were presented per dose group as dosing was dependent on age. (NCT02703272)
Timeframe: Up to Cycle 3 (each cycle of 21 or 28 days)

Interventionliter(s) (Median)
1-5 years6-11 years
Part 2: Ibrutinib: 440 mg/m^21.686.18

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Part 2: Apparent (Oral) Volume of Distribution (Vd/F) of Ibrutinib

Vd/F is defined as apparent (oral) volume of distribution of ibrutinib. As per planned analyses, PK parameters for Part 2 were presented per dose group (240 mg/m^2, 329 mg/m^2 and 440 mg/m^2) and age group (1-5, 6-11, 12-17 and >18 years). As planned in protocol, the PK parameters were presented per dose group as dosing was dependent on age. (NCT02703272)
Timeframe: Up to Cycle 3 (each cycle of 21 or 28 days)

Interventionliter(s) (Median)
12-17 years18+ years
Part 2: Ibrutinib: 329 mg/m^24.149.29

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Part 2: Area Under the Plasma Concentration-time Curve (AUC) of Ibrutinib

AUC is defined as area under the plasma concentration-time curve. As per planned analyses, PK parameters for Part 2 were presented per dose group (240 mg/m^2, 329 mg/m^2 and 440 mg/m^2) and age group (1-5, 6-11, 12-17 and >18 years). As planned in protocol, the PK parameters were presented per dose group as dosing was dependent on age. (NCT02703272)
Timeframe: Up to Cycle 3 (each cycle of 21 or 28 days)

Interventionh*ng/mL (Mean)
12-17 years
Part 2: Ibrutinib: 240 mg/m^2:215

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Part 2: Area Under the Plasma Concentration-time Curve (AUC) of Ibrutinib

AUC is defined as area under the plasma concentration-time curve. As per planned analyses, PK parameters for Part 2 were presented per dose group (240 mg/m^2, 329 mg/m^2 and 440 mg/m^2) and age group (1-5, 6-11, 12-17 and >18 years). As planned in protocol, the PK parameters were presented per dose group as dosing was dependent on age. (NCT02703272)
Timeframe: Up to Cycle 3 (each cycle of 21 or 28 days)

Interventionh*ng/mL (Mean)
1-5 years6-11 years
Part 2: Ibrutinib: 440 mg/m^2298655

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Part 2: Area Under the Plasma Concentration-time Curve (AUC) of Ibrutinib

AUC is defined as area under the plasma concentration-time curve. As per planned analyses, PK parameters for Part 2 were presented per dose group (240 mg/m^2, 329 mg/m^2 and 440 mg/m^2) and age group (1-5, 6-11, 12-17 and >18 years). As planned in protocol, the PK parameters were presented per dose group as dosing was dependent on age. (NCT02703272)
Timeframe: Up to Cycle 3 (each cycle of 21 or 28 days)

Interventionh*ng/mL (Mean)
12-17 years18+ years
Part 2: Ibrutinib: 329 mg/m^2499423

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Part 2: Maximum Observed Plasma Concentration (Cmax) of Ibrutinib

Cmax is defined as maximum plasma concentration of ibrutinib. As per planned analyses, PK parameters for Part 2 were presented per dose group (240 mg/m^2, 329 mg/m^2 and 440 mg/m^2) and age group (1-5, 6-11, 12-17 and >18 years). As planned in protocol, the PK parameters were presented per dose group as dosing was dependent on age. (NCT02703272)
Timeframe: Up to Cycle 3 (each cycle of 21 or 28 days)

Interventionng/mL (Median)
12-17 years
Part 2: Ibrutinib: 240 mg/m^22.93

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Part 2: Maximum Observed Plasma Concentration (Cmax) of Ibrutinib

Cmax is defined as maximum plasma concentration of ibrutinib. As per planned analyses, PK parameters for Part 2 were presented per dose group (240 mg/m^2, 329 mg/m^2 and 440 mg/m^2) and age group (1-5, 6-11, 12-17 and >18 years). As planned in protocol, the PK parameters were presented per dose group as dosing was dependent on age. (NCT02703272)
Timeframe: Up to Cycle 3 (each cycle of 21 or 28 days)

Interventionng/mL (Median)
1-5 years6-11 years
Part 2: Ibrutinib: 440 mg/m^23.794.15

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Part 2: Maximum Observed Plasma Concentration (Cmax) of Ibrutinib

Cmax is defined as maximum plasma concentration of ibrutinib. As per planned analyses, PK parameters for Part 2 were presented per dose group (240 mg/m^2, 329 mg/m^2 and 440 mg/m^2) and age group (1-5, 6-11, 12-17 and >18 years). As planned in protocol, the PK parameters were presented per dose group as dosing was dependent on age. (NCT02703272)
Timeframe: Up to Cycle 3 (each cycle of 21 or 28 days)

Interventionng/mL (Median)
12-17 years18+ years
Part 2: Ibrutinib: 329 mg/m^24.863.7

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Part 1 and Part 2: Number of Participants With Greater Than (>) 90% Bruton's Tyrosine Kinase (BTK) Occupancy

Number of participants with >90% BTK occupancy were reported. Blood samples were collected to assess BTK occupancy. (NCT02703272)
Timeframe: Up to 3 months

InterventionParticipants (Count of Participants)
Part 1: Ibrutinib5
Part 2: Ibrutinib5

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Part 1 and Part 2: Overall Response Rate (ORR)

ORR was defined as the percentage of participants achieving a best overall response of either complete response (CR) (including CR biopsy-negative [CRb] and unconfirmed CR [CRu]) or partial response (PR) as evaluated by International Pediatric non-Hodgkin lymphoma (NHL) response criteria. CR=disappearance of all disease; CRb=residual mass has no morphologic evidence of disease from limited or core biopsy, with no new lesions by imaging examination; bone marrow (BM) and CSF morphologically free of disease; no new or PD elsewhere, CRu=Residual mass is negative by FDG-PET; no new lesions by imaging examination; BM and CSF morphologically free of disease; no new or PD elsewhere, PR=50% decrease in SPD on CT or MRI; FDG-PET may be positive (deauville score or 4 or 5 with reduced lesional uptake compared with baseline); no new or PD; morphologic evidence of disease may be present in BM or CSF if present at diagnosis; however, there should be 50% reduction in percentage of lymphoma cells. (NCT02703272)
Timeframe: Up to 4 year and 4 months

InterventionPercentage of participants (Number)
Part 1: Ibrutinib+RICE81.8
Part 1: Ibrutinib+RVICI50.0
Part 2: Ibrutinib+CIT (RICE or RVICI)68.6
Part 2: Chemoimmunotherapy81.3

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Part 2: Duration of Response

Duration of response was defined as the duration from date of initial documentation of a response (CR or PR) to the date of first documented evidence of progressive disease (PD) or death, whichever occurred first. PD: >25% increase in SPD of residual lesions (calculated from nadir) on CT or MRI; Deauville score 4 or 5 on FDG-PET with increase in lesional uptake from baseline; documentation of new lesions or development of new morphologic evidence of disease in BM or CSF. (NCT02703272)
Timeframe: Up to 4 year and 4 months

InterventionMonths (Median)
Part 2: Ibrutinib+CIT (RICE or RVICI)6.01
Part 2: Chemoimmunotherapy6.51

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Part 2: Event Free Survival (EFS) Between the 2 Treatment Groups

EFS was the time interval from randomization to death, disease progression, or lack of complete response (CR) or partial response (PR) after 3 cycles of treatment, whichever occurred first based on blinded independent event review by the Independent Review Committee (IRC). CR was defined as computed tomography (CT) or magnetic resonance imaging (MRI) reveals no residual disease or new lesions, resected residual mass that was pathologically (morphologically) negative for disease, BM and CSF morphologically free of disease with no new lesions by imaging examination. PR was defined as 50 percent (%) decrease in sum of the products of the lesion diameters (SPD) on CT or MRI; fluorodeoxyglucose (FDG)-positron emission tomography (PET) may be positive, no new or progressive disease (PD); morphologic evidence of disease may be present in BM or cerebrospinal fluid (CSF) if present at diagnosis; however, there should be 50% reduction in percentage of lymphoma cells. (NCT02703272)
Timeframe: Time from Randomization to death, disease progression, or lack of CR or PR after 3 cycles of treatment (up to 4 year and 4 months)

InterventionMonths (Median)
Part 2: Ibrutinib+CIT (RICE or RVICI)6.05
Part 2: Chemoimmunotherapy6.97

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Part 2: Number of Participants Who Proceeded to Stem Cell Transplantation

Number of participants who proceeded to stem cell transplantation were reported. (NCT02703272)
Timeframe: Up to end of the study (Up to 4 year and 4 months)

InterventionParticipants (Count of Participants)
Part 2: Ibrutinib+CIT (RICE or RVICI)13
Part 2: Chemoimmunotherapy7

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Part 2: Apparent (Oral) Plasma Clearance (CL/F) of Ibrutinib

CL/F is defined as apparent plasma clearance of ibrutinib. As per planned analyses, PK parameters for Part 2 were presented per dose group (240 mg/m^2, 329 mg/m^2 and 440 mg/m^2) and age group (1-5, 6-11, 12-17 and >18 years). As planned in protocol, the PK parameters were presented per dose group as dosing was dependent on age. (NCT02703272)
Timeframe: Up to Cycle 3 (each cycle of 21 or 28 days)

InterventionmL/h (Median)
12-17 years
Part 2: Ibrutinib: 240 mg/m^21730

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Part 1: Maximum Observed Plasma Concentration (Cmax) of Ibrutinib

Cmax is defined as maximum plasma concentration of ibrutinib. As per planned analyses, pharmacokinetic (PK) parameters for Part 1 were presented per dose group (240 mg/m^2, 329 mg/m^2 and 440 mg/m^2) and age group (1-5, 6-11, 12-17 and >18 years). As planned in protocol, the PK parameters were presented per dose group as dosing was dependent on age. (NCT02703272)
Timeframe: Up to Cycle 3 (each cycle of 21 or 28 days)

,
Interventionnanograms per milliliter (ng/mL) (Median)
1-5 years6-11 years12-17 years
Part 1: Ibrutinib: 240 mg/m^23.863.464.88
Part 1: Ibrutinib: 329 mg/m^24.483.644.73

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Part 1: Maximum Observed Plasma Concentration (Cmax) of Ibrutinib

Cmax is defined as maximum plasma concentration of ibrutinib. As per planned analyses, pharmacokinetic (PK) parameters for Part 1 were presented per dose group (240 mg/m^2, 329 mg/m^2 and 440 mg/m^2) and age group (1-5, 6-11, 12-17 and >18 years). As planned in protocol, the PK parameters were presented per dose group as dosing was dependent on age. (NCT02703272)
Timeframe: Up to Cycle 3 (each cycle of 21 or 28 days)

Interventionnanograms per milliliter (ng/mL) (Median)
1-5 years6-11 years
Part 1: Ibrutinib: 440 mg/m^25.073.88

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Part 1: Area Under the Plasma Concentration-time Curve (AUC) of Ibrutinib

AUC is defined as area under the plasma concentration-time curve. As per planned analyses, pharmacokinetic (PK) parameters for Part 1 were presented per dose group (240 milligrams per meter square [mg/m^2], 329 mg/m^2 and 440 mg/m^2) and age group (1-5, 6-11, 12-17 and >18 years). As planned in protocol, the PK parameters were presented per dose group as dosing was dependent on age. (NCT02703272)
Timeframe: Up to Cycle 3 (each cycle of 21 or 28 days)

,
Interventionhours*nanogram per milliliter (h*ng/mL) (Median)
1-5 years6-11 years12-17 years
Part 1: Ibrutinib: 240 mg/m^21431451210
Part 1: Ibrutinib: 329 mg/m^2386349661

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Part 1: Area Under the Plasma Concentration-time Curve (AUC) of Ibrutinib

AUC is defined as area under the plasma concentration-time curve. As per planned analyses, pharmacokinetic (PK) parameters for Part 1 were presented per dose group (240 milligrams per meter square [mg/m^2], 329 mg/m^2 and 440 mg/m^2) and age group (1-5, 6-11, 12-17 and >18 years). As planned in protocol, the PK parameters were presented per dose group as dosing was dependent on age. (NCT02703272)
Timeframe: Up to Cycle 3 (each cycle of 21 or 28 days)

Interventionhours*nanogram per milliliter (h*ng/mL) (Median)
1-5 years6-11 years
Part 1: Ibrutinib: 440 mg/m^2310324

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Number of Participants With Complete Response (CR) of Rolapitant Hydrochloride Administered as a Single-dose

Complete response (CR) no emetic episodes and no rescue medications. (NCT02732015)
Timeframe: Days 1-10

InterventionParticipants (Count of Participants)
Cohort 10
Cohort 25

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Disease Control Rate (DCR): Percentage of Participants With a Best Overall Response of CR, PR, or Stable Disease (SD)

Disease control rate (DCR) is the percentage of participants with a best overall response of CR, PR or SD as defined by RECIST v1.1. CR is defined as the disappearance of all target and non-target lesions and no appearance of new lesions. PR is defined as at least a 30% decrease in the sum of the longest diameter (LD) of target lesions (taking as reference the baseline sum LD), no progression of non-target lesions, and no appearance of new lesions. SD is neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for progressive disease (PD) for target lesions, no progression of non-target lesions, and no appearance of new lesions. PD is defined as at least a 20% increase in the sum of the diameters of target lesions, with reference being the smallest sum on study and an absolute increase of at least 5 mm, or unequivocal progression of non-target lesions, or 1 or more new lesions. (NCT03283696)
Timeframe: Baseline until Disease Progression or Death Due to Any Cause (Up To 21 Months)

InterventionPercentage of participants (Number)
Olaratumab 15 mg/kg + Doxorubicin + Ifosfamide81.3
Olaratumab 20 mg/kg + Doxorubicin + Ifosfamide87.5

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Number of Participants With Olaratumab Dose Limiting Toxicities (DLTs)

"A Dose Limiting Toxicity is defined as an Adverse Event (AE) that is likely related to the study medication or combination, and fulfills any one of the following criteria, graded according to the NCI-CTCAE Version 4.0:~Grade 3 or 4 febrile neutropenia, or sepsis., or~Grade 4 neutropenia lasting 7 days or longer.~Grade 4 thrombocytopenia, or Grade 3 thrombocytopenia complicated by hemorrhage.~Nonhematologic Grade ≥3 toxicity, except for toxicities (such as nausea, vomiting, transient electrolyte abnormalities, or diarrhoea) that can be controlled with optimal medical management within 48 hours or clinically non-significant laboratory abnormalities." (NCT03283696)
Timeframe: Cycle 1 (Up To 24 days)

InterventionParticipants (Count of Participants)
Olaratumab 15 mg/kg + Doxorubicin + Ifosfamide4
Olaratumab 20 mg/kg + Doxorubicin + Ifosfamide4

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PK: Trough Serum Concentration (Cmin,ss) of Olaratumab at Steady-state

PK: Cmin of olaratumab at steady-state. (NCT03283696)
Timeframe: Cycle 3 - Day 1 (predose, end of infusion, 2 hours post olara, 5 hours post olara, 24 hours post olara, 72 hours post olara), Day 8 (predose, end of infusion, 2 hours post-olara, 5 hours post olara, 48 hours post olara, 168 hours post olara)

,
Interventionmicrograms per milliliter (μg/mL) (Geometric Mean)
Cycle 3 Day 1Cycle 3 Day 8
Olaratumab 15 mg/kg + Doxorubicin + Ifosfamide154126
Olaratumab 20 mg/kg + Doxorubicin + Ifosfamide177115

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PK: Trough Serum Concentration (Cmin)

PK: Cmin of olaratumab. (NCT03283696)
Timeframe: Cycle 1 - Day 1 (predose, end of infusion, 2 hours post olaratumab (olara), 6 hours post olara, 24 hours post olara, 72 hours post olara), Day 8 (predose, end of infusion, 2 hours post-olara, 6 hours post olara, 48 hours post olara, 168 hours post olara)

,
Interventionmicrograms per milliliter (μg/mL) (Geometric Mean)
Cycle 1 Day 1Cycle 1 Day 8
Olaratumab 15 mg/kg + Doxorubicin + Ifosfamide87.346.7
Olaratumab 20 mg/kg + Doxorubicin + Ifosfamide14053.3

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Number of Participants With Anti-Olaratumab Antibodies

Participants with treatment-emergent anti-drug antibody (TE ADA) positive were 1) a participant with a 4-fold (2 dilutions) increase over a positive baseline antibody titer; or 2) for a negative baseline titer, a participant with an increase from the baseline to a level of 1:20. (NCT03283696)
Timeframe: Baseline through Follow-up (Up To 21 Months)

InterventionParticipants (Count of Participants)
Olaratumab 15 mg/kg + Doxorubicin + Ifosfamide0
Olaratumab 20 mg/kg + Doxorubicin + Ifosfamide1

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Duration of Response (DoR)

Duration of response is defined as the time from the date measurement criteria for CR or PR (whichever is first recorded) are first met until the first date that disease is recurrent or objective progression is observed, per RECIST 1.1, or the date of death from any cause in the absence of objectively determined disease progression or recurrence. Participants known to be alive and without disease progression will be censored at the time of the last adequate tumor assessment. (NCT03283696)
Timeframe: Date of Complete Response (CR) or Partial Response (PR) to Objective Disease Progression or Death Due to Any Cause (Up To 21 Months)

InterventionMonths (Median)
Olaratumab 15 mg/kg + Doxorubicin + Ifosfamide8.25
Olaratumab 20 mg/kg + Doxorubicin + IfosfamideNA

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Objective Response Rate (ORR): Number of Participants Who Achieve Best Overall Tumor Response of Complete Response (CR) or Partial Response (PR)

Objective response rate is the best overall tumor response of complete response (CR) or partial response (PR) as classified by the independent central review according to the Response Evaluation Criteria In Solid Tumors (RECIST v1.1). CR is a disappearance of all target and non-target lesions and normalization of tumor marker level. PR is an at least 30% decrease in the sum of the diameters of target lesions (taking as reference the baseline sum diameter) without progression of non-target lesions or appearance of new lesions. (NCT03283696)
Timeframe: Baseline up to Short-Term Follow-Up Period (Up To 21 Months)

InterventionParticipants (Count of Participants)
Olaratumab 15 mg/kg + Doxorubicin + Ifosfamide6
Olaratumab 20 mg/kg + Doxorubicin + Ifosfamide1

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Overall Survival (OS)

Overall survival is defined as the time from the date of randomization to the date of death from any cause. For each participant who is not known to have died as of the data-inclusion cut-off date for a particular analysis, overall survival duration was censored for that analysis at the date of last prior contact. (NCT03283696)
Timeframe: Baseline to Date of Death Due to Any Cause (Up To 21 Months)

InterventionMonths (Median)
Olaratumab 15 mg/kg + Doxorubicin + Ifosfamide16.72
Olaratumab 20 mg/kg + Doxorubicin + IfosfamideNA

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Progression Free Survival (PFS)

Progression-free survival time was measured from randomization until the date of objective progression as defined by Response Evaluation Criteria in Solid Tumors v1.1 (RECIST v1.1), or death from any cause. PD is defined as at least a 20% increase in the sum of the diameters of target lesions, with reference being the smallest sum on study and an absolute increase of at least 5 mm, or unequivocal progression of non-target lesions, or 1 or more new lesions. Participants who have neither progressed nor died were censored at the day of their last radiographic tumor assessment, if available, or date of randomization if no post-baseline radiographic assessment is available. (NCT03283696)
Timeframe: Baseline to Objective Disease Progression or Death Due to Any Cause (Up To 21 Months)

InterventionMonths (Median)
Olaratumab 15 mg/kg + Doxorubicin + Ifosfamide9.53
Olaratumab 20 mg/kg + Doxorubicin + Ifosfamide6.93

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Pharmacokinetics (PK): Maximum Serum Concentration (Cmax) of Olaratumab

PK: Cmax of olaratumab. (NCT03283696)
Timeframe: Cycle 1 - Day 1 (predose, end of infusion, 2 hours post olaratumab (olara), 6 hours post olara, 24 hours post olara, 72 hours post olara), Day 8 (predose, end of infusion, 2 hours post-olara, 6 hours post olara, 48 hours post olara, 168 hours post olara)

,
Interventionmicrograms per milliliter (μg/mL) (Geometric Mean)
Cycle 1 Day 1Cycle 1 Day 8
Olaratumab 15 mg/kg + Doxorubicin + Ifosfamide408452
Olaratumab 20 mg/kg + Doxorubicin + Ifosfamide508671

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PK: Maximum Serum Concentration (Cmax,ss) of Olaratumab at Steady-state

PK: Cmax of olaratumab at steady-state. (NCT03283696)
Timeframe: Cycle 3 - Day 1 (predose, end of infusion, 2 hours post olara, 5 hours post olara, 24 hours post olara, 72 hours post olara), Day 8 (predose, end of infusion, 2 hours post-olara, 5 hours post olara, 48 hours post olara, 168 hours post olara)

,
Interventionmicrograms per milliliter (μg/mL) (Geometric Mean)
Cycle 3 Day 1Cycle 3 Day 8
Olaratumab 15 mg/kg + Doxorubicin + Ifosfamide533523
Olaratumab 20 mg/kg + Doxorubicin + Ifosfamide494545

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Percentage of Participants With Overall Survival at 1 Year or Month 12 (OS-1y)

OS-1y was defined as the time from the date of randomization to the date of death from any cause assessed up to 1 year. OS was calculated using the Kaplan-Meier method. Final analysis data was reported for this outcome measure. (NCT04154189)
Timeframe: Month 12 or 1 Year

Interventionpercentage of participants (Number)
Treatment Arm A: Lenvatinib + Ifosfamide + Etoposide49.2
Treatment Arm B: Ifosfamide + Etoposide72.1

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Percentage of Participants With PFS at 1 Year or Month 12 (PFS-1y Rate) by IIR Assessment

PFS-1y rate as assessed by IIR was defined as the percentage of participants who were alive and without PD at 1 year from randomization date using RECIST v1.1. PD was defined as at least a 20% increase or 5 mm increase in the sum of diameters of target lesions (taking as reference the smallest sum on study) recorded since the treatment started or the appearance of 1 or more new lesions. PFS-1y rate was estimated using Kaplan-Meier method. Final analysis data was reported for this outcome measure. (NCT04154189)
Timeframe: Month 12 or 1 Year

Interventionpercentage of participants (Number)
Treatment Arm A: Lenvatinib + Ifosfamide + EtoposideNA
Treatment Arm B: Ifosfamide + Etoposide14.9

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Percentage of Participants With PFS at Month 4 (PFS-4m Rate) by IIR Assessment

PFS rate at 4 months as assessed by IIR was defined as the percentage of participants who were alive and without PD at 4 months from the randomization date using RECIST v1.1. PD was defined as at least a 20% increase or 5 mm increase in the sum of diameters of target lesions (taking as reference the smallest sum on study) recorded since the treatment started or the appearance of 1 or more new lesions. The PFS-4m was estimated using the Kaplan-Meier method. Final analysis data was reported for this outcome measure. (NCT04154189)
Timeframe: Month 4

Interventionpercentage of participants (Number)
Treatment Arm A: Lenvatinib + Ifosfamide + Etoposide76.3
Treatment Arm B: Ifosfamide + Etoposide66.0

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Progression-free Survival (PFS) by Independent Imaging Review (IIR) Assessment

PFS as assessed by IIR was defined as the time from the date of randomization to the date of the first documentation of PD or date of death (whichever occurred first), as determined using RECIST v1.1. PD was defined as at least a 20 percent (%) increase or 5 millimeter (mm) increase in the sum of diameters of target lesions (taking as reference the smallest sum on study) recorded since the treatment started or the appearance of 1 or more new lesions. PFS was analyzed using Kaplan-Meier method. (NCT04154189)
Timeframe: From the date of randomization to the date of the first documentation of PD or date of death, whichever occurred first (up to 14.2 months)

Interventionmonths (Median)
Treatment Arm A: Lenvatinib + Ifosfamide + Etoposide6.5
Treatment Arm B: Ifosfamide + Etoposide5.5

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Number of Participants Categorized Based on Overall Palatability and Acceptability Questionnaire Responses for Suspension of Lenvatinib

The palatability and acceptability of lenvatinib oral suspension formulation was assessed using the Palatability Questionnaire. In the questionnaire, participants were asked to answer palatability and acceptability of lenvatinib suspension considering the following elements: taste, appearance, smell, how does it feel in the mouth and overall acceptability in terms of 7 responses: Super good, really good, good, may be good or may be bad, bad, really bad, super bad. In this outcome measure, number of participants have been reported per their overall palatability and acceptability responses. Final analysis data was reported for this outcome measure. (NCT04154189)
Timeframe: Cycle 1 Day 1 (Cycle length = 21 days)

InterventionParticipants (Count of Participants)
Super BadReally BadBadMay be Good or May be BadGoodReally GoodSuper Good
All Participants: Lenvatinib 14 mg/m^20002201

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Change From Baseline in Pediatric Quality of Life Inventory (PedsQL) Scale: Generic Core Scale Score at Month 4

Health-Related Quality of Life (HRQoL): PedsQL 4.0 Generic Core Scale is a multidimensional scale. It included assessment of 4 dimensions: physical functioning (8 items), emotional functioning (8 items), social functioning (8 items), and school functioning (5 items - children greater than or equal to [>=] 5 years, adults; 3 items - toddlers [aged 2-4 years]). Each item was reported using a 5-point Likert scale, items were then reverse-scored and linearly transformed to a 0 to 100 scale. Generic Core Scale total score: sum of all the items divided by the number of items answered across all the scales. Total score ranges from 0 to 100, where higher scores=better HRQoL, lower scores=worse HRQoL. Final analysis data was reported for this outcome measure. (NCT04154189)
Timeframe: Baseline and Month 4

Interventionscore on a scale (Mean)
Treatment Arm A: Lenvatinib + Ifosfamide + Etoposide2.61
Treatment Arm B: Ifosfamide + Etoposide2.65

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Change From Baseline in PedsQL Scale: Cancer Module Scale Score at Month 4

HRQoL: PedsQL 3.0 Cancer Module Scale measured pediatric cancer-specific HRQoL. It included assessment of 8 dimensions: pain and hurt (2 items), nausea (5 items), procedural anxiety (3 items), treatment anxiety (3 items), worry (3 items), cognitive problems (3 items - toddlers [aged 2-4], 4 items - young children [aged 5-7]; 5 items for children aged >=8 years, adults), perceived physical appearance (3 items), communication (3 items). Each item was reported using a 5-point Likert scale, items were then reverse-scored and linearly transformed to a 0 to 100 scale. Cancer Module total score: sum of all items divided by the number of items answered on all the scales. Total score ranges from 0 to 100, where higher scores=better HRQoL, lower scores=worse HRQoL. Final analysis data was reported for this outcome measure. (NCT04154189)
Timeframe: Baseline and Month 4

Interventionscore on a scale (Mean)
Treatment Arm A: Lenvatinib + Ifosfamide + Etoposide2.66
Treatment Arm B: Ifosfamide + Etoposide2.08

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Objective Response Rate at Month 4 (ORR-4m) by IIR Assessment

ORR-4m was defined as the percentage of participants with best overall response of complete response (CR) or partial response (PR) as determined by IIR using RECIST v1.1 within the first 4 months. CR: defined as the disappearance of all target and non-target lesions (non-lymph nodes). All pathological lymph nodes (whether target or non-target) must have a reduction in their short axis to less than (<) 10 mm. PR: defined as at least a 30% decrease in the sum of diameters of target lesions, taking as reference the baseline sum diameters. 95% confidence interval (CI) of ORR was calculated using the method of Clopper and Pearson. Final analysis data was reported for this outcome measure. (NCT04154189)
Timeframe: Month 4

Interventionpercentage of participants (Number)
Treatment Arm A: Lenvatinib + Ifosfamide + Etoposide15.0
Treatment Arm B: Ifosfamide + Etoposide7.3

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Treatment Arm A: Plasma Concentration of Lenvatinib

Plasma concentration of lenvatinib in participants from Treatment Arm A (Lenvatinib + Ifosfamide + Etoposide) at different time points were reported. As planned, data for this outcome measure was analyzed for treatment arm A only. Lenvatinib concentration in plasma was quantified using a validated liquid chromatography tandem mass spectrometry (LC-MS/MS) method. Final analysis data was reported for this outcome measure. (NCT04154189)
Timeframe: Cycle 1 Day 1: 0.5-4 hours and 6-10 hours post-dose; Cycle 1 Day 15: Pre-dose, 0.5-4 hours and 6-10 hours post-dose; Cycle 2 Day 1: Pre-dose (each Cycle length = 21 days)

Interventionnanograms per milliliter (ng/mL) (Mean)
Cycle 1, Day 1: 0.5-4 hours post-doseCycle 1, Day 1: 6-10 hours post-doseCycle 1, Day 15: Pre-doseCycle 1, Day 15: 0.5-4 hours post-doseCycle 1, Day 15: 6-10 hours post-doseCycle 2, Day 1: Pre-dose
Treatment Arm A: Lenvatinib + Ifosfamide + Etoposide147.9217.870.7222.3310.970.2

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ORR by IIR Assessment

ORR by IIR was defined as the percentage of participants with best overall response of CR or PR determined using RECIST v1.1. CR: defined as the disappearance of all target and non-target lesions (non-lymph nodes). All pathological lymph nodes (whether target or non-target) must have a reduction in their short axis to <10 mm. PR: defined as at least a 30% decrease in the sum of diameters of target lesions, taking as reference the baseline sum diameters. 95% CI of ORR was calculated using the method of Clopper and Pearson. Final analysis data was reported for this outcome measure. (NCT04154189)
Timeframe: From the date of randomization to the date of the first documentation of CR or PR, whichever occurred first (up to approximately 14.2 months)

Interventionpercentage of participants (Number)
Treatment Arm A: Lenvatinib + Ifosfamide + Etoposide15.0
Treatment Arm B: Ifosfamide + Etoposide9.8

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Event-Free Survival (EFS)

Duration of Event-Free Survival (EFS) in study participants. EFS is defined as the time from first dose to documented disease progression, death from any cause, or study dropout, whichever occurs first. (NCT04189952)
Timeframe: Up to 61 weeks

Interventionweeks (Number)
Acalabrutinib + R-ICENA

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Number of Treatment-Emergent Adverse Events

The safety profile and tolerability of acalabrutinib + R-ICE will be reported as the number of treatment-emergent adverse events (AEs) or abnormalities of laboratory tests; serious adverse events (SAEs); dose-limiting toxicities (DLTs), or AEs leading to discontinuation of study treatment, or death. Severity and relationship will be assessed by the treating physician using the Common Terminology Criteria for Adverse Events (CTCAE), Version 5.0. (NCT04189952)
Timeframe: 13 weeks

InterventionTreatment-emergent adverse events (Number)
Acalabrutinib + R-ICENA

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Overall Survival (OS)

Duration of Overall Survival (OS) in study participants. OS is defined as the time from first dose to death from any cause. Data for subjects who are still alive at the time of data cutoff date, lost to follow-up, have discontinued the study (or, if no post-baseline assessment, at the time of first dose plus 1 day) will be censored. (NCT04189952)
Timeframe: Up to 61 weeks

Interventionweeks (Number)
Acalabrutinib + R-ICENA

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Percentage of Participants Achieving Complete Response (CR)

The percentage of participants achieving complete response (CR) will be assessed using Response Evaluation Criteria in Lymphoma (RECIL 2017) criteria. (NCT04189952)
Timeframe: 9 weeks (End of Cycle 3)

Interventionpercentage of participants (Number)
Acalabrutinib + R-ICENA

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Percentage of Participants Achieving Mobilization Rate Greater Than or Equal to 2x10^6 CD34+ Cells/kg Body Weight

Percentage of study participants achieving a mobilization rate of greater than or equal to 2x10^6 CD34+ cells/kg body weight. Descriptive statistics will be used to summarize the mobilization rates. (NCT04189952)
Timeframe: 9 weeks

Interventionpercentage of participants (Number)
Acalabrutinib + R-ICENA

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Percentage of Participants Achieving Overall Response

Overall response is defined as the percentage of participants who achieved complete response (CR) or partial response (PR) to acalabrutinib + R-ICE therapy. Response will be assessed using Response Evaluation Criteria in Lymphoma (RECIL 2017) criteria. (NCT04189952)
Timeframe: 9 weeks

Interventionpercentage of participants (Number)
Acalabrutinib + R-ICENA

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Percentage of Participants Achieving Partial Response (PR)

The percentage of participants achieving partial response (PR) will be assessed using Response Evaluation Criteria in Lymphoma (RECIL 2017) criteria. (NCT04189952)
Timeframe: 9 weeks

Interventionpercentage of participants (Number)
Acalabrutinib + R-ICENA

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Progression-Free Survival (PFS)

Duration of Progression-Free Survival (PFS) in study participants. PFS is defined as the time from first dose to documented disease progression, or death from any cause, whichever occurs first. Data for subjects who are still alive and free from progression at the time of data cutoff date, lost to follow-up, or have discontinued the study will be censored on last assessment (or, if no post-baseline tumor assessment, at the time of first dose plus 1 day). (NCT04189952)
Timeframe: Up to 61 weeks

Interventionweeks (Number)
Acalabrutinib + R-ICENA

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