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procarbazine

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Description

Procarbazine: An antineoplastic agent used primarily in combination with mechlorethamine, vincristine, and prednisone (the MOPP protocol) in the treatment of Hodgkin's disease. [Medical Subject Headings (MeSH), National Library of Medicine, extracted Dec-2023]

procarbazine : A benzamide obtained by formal condensation of the carboxy group of 4-[(2-methylhydrazino)methyl]benzoic acid with the amino group of isopropylamine. An antineoplastic chemotherapy drug used for treatment of Hodgkin's lymphoma. Metabolism yields azo-procarbazine and hydrogen peroxide, which results in the breaking of DNA strands. [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]

Cross-References

ID SourceID
PubMed CID4915
CHEMBL ID1321
CHEBI ID71417
SCHEMBL ID4656
MeSH IDM0017616

Synonyms (110)

Synonym
procarbazin
AC-4547
BIDD:GT0183
unii-35s93y190k
35s93y190k ,
procarbazina
procarbazinum
SRI-10847-10
p-toluamide, n-isopropyl-.alpha.-(2-methylhydrazino)-
benzamide, n-(1-methylethyl)-4-[(2-methylhydrazino)methyl]-
NCI60_041703
n-(1-methylethyl)-4-[(2-methylhydrazino)methyl]benzamide
ibenzmethyzin
ro 4-6467
MIH ,
procarbazine [inn:ban]
procarbazina [inn-spanish]
einecs 211-582-2
procarbazinum [inn-latin]
hsdb 3250
brn 0958270
cb 400-497
p-toluamide, n-isopropyl-alpha-(2-methylhydrazino)-
benzamide, n-(1-methylethyl)-4-((2-methylhydrazino)methyl)-
procarbazin [german]
ccris 2389
p-(n'-methylhydrazinomethyl)-n-isopropylbenzamide
cas-366-70-1
NCGC00016438-01
n-isopropyl-4-[(2-methylhydrazino)methyl]benzamide
PRESTWICK3_001112
BPBIO1_001369
PRESTWICK2_001112
PCX ,
SRI-10847 ,
671-16-9
C07402
procarbazine
IBZ ,
n-isopropyl-alpha-(2-methylhydrazino)-p-toluamide
p-(2-methylhydrazinomethyl)-n-isopropylbenzamide
DB01168
n-4-isopropylcarbamoylbenzyl-n'-methylhydrazine
2-(p-isopropylcarbamoylbenzyl)-1-methylhydrazine
4-((2-methylhydrazino)methyl)-n-isopropylbenzamide
1-methyl-2-(p-(isopropylcarbamoyl)benzyl)hydrazine
n-(1-methylethyl)-4-((2-methylhydrazino)methyl)benzamide
n-isopropyl-p-(2-methylhydrazinomethyl)-benzamide
SPBIO_003112
PRESTWICK0_001112
NCIOPEN2_004074
PRESTWICK1_001112
BSPBIO_001244
NCGC00016438-02
HMS2090J09
procarbazine (inn)
D08423
procarbacine
ro-4-6467
CHEMBL1321
ro-4-6467 free base
chebi:71417 ,
4-[(2-methylhydrazinyl)methyl]-n-propan-2-ylbenzamide
dtxcid301189
tox21_301738
cas-671-16-9
NCGC00255280-01
dtxsid4021189 ,
nsc-759626
pharmakon1600-01502326
nsc759626
ibenzmethyzine
NCGC00016438-05
ro-4-6467/1
AKOS015891211
4-[(2-methylhydrazin-1-yl)methyl]-n-(propan-2-yl)benzamide
ro-4646711
gtpl7278
procarbazine [who-dd]
n-isopropyl-.alpha.-(2-methylhydrazino)-p-toluamide
procarbazine [inn]
procarbazine [hsdb]
procarbazine [vandf]
procarbazine [mi]
CCG-213031
SCHEMBL4656
SRI-10847-09
CPTBDICYNRMXFX-UHFFFAOYSA-N
mbh (salt/mix)
matulane (salt/mix)
natunalar (salt/mix)
n-isopropyl-4-[(2-methylhydrazino)methyl]benzamide #
nathulane (salt/mix)
n-isopropyl-4-((2-methylhydrazinyl)methyl)benzamide
SRI-10847_11
SRI-10847_13
STL483417
4-[(2-methylhydrazinyl)methyl]-n-(propan-2-yl)benzamide
SR-01000763375-3
sr-01000763375
FT-0737820
Q418656
procarbazine free base
671-16-9 (free base)
BCP12198
cb 400-497; ibenzmethyzine; mih
A917829
CS-0012387
HY-13733A
EN300-708801

Research Excerpts

Overview

Procarbazine (P) is an effective chemotherapeutic drug especially used in lymphoma treatment. Testicular toxicity is a limiting factor. Procarbazine hydrochloride is an oral alkylating agent.

ExcerptReferenceRelevance
"Procarbazine is a primary component of antineoplastic combination chemotherapy often used for the treatment of Hodgkin's lymphoma. "( Spectrum of Pig-a mutations in T lymphocytes of rats treated with procarbazine.
Bhalli, JA; Dobrovolsky, VN; Felton, N; McKinzie, P; Noteboom, J; Pearce, MG; Revollo, J; Tebbe, C; Thomas, D, 2017
)
2.13
"Procarbazine is a genotoxic carcinogen whose DNA-damaging activities are not reliably detected in vitro. "( Flow cytometric analysis of Pig-a gene mutation and chromosomal damage induced by procarbazine hydrochloride in CD-1 mice.
Avlasevich, SL; Bemis, JC; Dertinger, SD; Macgregor, JT; Mereness, J; Phonethepswath, S; Torous, DK, 2013
)
2.06
"Procarbazine is an anticancer agent that also inhibits monoamine oxidase, an enzyme responsible for the metabolism of various catecholamines, including serotonin."( Procarbazine and antidepressants: a retrospective review of the risk of serotonin toxicity.
Baker, NM; Bostwick, JR; Carpenter, J; Kraft, SL, 2014
)
3.29
"Procarbazine (P) is an effective chemotherapeutic drug especially used in lymphoma treatment; however testicular toxicity is a limiting factor. "( The effect of melatonin on procarbazine induced testicular toxicity on rats.
Akgül, EÖ; Alp, BF; Babacan, O; Erdem, O; Gulgun, M; Kesik, V; Korkmazer, N; Malkoç, E; Poyrazoglu, Y; Saldır, M; Yiğit, N, 2014
)
2.14
"Procarbazine hydrochloride is an oral alkylating agent primarily used as a component of chemotherapy regimens for Hodgkin's lymphoma, as well as in regimens for primary central nervous system lymphoma and high-grade gliomas. "( Procarbazine-induced hepatotoxicity: case report and review of the literature.
Becker-Koepke, S; Di Bisceglie, AM; Fesler, MJ; Petruska, PJ, 2010
)
3.25
"Procarbazine is a cytotoxic chemotherapeutic agent used in the treatment of lymphomas and brain tumors. "( Determination of procarbazine in human plasma by liquid chromatography with electrospray ionization mass spectrometry.
Batchelor, TT; Grossman, S; He, X; Supko, JG, 2004
)
2.11
"Procarbazine hydrochloride is an oral alkylating agent with activity against lymphoma. "( Procarbazine for non-Hodgkin's lymphoma.
Chaar, BT; Petruska, PJ; Salem, P, 2006
)
3.22
"Procarbazine (PCZ) is an antineoplastic agent useful in the treatment of Hodgkin's disease, brain tumors, and chronic leukemia. "( Profile of procarbazine-induced embryotoxicity in an embryo hepatocyte co-culture system and after in utero glutathione depletion.
Andrews, JE; Ebron-McCoy, MT; Kavlock, RJ; Nichols, HP, 1995
)
2.12
"Procarbazine is a chemotherapy methylating agent that has been used in combination with other drugs, perhaps most successfully in the treatment of Hodgkin's disease. "( Pulmonary toxicity secondary to procarbazine.
Mahmood, T; Mudad, R, 2002
)
2.04
"Procarbazine is a 1,2-disubstituted hydrazine derivative that is used to treat human leukemias. "( Methylazoxyprocarbazine, the active metabolite responsible for the anticancer activity of procarbazine against L1210 leukemia.
Harker, WG; Horstman, MG; Jaw, JY; Meadows, GG; Swaffar, DS; Thrall, BD; Yost, GS, 1989
)
2.11
"Procarbazine (Natulan) is a potent inducer of gene mutations at the heterozygous tk +/- locus in L5178Y mouse lymphoma cells in the presence of Aroclor-induced rat liver S9 metabolic activation (approximately 10(-3) mutant frequency at 10 micrograms/ml) while exerting a far weaker effect in the absence of S9. "( Procarbazine is a potent mutagen at the heterozygous thymidine kinase (tk +/-) locus of mouse lymphoma assay.
Clive, D; Krehl, R; Turner, N, 1988
)
3.16

Effects

Procarbazine (PCB) has been used for treating gliomas for many years and here both agents were combined in the treatment. Procarbazine has been implicated as a cause of infertility.

ExcerptReferenceRelevance
"Procarbazine (PCB) has been used for treating gliomas for many years and here both agents were combined in the treatment."( Phase I study of temozolamide (TMZ) combined with procarbazine (PCB) in patients with gliomas.
Foster, T; Newlands, ES; Zaknoen, S, 2003
)
1.29
"Procarbazine has been implicated as a cause of infertility. "( Regional procarbazine delivery reduces testicular toxicity.
Farr, SA; Johnson, FE; Sunwoo, YC; Susman, RS, 1993
)
2.15
"Procarbazine has been shown to be a hypoxic cell sensitizer of moderate ability in E. "( Radiosensitization of E. coli B/r by the cytotoxic agent procarbazine: a hypoxic cell sensitizer preferentially toxic to aerobic cells and easily oxidized.
Roberts, PB, 1979
)
1.95
"Procarbazine may have been the responsible agent."( Diffuse pulmonary disease after therapy with nitrogen mustard, vincristine, procarbazine, and prednisone.
Armstrong, JD; Farney, RJ; Hammer, S; Morris, AH, 1977
)
1.21

Actions

ExcerptReferenceRelevance
"Procarbazine did not inactivate monoamine oxidase like other hydrazines; this most likely reflects the fact that the oxidation product of the 1,2-disubstituted hydrazines is a stable azo derivative."( The mitochondrial metabolism of 1,2-disubstituted hydrazines, procarbazine and 1,2-dimethylhydrazine.
Coomes, MW; Prough, RA,
)
1.09

Treatment

Procarbazine had essentially no effect on the number of LPS antibody-producing cells in spleens of mice. Treatment with procarbazine was significantly correlated with survival time. Procarbazine treatment with doses of 200-400 mg/kg/day given IP for 3 consecutive days increased mean lifespan by 39%-46%.

ExcerptReferenceRelevance
"Procarbazine-treated dogs must be monitored for adverse reactions."( Procarbazine as adjunctive therapy for treatment of dogs with presumptive antemortem diagnosis of granulomatous meningoencephalomyelitis: 21 cases (1998-2004).
Barone, G; Coates, JR; Dewey, CW; Holloway-Azene, NM; Sessions, JK; Vitale, CL,
)
2.3
"Procarbazine treatment with doses of 200-400 mg/kg/day given IP for 3 consecutive days increased mean lifespan by 39%-46%."( The in vivo cytotoxic activity of procarbazine and procarbazine metabolites against L1210 ascites leukemia cells in CDF1 mice and the effects of pretreatment with procarbazine, phenobarbital, diphenylhydantoin, and methylprednisolone upon in vivo procarba
Shiba, DA; Weinkam, RJ, 1983
)
1.27
"Procarbazine treatment had essentially no effect on the number of LPS antibody-producing cells in spleens of mice in the entire range of PCZ dose and time, while the circulating antibody to LPS in serum diminished in mice treated with 600 mg/kg dose."( Alterations of immune response of DBA/2 mice by procarbazine treatment.
Ansari, AA; Baig, MA, 1981
)
1.24
"In procarbazine-treated rats, infusion of inhibin reduced the number of pachytene spermatocytes and reduced blood FSH levels simultaneously."( Testicular germ cell populations in the adult rat after continuous in-vivo testicular infusion of inhibin-A and activin-A.
Adeeko, AO; Dunne, E; Mather, J; Moore, A; Morris, ID, 1996
)
0.81
"Procarbazine treatment induced minimal disruption of normal interest in a receptive female, copulatory measures (intromissions or ejaculations) and structural integrity of seminal vesicles, bulbospongiosus muscles and ventral prostate glands."( Sociosexual behaviour and paternity in procarbazine-exposed rats with or without regional testicular circulatory isolation.
Farr, SA; Johnson, FE; Taylor, GT, 1997
)
1.29
"Treatment with procarbazine was significantly correlated with survival time (P < .001)."( Procarbazine as adjunctive therapy for treatment of dogs with presumptive antemortem diagnosis of granulomatous meningoencephalomyelitis: 21 cases (1998-2004).
Barone, G; Coates, JR; Dewey, CW; Holloway-Azene, NM; Sessions, JK; Vitale, CL,
)
1.91

Toxicity

Toxic effects resulted when procarbazine, a drug of this class, was used in treating a child with a CNS tumor. Procarbazine without S10 fraction is highly toxic and induced mitotic crossover, gene conversion, and reverse mutation in D7.

ExcerptReferenceRelevance
" Procarbazine, without S10 fraction, is highly toxic and induced mitotic crossover, gene conversion, and reverse mutation in D7."( Genetic toxicity of procarbazine in bacteria and yeast.
Bronzetti, G; Malling, HV; Zeiger, E, 1979
)
1.49
" A number of the toxic effects of procarbazine seen in humans were also noted in this series of monkeys, including vomiting and myelosuppression."( Carcinogenic and other adverse effects of procarbazine in nonhuman primates.
Adamson, RH; Correa, P; Dalgard, DW; Sieber, SM, 1978
)
0.8
" This side effect could be explained by a cycling of the hematopoietic stem-cells and call to some caution when androgens are used during cancer chemotherapy."( [Increased hematological toxicity of antineoplastic drugs with simultaneous androgenotherapy (author's transl)].
Barthélémy, M; Bilski-Pasquier, G; Blanc, CM; Bouchard, M; Bousser, J; Zittoun, R, 1977
)
0.26
"Pulmonary toxicity is a well recognised side effect of anticancer agents particularly bleomycin, cyclophosphamide, methotrexate, and busulphan."( Pulmonary toxicity following MOPP chemotherapy.
Byrne, MJ; Cohney, SJ; Millward, MJ; Ryan, GF, 1990
)
0.28
" There were three fatal toxic events, two due to viral infection and one to a second malignant tumor (NHL)."( Hodgkin's disease in children: treatment with MOPP and low-dose, extended field irradiation without laparotomy. Late results and toxicity.
Berry, M; Blanchette, V; Chan, H; Doherty, M; Doyle, J; Freedman, M; Greenberg, M; Jenkin, D; Panzarella, T; Saunders, F, 1990
)
0.28
" Toxic effects resulted when procarbazine, a drug of this class, was used in treating a child with a CNS tumor."( Monoamine oxidase inhibitor toxicity.
Pack, R; Pfefferbaum, B; van Eys, J, 1989
)
0.57
" When cell growth is expressed as percentage survival of L1210 cells, the azoxy 2 isomer was approximately 7-fold more toxic than the azoxy 1 metabolite."( Cytotoxicity and DNA damage caused by the azoxy metabolites of procarbazine in L1210 tumor cells.
Ducore, JM; Erikson, JM; Prough, RA; Tweedie, DJ, 1989
)
0.52
" The decrease in toxicity caused by deuterium substitution at the benzylic position, coupled with the absence of an effect with the methyl-labeled analog, indicate the requirement for regioselective oxidative metabolism of procarbazine at the benzylic position prior to the toxic event."( Procarbazine spermatogenesis toxicity: deuterium isotope effects point to regioselective metabolism in mice.
el Walily, AF; Gordon, WP; Horstman, MG; Nelson, SD; Yost, GS, 1985
)
1.9
" In 59 patients with advanced disease who received no other treatment, a 5-year survival rate of 66% was comparable with that achieved by more toxic mustine-containing combinations."( Five years' experience with ChlVPP: effective low-toxicity combination chemotherapy for Hodgkin's disease.
Austin, DE; Barrett, A; Dady, PJ; McElwain, TJ; Peckham, MJ, 1982
)
0.26
" Although the neurotoxic effects produced by different cytostatics present a different appearance and are partly of only sporadic or slight clinical importance, there is hardly a cytostatic which does not exercise a side effect on the nervous system."( [Neurotoxic side effects of cytostatic therapy (author's transl)].
Maurach, R; Strian, F, 1981
)
0.26
" Studies have shown that the formation of toxic metabolites can result from glutathione (GSH) conjugation of toxicants in the liver."( Profile of procarbazine-induced embryotoxicity in an embryo hepatocyte co-culture system and after in utero glutathione depletion.
Andrews, JE; Ebron-McCoy, MT; Kavlock, RJ; Nichols, HP, 1995
)
0.68
" LD50 at day 59 for procarbazine appears to be approximately 600 mg kg-1 body weight using this regimen."( Testicular cytotoxicity of intravenous procarbazine in rats.
Doubek, WG; Janney, CG; Johnson, FE; Tolman, KC, 1993
)
0.88
"Cardiotoxicity is a well recognized side effect of anthracyclines (doxorubicin and epirubicin) or antracenadiones (mitoxantrone) at cumulative or high doses."( Late cardiac toxicity of doxorubicin, epirubicin, and mitoxantrone therapy for Hodgkin's disease in adults.
Arévila, N; Avilés, A; Díaz Maqueo, JC; García, R; Gómez, T; Nambo, MJ, 1993
)
0.29
"Several hydrazine derivatives (HD) tested so far have pharmacological activities, but many also have toxic side effects, including carcinogenesis."( Contribution of hydrazines-derived alkyl radicals to cytotoxicity and transformation induced in normal c-myc-overexpressing mouse fibroblasts.
Armelin, MC; Cidade, MR; Gamberini, M; Leite, LC; Valotta, LA, 1998
)
0.3
" Despite increased hematotoxicity, moderate dose escalation is safe for the majority of the patients with G-CSF assistance and standard supportive treatment."( Acute hematologic toxicity and practicability of dose-intensified BEACOPP chemotherapy for advanced stage Hodgkin's disease. German Hodgkin's Lymphoma Study Group (GHSG).
Diehl, V; Engel, C; Loeffler, M; Schmitz, S; Tesch, H, 2000
)
0.31
"Peripheral neurotoxicity is a crucial side effect of chemotherapeutic agents."( [Peripheral nervous system neurotoxicity secondary to chemotherapy treatment] .
Iñiguez, C; Larrodé, P; Mauri, JA; Mayordomo, JI; Morales, F; Trés, A, 2000
)
0.31
"In this study we aimed to discuss whether the gonadal suppression is effective or not in preventing the gonadal toxic effects of some chemotherapeutics."( The effects of GnRH analogues and antiandrogenes in preventing the gonadotoxic effects of COPP chemotherapy.
Akay, AF; Bircan, MK; Deniz, M; Göçmen, M; Nergiz, Y; Sahin, H, 2001
)
0.31
"As a conclusion we think that gonadal suppression applied during chemotherapy regimen could decrease the testicular toxic effects of chemotherapeutic but more clinical investigations needed for routine application."( The effects of GnRH analogues and antiandrogenes in preventing the gonadotoxic effects of COPP chemotherapy.
Akay, AF; Bircan, MK; Deniz, M; Göçmen, M; Nergiz, Y; Sahin, H, 2001
)
0.31
"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
" The use of most cytotoxic agents is associated with potential hypersensitivity reactions, and the constant increase of their administration has caused an increase in incidence of these adverse effects, thus becoming a relevant problem for clinicians."( The complex clinical picture of presumably allergic side effects to cytostatic drugs: symptoms, pathomechanism, reexposure, and desensitization.
Pagani, M, 2010
)
0.36
"The majority of patients with Hodgkin's disease can be cured by combination of polychemotherapy and radiotherapy (RT) that can produce late toxic pulmonary and cardiac effects which often remain at a subclinical level."( Cardiopulmonary toxicity of different chemoradiotherapy combined regimens for Hodgkin's disease.
Bonfante, V; Busia, A; Laffranchi, A; Villani, F; Viviani, S, 2010
)
0.36
"These data confirm that the combination of mediastinal RT with the more commonly used polychemotherapy regimens produce late toxic effects."( Cardiopulmonary toxicity of different chemoradiotherapy combined regimens for Hodgkin's disease.
Bonfante, V; Busia, A; Laffranchi, A; Villani, F; Viviani, S, 2010
)
0.36
"Previously, adverse event reports (AERs) submitted to the US Food and Drug Administration (FDA) database were reviewed to confirm platinum agent-associated hypersensitivity reactions."( Hypersensitivity reactions to anticancer agents: data mining of the public version of the FDA adverse event reporting system, AERS.
Brown, JB; Kadoyama, K; Kuwahara, A; Okuno, Y; Sakaeda, T; Yamamori, M, 2011
)
0.37
" However, the total number of adverse events occurring with procarbazine, asparaginase, teniposide, or etoposide was not large enough to detect signals."( Hypersensitivity reactions to anticancer agents: data mining of the public version of the FDA adverse event reporting system, AERS.
Brown, JB; Kadoyama, K; Kuwahara, A; Okuno, Y; Sakaeda, T; Yamamori, M, 2011
)
0.61
"The FDA's adverse event reporting system, AERS, and the data mining methods used herein are useful for confirming drug-associated adverse events, but the number of co-occurrences is an important factor in signal detection."( Hypersensitivity reactions to anticancer agents: data mining of the public version of the FDA adverse event reporting system, AERS.
Brown, JB; Kadoyama, K; Kuwahara, A; Okuno, Y; Sakaeda, T; Yamamori, M, 2011
)
0.37
" Information evaluated included patient signalment, feline immunodeficiency virus/feline leukemia virus status, anatomic location(s) of lymphoma, prior protocols (type and number), MOPP doses, MOPP response, remission duration, hematologic and biochemical parameters, and owner-reported adverse effects."( Efficacy and toxicity of mustargen, vincristine, procarbazine and prednisone (MOPP) for the treatment of relapsed or resistant lymphoma in cats.
Brown, DC; Krick, EL; MaloneyHuss, MA; Mauldin, GE; Veluvolu, SM, 2020
)
0.81
" The most common adverse effects were neutropenia and gastrointestinal upset, which were reported in 18."( Efficacy and toxicity of mustargen, vincristine, procarbazine and prednisone (MOPP) for the treatment of relapsed or resistant lymphoma in cats.
Brown, DC; Krick, EL; MaloneyHuss, MA; Mauldin, GE; Veluvolu, SM, 2020
)
0.81
"MOPP is a safe protocol for the treatment of relapsed or refractory feline lymphoma, with a promising overall response rate and median remission time."( Efficacy and toxicity of mustargen, vincristine, procarbazine and prednisone (MOPP) for the treatment of relapsed or resistant lymphoma in cats.
Brown, DC; Krick, EL; MaloneyHuss, MA; Mauldin, GE; Veluvolu, SM, 2020
)
0.81
"Evidently, the conclusion of this study will provide an assessment on whether combined procarbazine, lomustine, and vincristine provides an effective and safe form of treatment for recurrent high-grade glioma."( A comparative study of the effectiveness and safety of combined procarbazine, lomustine, and vincristine as a therapeutic method for recurrent high-grade glioma: A protocol for systematic review and meta-analysis.
Cai, Y; Jiang, YG; Jiang, ZH; Tan, ZG; Wang, M, 2020
)
1.02

Pharmacokinetics

ExcerptReferenceRelevance
"Dibromdulcitol (Elobromol) has favorable pharmacokinetic parameters for the treatment of brain tumors: high spinal fluid/plasma ratio and long half-life in spinal fluid."( Treatment of malignant scala posterior brain tumors in children: the chemotherapy of relapsed medulloblastoma with a dibromdulcitol containing drug regime and pharmacokinetic studies of dibromdulcitol in children.
Kálmánchey, R; Koóos, R; Paraicz, E; Schuler, D; Somló, P, 1992
)
0.28
" The elimination half-life (t1/2 less than 80 min) allows autologous bone marrow transplantation 24 h after the drug administration."( Pharmacokinetics of high-dose melphalan in children and adults.
Gouyette, A; Hartmann, O; Pico, JL, 1986
)
0.27
"004), the elimination half-life was 35% shorter (12."( Cytochrome P450-inducing antiepileptics increase the clearance of vincristine in patients with brain tumors.
Joensuu, H; Kivistö, KT; Mäenpää, H; Neuvonen, PJ; Villikka, K, 1999
)
0.3
" Pharmacokinetic studies were done with a new electrospray ionization mass spectrometry assay."( The effect of enzyme-inducing antiseizure drugs on the pharmacokinetics and tolerability of procarbazine hydrochloride.
Alavi, JB; Batchelor, TT; Carson, KA; Fisher, JD; Grossman, SA; Hammour, T; Lesser, G; Mikkelsen, T; Phuphanich, S; Supko, JG, 2006
)
0.55
"Three plasma samples and a 24-hour urine collection for day 1 of the first three cycles of chemotherapy were analysed in 30 patients, and the pharmacokinetic parameters of the respective drugs were estimated by population pharmacokinetic methods (nonlinear mixed-effects model [NONMEM] software)."( Population pharmacokinetics of the BEACOPP polychemotherapy regimen in Hodgkin's lymphoma and its effect on myelotoxicity.
Busse, D; Diehl, V; Engert, A; Fuhr, U; Hempel, G; Jaehde, U; Jetter, A; Josting, A; Kasel, D; Klimm, B; Merkel, U; Reif, S; Rietbrock, S; Schwab, M; Wilde, S, 2007
)
0.34
"The pharmacokinetic parameters and respective covariates were similar to the published data."( Population pharmacokinetics of the BEACOPP polychemotherapy regimen in Hodgkin's lymphoma and its effect on myelotoxicity.
Busse, D; Diehl, V; Engert, A; Fuhr, U; Hempel, G; Jaehde, U; Jetter, A; Josting, A; Kasel, D; Klimm, B; Merkel, U; Reif, S; Rietbrock, S; Schwab, M; Wilde, S, 2007
)
0.34

Compound-Compound Interactions

Fotemustine combined with a fixed dose of procarbazine (PCZ) to evaluate extent of O6-alkylguanine-DNA alkyltransferase (ATase) depletion in circulating lymphocytes. BCNU in combination with Vincristine and Procarbazine every 6 weeks.

ExcerptReferenceRelevance
" All other disease stages will require a different strategy that should consist of radiotherapy combined with short-term effective regimens, such as ABVD (doxorubicin, bleomycin, vinblastine and decarbazine) or VBM (vinblastine, bleomycin and methotrexate) to reduce the incidence of MOPP-associated gonadal dysfunction and leukaemogenesis."( Early stage Hodgkin's disease: ten-year results of a non-randomised study with radiotherapy alone or combined with MOPP.
Banfi, A; Bonadonna, G; Bonfante, V; Devizzi, L; Santoro, A; Tesoro Tess, JD; Valagussa, P; Viviani, S; Zanini, M; Zucali, R, 1992
)
0.28
" It is noteworthy that in all subsets, ABVD (Adriamycin + bleomycin + vinblastine + dacarbazine), either combined with irradiation or alternated with MOPP (mechlorethamine + vincristine + procarbazine + prednisone), yielded superior results compared with MOPP with or without irradiation."( Prognosis of bulky Hodgkin's disease treated with chemotherapy alone or combined with radiotherapy.
Bonadonna, G; Santoro, A; Valagussa, P, 1985
)
0.46
" From 1980 to 1982, 96 patients with SCLC were treated, 37 of whom by chemotherapy combined with surgery."( [Chemotherapy combined with selective resection in small cell lung cancer--analysis of 239 patients].
Cao, YF; Chen, YR; Fang, MS; Huang, OL; Liao, ML; Wu, SC; Wu, SF; Wu, SZ; Xu, CW; Yang, XF, 1986
)
0.27
"From 1976 to 1981, 335 patients with untreated Hodgkin's disease, clinical stages I, II, and IIIA, have been treated by MOPP (nitrogen mustard, vincristine, procarbazine, prednisone) chemotherapy, three to six cycles according to the prognostic factors, combined with radiotherapy."( Extended versus involved fields irradiation combined with MOPP chemotherapy in early clinical stages of Hodgkin's disease.
Audebert, A; Bernadou, A; Diebold, J; Eghbali, H; Hoerni, B; Krulik, M; Merle-Béral, H; Parlier, Y; Rojouan, J; Zittoun, R, 1985
)
0.47
" BCNU in combination with Vincristine and Procarbazine every 6 weeks."( Complications associated with intra-arterial BCNU administered in combination with vincristine and procarbazine for the treatment of malignant brain tumors.
Balsys, R; Bremer, AM; Duarte, P; Gonzalez, N; Kleriga, E; Miller, RI; Nguyen, TQ; Northup, HM, 1984
)
0.75
"The clinical efficacy of COP-BLAM chemotherapy combined with human recombinant granulocyte colony-stimulating factor (G-CSF) was evaluated in 104 previously untreated patients with non-Hodgkin's lymphoma (NHL)."( COP-BLAM regimen combined with granulocyte colony-stimulating factor and high-grade non-Hodgkin's lymphoma.
Niitsu, N; Umeda, M, 1995
)
0.29
"We evaluated the efficacy and adverse effects of biweekly COP-BLAM (cyclophosphamide, vincristine, prednisone, bleomycin, doxorubicin and procarbazine) therapy combined with granulocyte colony-stimulating factor (G-CSF) for treating non-Hodgkin's lymphoma (NHL)."( Biweekly COP-BLAM (cyclophosphamide, vincristine, prednisone, bleomycin, doxorubicin and procarbazine) regimen combined with granulocyte colony stimulating factor (G-CSF) for intermediate-grade non-Hodgkin's lymphoma.
Niitsu, N; Umeda, M, 1996
)
0.72
"One hundred and sixty seven patients with non-Hodgkin's lymphoma were randomly divided into two groups, the treatment group, which consisted of 112 cases using Chinese herbs combined with chemotherapy and 55 cases of control group were treated by chemotherapy only."( [Clinical observation on 112 cases with non-Hodgkin's lymphoma treated by Chinese herbs combined with chemotherapy].
Guo, XM; Li, JX; Yang, XF, 1997
)
0.3
" These showed that Chinese herbs combined with chemotherapy was a safe and effective method for treating NHL and deserve to be recommended."( [Clinical observation on 112 cases with non-Hodgkin's lymphoma treated by Chinese herbs combined with chemotherapy].
Guo, XM; Li, JX; Yang, XF, 1997
)
0.3
"The aims of this phase I study in patients with recurrent malignant gliomas were to determine the maximum tolerated dose (MTD) and toxicity profile of fotemustine when combined with a fixed dose of procarbazine (PCZ), and to evaluate the extent of O6-alkylguanine-DNA alkyltransferase (ATase) depletion in circulating lymphocytes during treatment."( Fotemustine combined with procarbazine in recurrent malignant gliomas: a phase I study with evaluation of lymphocyte 06-alkylguanine-DNA alkyltransferase activity.
Berger, E; Boiardi, A; Ciusani, E; Giroux, B; Lucas, C; Margison, G; Silvani, A; Watson, A, 2001
)
0.8
"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
" This phase I study was designed to evaluate the efficacy and safety of TMZ alone (course 1) and TMZ in combination with PCB in subsequent courses in chemotherapy-naïve patients with malignant glioma."( Phase I study of temozolamide (TMZ) combined with procarbazine (PCB) in patients with gliomas.
Foster, T; Newlands, ES; Zaknoen, S, 2003
)
0.57
"To improve survival of elderly patients with primary central nervous system lymphoma (PCNSL), we conducted a phase II study with high-dose methotrexate (MTX) combined with procarbazine and CCNU."( High-dose methotrexate combined with procarbazine and CCNU for primary CNS lymphoma in the elderly: results of a prospective pilot and phase II study.
Deckert, M; Feuerhake, F; Finke, J; Ihorst, G; Illerhaus, G; Marks, R; Müller, F; Ostertag, C, 2009
)
0.82
"Intrinsic subtypes are highly prognostic in EORTC 26951 and improve outcome prediction when combined with other prognostic factors."( Intrinsic molecular subtypes of glioma are prognostic and predict benefit from adjuvant procarbazine, lomustine, and vincristine chemotherapy in combination with other prognostic factors in anaplastic oligodendroglial brain tumors: a report from EORTC stu
de Rooi, J; den Dunnen, WF; Eilers, PH; Erdem-Eraslan, L; French, PJ; Gorlia, T; Gravendeel, LA; Idbaih, A; Kros, JM; Sillevis Smitt, PA; Spliet, WG; Teepen, JL; van den Bent, MJ; Wesseling, P, 2013
)
0.61
"To investigate the efficacy and safety of Rituximab combined with second line regimen for treatment of relapsed and refractory Hodgkin lymphoma."( [Rituximab combined with second line regimens for treatment of seven relapsed and refractory Hodgkin lymphoma patients].
Li, H; Liu, H; Qiu, L; Xiong, W; Yi, S; Zou, D, 2015
)
0.42
"Seven patients with relapsed and refractory Hodgkin lymphoma were treated with Rituximab combined with second line regimen."( [Rituximab combined with second line regimens for treatment of seven relapsed and refractory Hodgkin lymphoma patients].
Li, H; Liu, H; Qiu, L; Xiong, W; Yi, S; Zou, D, 2015
)
0.42
"These results indicate that the Rituximab combined with second line regimen is an effective therapy for relapsed and refractory Hodgkin lymphoma."( [Rituximab combined with second line regimens for treatment of seven relapsed and refractory Hodgkin lymphoma patients].
Li, H; Liu, H; Qiu, L; Xiong, W; Yi, S; Zou, D, 2015
)
0.42

Bioavailability

ExcerptReferenceRelevance
" Since the absorption rate is not clinically relevant in patients on long-term glycoside therapy, our results indicate that digitoxin is preferable to digoxin in such patients."( Cytostatic drugs are without significant effect on digitoxin plasma level and renal excretion.
Kuhlmann, J; Rietbrock, N; Wilke, J, 1982
)
0.26
" The aim of the study was to determine the oral bioavailability of high dose methylprednisolone and to establish whether this is a feasible and more convenient route of administration."( Pharmacokinetics of high dose methylprednisolone and use in hematological malignancies.
Graham, MA; McElwain, TJ; Newell, DR; Patel, PM; Selby, PJ; Viner, C,
)
0.13
" Interaction between copper and other stressors operating only in the field probably balance the higher bioavailability in spiked soil."( Effect of a copper gradient on plant community structure.
Attrill, MJ; Axelsen, JA; Jensen, J; Pedersen, MB; Strandberg, B, 2006
)
0.33
"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

Study of 5-year HL survivors found a dose-response association between radiation therapy and colorectal cancer risk, and modification of this association by procarbazine.

ExcerptRelevanceReference
" Because of rapid progression of the amyloidosis and further infections, cytotoxic drug therapy was stopped, corticosteroid dosage was decreased, and supplementary immunoglobulin therapy was instituted."( Amyloidosis associated with dermatomyositis and features of multiple myeloma. The progression of amyloidosis associated with corticosteroid and cytotoxic drug therapy.
Dawkins, RL; Zilko, PJ, 1975
)
0.25
" On the other side, dosage and the interval between cycles of chemotherapy appear to be a determining factor in the activity, but the limits are very narrow."( [A study of the use of sequential chemotherapy in 176 cases of glioblastoma (author's transl)].
Buge, A; Poisson, M; Pouillart, P, 1978
)
0.26
"We investigated the effect of two variables, the time interval between drug administration and transplant removal and the dosage of the drug, on the prolongation of rat heart allograft survival via donor pretreatment."( Prolongation of rat cardiac allograft survival by donor pretreatment. Impact of dose and timing of drug administration.
Häyry, P; Soots, A, 1979
)
0.26
" Male mice were dosed once and mated with fresh virgin females each week."( Action of N-isopropyl-alpha-(2-methylhydrazino)-p-toluamide hydrochloride (procarbazine hydrochloride) in the germ tissue of mice: dominant lethal effects.
Johnson, FM; Malling, HV; Roberts, GT; Sharma, RK, 1979
)
0.49
" Methodology and dosage schemes are discussed."( Towards curative treatment of advanced Hodgkin's disease.
Falkson, G; Falkson, HC, 1975
)
0.25
" In a multivariate analysis where both disease-related and treatment-related factors were taken into account drug dosage remained a significant prognostic factor."( Treatment of Hodgkin's disease with MOPP chemotherapy: effect of dose and schedule modification on treatment outcome.
Bezwoda, MA; Bezwoda, WR; Dansey, R, 1990
)
0.28
"5 micrograms/kg/day, sc), which significantly shortened the duration of neutropenia and decreased the number of days with episodes of fever when compared with those not given rhG-CSF, consequently facilitating the treatment without prolonging the dosing intervals."( [The COP-BLAM III therapy of non-Hodgkin's lymphoma].
Arai, N; Hara, A; Shirai, T; Umeda, M, 1991
)
0.28
" In addition to the high mean MPE frequency observed after 2 doses of 116 mg/kg of PC at the 48-h sampling time, a late increase in micronucleus induction was also seen after triple dosing at the 96-h sampling time."( Comparison of single/multiple-dose protocols using triethylenemelamine and procarbazine hydrochloride for the mouse bone marrow micronucleus test.
Romagna, F; Schneider, BM,
)
0.36
" The predictive value of mechlorethamine dosage with regard to OS was retained in an analysis restricted to the patients receiving greater than or equal to six cycles of chemotherapy."( Dose intensity of MOPP chemotherapy and survival in Hodgkin's disease.
de Meijer, AJ; Dekker, AW; Haanen, C; van Rijswijk, RE; Verbeek, J, 1989
)
0.28
" The CVPP schedule gave: (1) a constant drug dosage for each patient independent of body surface or weight; and (2) a total drug dosage dependent on haematological tolerance, since the treatment was given for 21 days or until the leukocyte count dropped to 2 x 10(9) l-1."( Influence of dose intensity and density on therapeutic and toxic effects in Hodgkin's disease.
Bonichon, F; Chauvergne, J; de Mascarel, I; Eghbali, H; Hoerni, B; Lagarde, P, 1989
)
0.28
" The subsequent radiotherapy was limited to the initially involved fields, the dosage of 35, 30 or 25 Gy depending on the extent of chemotherapy."( [Significance of procarbazine in the chemotherapy of Hodgkin's disease--a report of the Cooperative Therapy Study DAL-HD-85].
Bökkerink, JP; Brämswig, J; Heinecke, H; Hörnig, I; Ludwig, R; Niethammer, D; Reiter, A; Schellong, G; Steinhoff, A; von Lengerke, HJ,
)
0.47
" Buserelin (d-Ser-[TBU]6 LHRH ethylamide) was prescribed in two different dosage schedules to twenty men, and in a single dosage schedule to eight women."( Failure to preserve fertility in patients with Hodgkin's disease.
Ahmed, R; Besser, GM; Crowther, D; Gregory, W; Malpas, JS; Rees, LH; Shalet, S; Smith, D; Waxman, JH; Wrigley, PF, 1987
)
0.27
" The optimal dosing for MV26PD remains to be determined."( Treatment of refractory lymphoma with methotrexate, VM-26 (teniposide), procarbazine, and dexamethasone: Cancer and Leukemia Group B study 7902.
Anderson, J; Bloomfield, CD; Cooper, MR; Ginsberg, SJ; Gottlieb, AJ; Hurd, DD; Lachant, NA, 1988
)
0.51
" The enhancement of damage may have been caused by either a change in the shoulder width of the cell-survival curve, or additive cell-killing as indicated by a dose-response study."( Survival of murine clonogenic stem spermatogonia following combined radiation and cytotoxic drug treatments.
Bush, C; Delic, JI; Steel, GG, 1986
)
0.27
" Enhancement in the case of PCB consisted largely of a vertical displacement of the radiation dose-response curves, but with additional evidence for possible changes in slope."( Influence of timing of cytotoxic drug treatment on the response of murine clonogenic spermatogonia to X-irradiation.
Bush, C; Delic, JI; Steel, GG, 1986
)
0.27
" Demonstration of systemic signs, bioptically confirmed bone-marrow infiltration and suboptimal cytostatic dosage correlated significantly with a lower full-remission rate."( [Chemotherapy of advanced lymphogranulomatosis. Results of MOPP/COPP treatment at the West German Tumor Center, Essen].
Becher, R; Höffken, K; Ippisch, A; Pfeiffer, R; Schmidt, CG; Seeber, S, 1985
)
0.27
" In the absence of evidence of a dose-response curve for platinum, the lower dosage schedules that can be used with acceptable toxicity on an outpatient basis should be selected."( Chemotherapy for squamous cell carcinoma of the head and neck: a progress report.
Glick, JH; Taylor, SG; Zehngebot, LM, 1980
)
0.26
" From 1976 to 1979 patients with Stage IV disease were treated wither with MOPP or with MOPP plus bleomycin at low dosage (B-MOPP); the incidence of complete remission was not significantly different in the two groups of patients (52 vs."( Combination chemotherapy for stage IV Hodgkin's disease (Report no 14).
Goldman, JM, 1981
)
0.26
" Time-response and dose-response were studied for chromosomal aberrations induced by transplacental treatment of mouse embryos."( New approaches to mutagenicity studies in animals for carcinogenic and mutagenic agents. II. Clastogenic effects determined in transplacentally treated mouse embryos.
Adler, ID, 1983
)
0.27
" It has become evident that DES at a dosage of 3 mg/day carries a significantly higher risk of overall cardiovascular toxicity than does cyproterone acetate, but severe cardiovascular complications did not differ between treatment groups."( Treatment of prostatic cancer: the EORTC experience--preliminary results of prostatic carcinoma trials.
Schroeder, FH, 1984
)
0.27
" Dose-response relationships of 3 triple-drug combinations and their component agents were explored, allowing the relative contributions of single agents in each combination to be assessed."( Experimental combination and single-agent chemotherapy in human lung-tumour xenografts.
Jones, JM; Peckham, MJ; Shorthouse, AJ; Steel, GG, 1982
)
0.26
" cytostatic antibiotic), the dosage (20% LD50 vs."( Immunosuppression by cytostatic drugs?
Duncker, D; Müller-Ruchholtz, W; Ulrichs, K; Yu, MY, 1984
)
0.27
" There were no differences in dosage of these two agents between patients who remain alive in CR and those who relapsed and died."( Simultaneous low-dose radiation and low-dose chemotherapy in the treatment of advanced Hodgkin's disease.
Gomez, GA; Han, T; Henderson, ES; Ozer, H; Panahon, AM; Stutzman, L, 1984
)
0.27
"A dose-response analysis of the results of MOPP chemotherapy in 132 patients with Hodgkin's disease was carried out."( A dose and time response analysis of the treatment of Hodgkin's disease with MOPP chemotherapy.
Carde, P; MacKintosh, FR; Rosenberg, SA, 1983
)
0.27
" A comparison of drug dosage in the group receiving TPN and the group receiving standard nutrition is a measure of drug tolerance in these patients."( A prospective randomized study of adjuvant parenteral nutrition in the treatment of diffuse lymphoma: effect on drug tolerance.
Brennan, MF; Fisher, RI; Popp, MB; Simon, RM, 1981
)
0.26
" The planned dosage intensity had to be significantly reduced in over half of the patients because of marrow toxicity."( Measurement of drug dosage intensity in MVPP therapy in Hodgkin's disease.
Dawson, AA; Fell, LF; Green, JA; Murray, S, 1980
)
0.26
" The administration of 500 mg PCB/kg 1 day before procarbazine dosage was suitable for the detection of the mutagenicity."( Detection of mutagenicity of procarbazine by the host-mediated assay with polychlorinated biphenyl (aroclor 1254) as enzyme inducer.
Moriya, M; Ohta, T; Shirasu, Y; Watanabe, K, 1980
)
0.81
" The COPP patients received 84% of the calculated ideal doses of cyclophosphamide and 78% of the ideal dosage of procarbazine."( Nodular mixed lymphoma: results of a randomized trial failing to confirm prolonged disease-free survival with COPP chemotherapy.
Barnes, JM; Bennett, JM; Berard, CW; Ezdinli, EZ; Glick, JH; Orlow, EL, 1981
)
0.47
" At equivalent germ-cell stages and dosage the mouse UDS assay is more sensitive, by a factor of 2 to 3, than the rabbit assay for the induction of UDS by procarbazine and MMS."( Induction of unscheduled DNA synthesis in the germ cells of male mice after treatment with hydrazine or procarbazine.
Chauhan, PS; Ehling, UH; Sotomayor, RE, 1982
)
0.68
" The time of expression and dose-response relationships obtained with gamma-radiation, methyl methanesulphonate, procarbazine, mitomycin C and benzo[a]pyrene are analysed in terms of this model."( Short-term tests for transplacentally active carcinogens. I. Micronucleus formation in fetal and maternal mouse erythroblasts.
Arlett, CF; Cole, J; Cole, RJ; Taylor, N, 1981
)
0.47
" Using appropriate dosage schedules, cyclophosphamide, methotrexate and procarbazine either potentiated or had no effect on DTH."( Selective effects of immunosuppressive agents against the delayed hypersensitivity response and humoral response to sheep red blood cells in mice.
Doherty, NS, 1981
)
0.5
" Therefore, in a second set of experiments, rat embryos were cultured in serum from rats pretreated with two GSH depleters (phorone and buthionine sulfoximine) and subsequently dosed with PCZ."( Profile of procarbazine-induced embryotoxicity in an embryo hepatocyte co-culture system and after in utero glutathione depletion.
Andrews, JE; Ebron-McCoy, MT; Kavlock, RJ; Nichols, HP, 1995
)
0.68
" Pretreatment of mice with O6-benzylguanine increased temozolomide-induced mortality, requiring reduction of the dosage from 1200 to 750 mg/m2 on the single-day regimen."( Activity of temozolomide in the treatment of central nervous system tumor xenografts.
Bigner, DD; Catino, JJ; Dolan, ME; Friedman, HS; Keir, S; Marcelli, S; Pegg, AE; Schold, SC, 1995
)
0.29
" Comparison of the dose-response relationships for humans and rats indicates that, under conditions of no depletion of O6-alkylguanine-DNA alkyltransferase (AGT), O6-meG accumulates in blood leukocyte DNA of humans at a rate which is only approximately 2-fold lower than in rats, implying that, to the extent to which O6-meG contributes to the genotoxic activity of procarbazine, human susceptibility to it is likely to be comparable to that of the rat."( Comparative dosimetry of O6-methylguanine in humans and rodents treated with procarbazine.
Boussiotis, VA; Kyrtopoulos, SA; Pangalis, GA; Souliotis, VL; Valavanis, C, 1994
)
0.69
"Because several previous authors have repeatedly described treatment with thiamine as one of the sufficient prophylactic measures in slowing the development of viscerocranial malformations, especially cleft alveolus and palate, it is of utmost importance that the timing of treatment and dosage of thiamine be taken into consideration not only in animal experiments but also when applying results to humans."( Application of thiamine in preventing malformations, specifically cleft alveolus and palate, during the intrauterine development of rats.
Bienengräber, V; Fanghänel, J; Kundt, G; Malek, FA, 1997
)
0.3
" Prognostic factors other than age should be taken into account, particularly when doses and dosing intervals are determined."( Prognostic factors in elderly patients with non-Hodgkin's lymphoma treated with cyclophosphamide, vincristine, prednisone, bleomycin, Adriamycin, procarbazine (COP-BLAM) therapy.
Niitsu, N, 1997
)
0.5
" Further follow-up is required to assess the effect of dosage and the effect on survival and late toxicities."( BEACOPP, a new dose-escalated and accelerated regimen, is at least as effective as COPP/ABVD in patients with advanced-stage Hodgkin's lymphoma: interim report from a trial of the German Hodgkin's Lymphoma Study Group.
Bischoff, H; Diehl, V; Duehmke, E; Engert, A; Franklin, J; Georgii, A; Glunz, A; Haedicke, C; Hasenclever, D; Hermann, R; Holmer, L; Krause, S; Lathan, B; Loeffler, M; Paulus, U; Pfreundschuh, M; Rueffer, JU; Sextro, M; Sieber, M; Stappert-Jahn, U; Tesch, H; von Kalle, K; Winnerlein-Trump, E; Wolf, J; Wulf, G, 1998
)
0.3
" Despite prompt initiation of antimycotic therapy the outcome was fatal; dosage of conventional and liposomal amphotericin B was limited due to treatment-related toxicities."( A novel type of metastatically spreading subcutaneous aspergillosis without epidermal lesions following allogeneic stem cell transplantation.
Bethe, U; Cornely, OA; Pels, H; Ritzkowsky, A; Seibold, M; Soehngen, D; Toepelt, K, 2001
)
0.31
" Parameters were evaluated by age at diagnosis, gender, ethnic origin, pre- and postsurgery Karnofsky Performance Status (KPS) score, limit and amount of surgical resection, histopathologic type, number of chemotherapy courses, time between surgery and radiotherapy, response to combined therapy, and dosage and type of radiotherapy."( Long-term follow-up in managing anaplastic astrocytoma by multimodality approach with surgery followed by postoperative radiotherapy and PCV-chemotherapy: phase II trial.
Gal, O; Kovner, F; Ron, IG; Vishne, TH, 2002
)
0.31
" 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
" Prednisone was reduced in dosage or discontinued in 17 dogs."( Procarbazine as adjunctive therapy for treatment of dogs with presumptive antemortem diagnosis of granulomatous meningoencephalomyelitis: 21 cases (1998-2004).
Barone, G; Coates, JR; Dewey, CW; Holloway-Azene, NM; Sessions, JK; Vitale, CL,
)
1.57
"The results show that the individual pharmacokinetics of BEACOPP drugs are an important link between dosage and toxicity."( Population pharmacokinetics of the BEACOPP polychemotherapy regimen in Hodgkin's lymphoma and its effect on myelotoxicity.
Busse, D; Diehl, V; Engert, A; Fuhr, U; Hempel, G; Jaehde, U; Jetter, A; Josting, A; Kasel, D; Klimm, B; Merkel, U; Reif, S; Rietbrock, S; Schwab, M; Wilde, S, 2007
)
0.34
" The dose-response of ethylnitrosourea-induced mutation was found to be very close to that previously established using a pedigree-based approach for ESTR mutation detection."( Single-molecule PCR analysis of germ line mutation induction by anticancer drugs in mice.
Dubrova, YE; Glen, CD; Smith, AG, 2008
)
0.35
" Since survival rates for patients receiving risk-adapted programs (DAL-Hd, SPBLKH-05) were higher than in control (MOPP), relevant protocols using lower drug dosage should be recommended in groups of favorable and intermediate risk."( [Use of risk-adapted programs of treatment of Hodgkin's disease in children and adolescents].
Kuleva, SA, 2008
)
0.35
" It is suggested that total focal dosage used after chemotherapy be reviewed since total dosage for the entire lymph collector in excess of 30 Gy might contribute to hazards of cardiopathology."( [Multivariate analysis of risk of cardiac complications in Hodgkin's lymphoma].
Bozhenko, VK; Datsenko, PV; Ivashin, AV; Mel'nik, IuD; Pan'shin, GA; Podol'skiĭ, PN; Sotnikov, VM, 2009
)
0.35
" 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
" Prospective pharmacokinetic studies to devise a rational dosing strategy for vinblastine in patients receiving ritonavir/lopinavir are warranted."( Incidence, predictors and significance of severe toxicity in patients with human immunodeficiency virus-associated Hodgkin lymphoma.
Boro, J; Cheung, MC; Ezzat, HM; Harris, M; Hicks, LK; Leitch, HA; Lima, VD; Montaner, JS, 2012
)
0.38
" With delphinidin and malvidin, a biphasic dose-response was observed for protection against cyclophosphamide."( Protective effects of common anthocyanidins against genotoxic damage induced by chemotherapeutic drugs in mice.
Abraham, SK; Khandelwal, N, 2014
)
0.4
" There are no indications that endogenous and exogenous gonadal hormones affect the radiation dose-response relationship."( Breast Cancer Risk After Radiation Therapy for Hodgkin Lymphoma: Influence of Gonadal Hormone Exposure.
Aleman, BMP; Broeks, A; De Bruin, ML; de Vathaire, F; Diallo, I; Fase, S; Hauptmann, M; Janus, CPM; Kesminiene, A; Kooijman, KR; Krol, ADG; Krul, IM; Lybeert, ML; Opstal-van Winden, AWJ; Russell, NS; Schaapveld, M; van der Maazen, RWM; van Eggermond, AM; van Leeuwen, FE; Zijlstra, JM, 2017
)
0.46
"Although G-CSF is widely used to prevent or ameliorate leukopenia during cytotoxic chemotherapies, its optimal use is still under debate and depends on many therapy parameters such as dosing and timing of cytotoxic drugs and G-CSF, G-CSF pharmaceuticals used and individual risk factors of patients."( Model-based optimization of G-CSF treatment during cytotoxic chemotherapy.
Engel, C; Loeffler, M; Loibl, S; Schirm, S; Scholz, M, 2018
)
0.48
" Because the dosing interval used for BV therapy was longer than that in the recommended schedule, we could not definitively attribute her recurrence to BV resistance."( [Successful treatment with brentuximab vedotin maintenance therapy after autologous stem cell transplantation in high-risk Hodgkin lymphoma].
Azuma, Y; Fujita, S; Hotta, M; Ishii, K; Ito, T; Konishi, A; Miyaji, M; Nakanishi, T; Nakaya, A; Nomura, S; Satake, A; Tsubokura, Y; Yoshimura, H,
)
0.13
" Furthermore, comparison of the magnitude of the genotoxicity responses indicated that the micronucleus and Comet endpoints generally produced greater responses with the higher dose, short-term treatments in the 3-day study, while the Pig-a assay responded better to the cumulative effects of the lower dose, but repeated subchronic dosing in the 28-day study."( Assessment of the Pig-a, micronucleus, and comet assay endpoints in rats treated by acute or repeated dosing protocols with procarbazine hydrochloride and ethyl carbamate.
Chen, G; Huang, Z; Jiang, H; Mao, Z; Miao, Y; Song, J; Wang, C; Wang, W; Wang, X; Wen, H; Yang, Y, 2019
)
0.72
" Although radiation dose-response associations with breast, lung, stomach, pancreatic, and esophageal cancer after HL have been demonstrated, the association of radiation therapy with colorectal cancer remains unclear."( Association of Radiation and Procarbazine Dose With Risk of Colorectal Cancer Among Survivors of Hodgkin Lymphoma.
Aleman, BMP; Aznar, MC; Cutter, DJ; Darby, SC; Geurts, YM; Janus, CPM; John, KM; Krol, ADG; Ntentas, G; Ramroth, J; Roberti, S; Roesink, JM; Schaapveld, M; Shakir, R; van der Maazen, RWM; van Leeuwen, FE; Zijlstra, JM, 2023
)
1.2
"This nested case-control study of 5-year HL survivors found a dose-response association between radiation therapy and colorectal cancer risk, and modification of this association by procarbazine."( Association of Radiation and Procarbazine Dose With Risk of Colorectal Cancer Among Survivors of Hodgkin Lymphoma.
Aleman, BMP; Aznar, MC; Cutter, DJ; Darby, SC; Geurts, YM; Janus, CPM; John, KM; Krol, ADG; Ntentas, G; Ramroth, J; Roberti, S; Roesink, JM; Schaapveld, M; Shakir, R; van der Maazen, RWM; van Leeuwen, FE; Zijlstra, JM, 2023
)
1.39
[information is derived through text-mining from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Roles (1)

RoleDescription
antineoplastic agentA substance that inhibits or prevents the proliferation of neoplasms.
[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 (2)

ClassDescription
hydrazinesHydrazine (diazane) and its substituted derivatives.
benzamides
[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]

Protein Targets (11)

Potency Measurements

ProteinTaxonomyMeasurementAverage (µ)Min (ref.)Avg (ref.)Max (ref.)Bioassay(s)
acetylcholinesteraseHomo sapiens (human)Potency39.91490.002541.796015,848.9004AID1347395; AID1347398
15-lipoxygenase, partialHomo sapiens (human)Potency7.94330.012610.691788.5700AID887
USP1 protein, partialHomo sapiens (human)Potency39.81070.031637.5844354.8130AID504865
GLS proteinHomo sapiens (human)Potency25.11890.35487.935539.8107AID624170
aldehyde dehydrogenase 1 family, member A1Homo sapiens (human)Potency17.78280.011212.4002100.0000AID1030
nuclear receptor subfamily 1, group I, member 3Homo sapiens (human)Potency61.13060.001022.650876.6163AID1224838; AID1224893
EWS/FLI fusion proteinHomo sapiens (human)Potency0.00170.001310.157742.8575AID1259256
estrogen-related nuclear receptor alphaHomo sapiens (human)Potency61.13060.001530.607315,848.9004AID1224849
pregnane X nuclear receptorHomo sapiens (human)Potency54.48270.005428.02631,258.9301AID1346982
cytochrome P450 2C19 precursorHomo sapiens (human)Potency5.01190.00255.840031.6228AID899
lamin isoform A-delta10Homo sapiens (human)Potency3.16230.891312.067628.1838AID1487
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Bioassays (99)

Assay IDTitleYearJournalArticle
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.
AID496827Antimicrobial activity against Leishmania amazonensis2010Bioorganic & medicinal chemistry, Mar-15, Volume: 18, Issue:6
Multi-target spectral moment QSAR versus ANN for antiparasitic drugs against different parasite species.
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).
AID496820Antimicrobial activity against Trypanosoma brucei2010Bioorganic & medicinal chemistry, Mar-15, Volume: 18, Issue:6
Multi-target spectral moment QSAR versus ANN for antiparasitic drugs against different parasite species.
AID1079946Presence of at least one case with successful reintroduction. [column 'REINT' in source]
AID1079937Severe hepatitis, defined as possibly life-threatening liver failure or through clinical observations. Value is number of references indexed. [column 'MASS' in source]
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]
AID496826Antimicrobial activity against Entamoeba histolytica2010Bioorganic & medicinal chemistry, Mar-15, Volume: 18, Issue:6
Multi-target spectral moment QSAR versus ANN for antiparasitic drugs against different parasite species.
AID189629The capillary permeability of radioligand was measured in Rat brain1980Journal of medicinal chemistry, Jun, Volume: 23, Issue:6
Relationship of octanol/water partition coefficient and molecular weight to rat brain capillary permeability.
AID496818Antimicrobial activity against Trypanosoma brucei brucei2010Bioorganic & medicinal chemistry, Mar-15, Volume: 18, Issue:6
Multi-target spectral moment QSAR versus ANN for antiparasitic drugs against different parasite species.
AID497005Antimicrobial activity against Pneumocystis carinii2010Bioorganic & medicinal chemistry, Mar-15, Volume: 18, Issue:6
Multi-target spectral moment QSAR versus ANN for antiparasitic drugs against different parasite species.
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.
AID1079934Highest frequency of acute liver toxicity observed during clinical trials, expressed as a percentage. [column '% AIGUE' in source]
AID496824Antimicrobial activity against Toxoplasma gondii2010Bioorganic & medicinal chemistry, Mar-15, Volume: 18, Issue:6
Multi-target spectral moment QSAR versus ANN for antiparasitic drugs against different parasite species.
AID496819Antimicrobial activity against Plasmodium falciparum2010Bioorganic & medicinal chemistry, Mar-15, Volume: 18, Issue:6
Multi-target spectral moment QSAR versus ANN for antiparasitic drugs against different parasite species.
AID1079942Steatosis, proven histopathologically. Value is number of references indexed. [column 'STEAT' 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.
AID496823Antimicrobial activity against Trichomonas vaginalis2010Bioorganic & medicinal chemistry, Mar-15, Volume: 18, Issue:6
Multi-target spectral moment QSAR versus ANN for antiparasitic drugs against different parasite species.
AID134250Mean life extension in mice bearing Trypanosoma rhodesiense, after ip administration at 0.9 mmol/kg dose1990Journal of medicinal chemistry, Feb, Volume: 33, Issue:2
Methylating agents as trypanocides.
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.
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]
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.
AID496831Antimicrobial activity against Cryptosporidium parvum2010Bioorganic & medicinal chemistry, Mar-15, Volume: 18, Issue:6
Multi-target spectral moment QSAR versus ANN for antiparasitic drugs against different parasite species.
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).
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).
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.
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.
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).
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.
AID1079940Granulomatous liver disease, proven histopathologically. Value is number of references indexed. [column 'GRAN' in source]
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.
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).
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.
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).
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).
AID496830Antimicrobial activity against Leishmania major2010Bioorganic & medicinal chemistry, Mar-15, Volume: 18, Issue:6
Multi-target spectral moment QSAR versus ANN for antiparasitic drugs against different parasite species.
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]
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).
AID319656Increase in mushroom tyrosinase catalysed oxidation of 4-tert-butyl catechol assessed as oxygen consumption after 30 mins2008Bioorganic & medicinal chemistry letters, Jun-01, Volume: 18, Issue:11
Indirect oxidation of the antitumor agent procarbazine by tyrosinase--possible application in designing anti-melanoma prodrugs.
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).
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]
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).
AID134111Mean life extension in mice bearing Trypanosoma rhodesiense, after ip administration at a dose of 0.2 mmol/kg1990Journal of medicinal chemistry, Feb, Volume: 33, Issue:2
Methylating agents as trypanocides.
AID496825Antimicrobial activity against Leishmania mexicana2010Bioorganic & medicinal chemistry, Mar-15, Volume: 18, Issue:6
Multi-target spectral moment QSAR versus ANN for antiparasitic drugs against different parasite species.
AID1079932Highest frequency of moderate liver toxicity observed during clinical trials, expressed as a percentage. [column '% BIOL' in source]
AID1079945Animal toxicity known. [column 'TOXIC' in source]
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).
AID496828Antimicrobial activity against Leishmania donovani2010Bioorganic & medicinal chemistry, Mar-15, Volume: 18, Issue:6
Multi-target spectral moment QSAR versus ANN for antiparasitic drugs against different parasite species.
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).
AID496832Antimicrobial activity against Trypanosoma brucei rhodesiense2010Bioorganic & medicinal chemistry, Mar-15, Volume: 18, Issue:6
Multi-target spectral moment QSAR versus ANN for antiparasitic drugs against different parasite species.
AID1079948Times to onset, minimal and maximal, observed in the indexed observations. [column 'DELAI' in source]
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.
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
AID1079947Comments (NB not yet translated). [column 'COMMENTAIRES' in source]
AID409954Inhibition of mouse brain MAOA2008Journal of medicinal chemistry, Nov-13, Volume: 51, Issue:21
Quantitative structure-activity relationship and complex network approach to monoamine oxidase A and B inhibitors.
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.
AID1079949Proposed mechanism(s) of liver damage. [column 'MEC' in source]
AID496829Antimicrobial activity against Leishmania infantum2010Bioorganic & medicinal chemistry, Mar-15, Volume: 18, Issue:6
Multi-target spectral moment QSAR versus ANN for antiparasitic drugs against different parasite species.
AID26811Partition coefficient (logP)1980Journal of medicinal chemistry, Jun, Volume: 23, Issue:6
Relationship of octanol/water partition coefficient and molecular weight to rat brain capillary permeability.
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).
AID1079943Malignant tumor, proven histopathologically. Value is number of references indexed. [column 'T.MAL' in source]
AID1079939Cirrhosis, proven histopathologically. Value is number of references indexed. [column 'CIRRH' in source]
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).
AID1079944Benign tumor, proven histopathologically. Value is number of references indexed. [column 'T.BEN' in source]
AID496817Antimicrobial activity against Trypanosoma cruzi2010Bioorganic & medicinal chemistry, Mar-15, Volume: 18, Issue:6
Multi-target spectral moment QSAR versus ANN for antiparasitic drugs against different parasite species.
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]
AID496821Antimicrobial activity against Leishmania2010Bioorganic & medicinal chemistry, Mar-15, Volume: 18, Issue:6
Multi-target spectral moment QSAR versus ANN for antiparasitic drugs against different parasite species.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
AID1745845Primary qHTS for Inhibitors of ATXN expression
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.
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.
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.
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.
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.
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.
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.
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023]

Research

Studies (3,090)

TimeframeStudies, This Drug (%)All Drugs %
pre-19901606 (51.97)18.7374
1990's673 (21.78)18.2507
2000's419 (13.56)29.6817
2010's335 (10.84)24.3611
2020's57 (1.84)2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Market Indicators

Research Demand Index: 55.80

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 Index55.80 (24.57)
Research Supply Index8.30 (2.92)
Research Growth Index4.30 (4.65)
Search Engine Demand Index98.07 (26.88)
Search Engine Supply Index2.00 (0.95)

This Compound (55.80)

All Compounds (24.57)

Study Types

Publication TypeThis drug (%)All Drugs (%)
Trials691 (20.83%)5.53%
Reviews333 (10.04%)6.00%
Case Studies452 (13.62%)4.05%
Observational1 (0.03%)0.25%
Other1,841 (55.49%)84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Clinical Trials (70)

Trial Overview

TrialPhaseEnrollmentStudy TypeStart DateStatus
Phase 11 Study of Cilengitide in Combination With Concurrent Chemotherapy and Radiotherapy Followed by Protracted Daily Low Dose Temozolomide and Low Dose Procarbazine D1 - 20 in Newly Diagnosed Glioblastoma Without Methylation of the MGMT Promoter Gene [NCT01124240]Phase 248 participants (Anticipated)Interventional2009-11-30Recruiting
[NCT01569204]Phase 2100 participants (Anticipated)Interventional2012-10-31Completed
A Phase Ib/II Trial of Combined SGN-35 (BrentuximabVedotin) Therapy With Cyclophosphamide, Procarbazine, Prednisone, Etoposide and Mitoxantrone (BrEPEM) for Older Patients With Untreated Hodgkin Lymphoma (HL) [NCT03576378]Phase 1/Phase 241 participants (Actual)Interventional2018-08-08Active, not recruiting
Phase II Trial of Anti-Angiogenic Therapy With RT-PEPC in Patients With Relapsed Mantle Cell Lymphoma [NCT00151281]Phase 225 participants (Actual)Interventional2004-11-30Completed
Improvement of Functional Outcome for Patients With Newly Diagnosed Grade II or III Glioma With Co-deletion of 1p/19q - IMPROVE CODEL: the NOA-18 Trial [NCT05331521]Phase 3406 participants (Anticipated)Interventional2021-04-07Recruiting
A Pilot Phase II Study Of Sequential Treatment With Chemotherapy, Radioimmunotherapy and Autologous Hematopoietic Stem Cell Transplantation in Patients With Follicular Lymphoma [NCT01130194]Phase 229 participants (Actual)Interventional2006-07-31Completed
HD17 for Intermediate Stages - Treatment Optimization Trial in the First-Line Treatment of Intermediate Stage Hodgkin Lymphoma [NCT01356680]Phase 31,100 participants (Actual)Interventional2012-01-13Completed
Prospective Randomized Comparison of ABVD Versus BEACOPP Chemotherapy With or Without Radiotherapy for Advanced Stage or Unfavorable Hodgkin's Lymphoma (HL) [NCT01251107]Phase 3331 participants (Actual)Interventional2000-03-31Completed
Randomized Phase II Trial on Fitness- and Comorbidity- Tailored Treatment in Elderly Patients With Newly Diagnosed Primary CNS Lymphoma (FIORELLA Trial) [NCT03495960]Phase 2208 participants (Anticipated)Interventional2019-06-15Recruiting
Fludarabine, Mitoxantrone, and Dexamethasone (FND) Plus Chimeric Anti-CD20 Monoclonal Antibody (Rituximab) for Stage IV Indolent Lymphoma [NCT00577993]Phase 3210 participants (Actual)Interventional1998-03-16Completed
A Pilot Study Incorporating Motexafin Gadolinium (MGd) Into High-dose Methotrexate (MTX)-Based Chemo-immunotherapy and Radiation for Patients With Newly Diagnosed Primary CNS Lymphoma [NCT00734773]Early Phase 10 participants (Actual)Interventional2008-11-30Withdrawn(stopped due to Lack of funding)
Multicenter Clinical Study With Early Treatment Intensification In Patients With High- Risk Hodgkin Lymphoma, Identified As FDG-PET Scan Positive After 2 Conventional ABVD Courses [NCT00795613]Phase 2450 participants (Anticipated)Interventional2008-06-30Active, not recruiting
Phase III Randomized Trial of Adjuvant Involved-Field Radiotherapy vs No Adjuvant Therapy Following Remission Induction With MOPP/ABV Hybrid Chemotherapy in Patients With Stage III/IV Hodgkin's Disease [NCT00002462]Phase 3615 participants (Actual)Interventional1989-09-30Active, not recruiting
Phase 2 Study of Pembrolizumab and Chemotherapy in Patients With Newly Diagnosed Classical Hodgkin Lymphoma (KEYNOTE-C11) [NCT05008224]Phase 2146 participants (Actual)Interventional2021-10-07Active, not recruiting
Treatment of Patients Over 65 Years With Primary CNS Lymphoma: High-dose Methotrexate Combined With Chemo-immunotherapy Followed by Maintenance Therapy [NCT00989352]Phase 256 participants (Anticipated)Interventional2009-09-30Recruiting
A Randomized Phase 3 Interim Response Adapted Trial Comparing Standard Therapy With Immuno-oncology Therapy for Children and Adults With Newly Diagnosed Stage I and II Classic Hodgkin Lymphoma [NCT05675410]Phase 31,875 participants (Anticipated)Interventional2023-05-11Recruiting
A Phase II Trial of Response-Adapted Therapy of Stage III-IV Hodgkin Lymphoma Using Early Interim FDG-PET Imaging [NCT00822120]Phase 2371 participants (Actual)Interventional2009-07-31Completed
A Pilot Study of Combined Immunochemotherapy Followed by Reduced Dose RT for Patients With Newly Diagnosed Primary Central Nervous System Lymphoma [NCT00594815]52 participants (Actual)Interventional2002-08-28Completed
Phase II Randomized Study of Rituximab, Methotrexate, Procarbazine, Vincristine, and Cytarabine With and Without Low-Dose Whole-Brain Radiotherapy for Primary Central Nervous System Lymphoma [NCT01399372]Phase 291 participants (Actual)Interventional2011-09-30Completed
Rituximab, Methotrexate, Procarbazine, Vincristine, Lenalidomide (RL-MPV) Followed by BBC (BCNU, Busulfan, Cyclophosphamide) High-dose Chemotherapy With Auto-HCT and Maintenance Therapy With Nivolumab in Newly Diagnosed Primary CNS Lymphoma [NCT05425654]Phase 230 participants (Anticipated)Interventional2021-05-17Recruiting
Phase II Study of Rituximab Given in Conjunction With Standard Chemotherapy in Primary Central Nervous System (CNS) Lymphoma [NCT00335140]Phase 226 participants (Actual)Interventional2007-08-23Terminated(stopped due to slow accrual)
Phase II Trial of Response-Adapted Chemotherapy Based on Positron Emission Tomography for Non-Bulky Stage I and II Hodgkin Lymphoma [NCT01132807]Phase 2164 participants (Actual)Interventional2010-05-31Completed
Phase II Study Evaluating the Toxicity and Efficacy of a Modified German Paediatric Hodgkin's Lymphoma Protocol (HD95) in Young Adults (Aged 18-30 Years) With Hodgkin's Lymphoma [NCT00666484]Phase 247 participants (Actual)Interventional2008-03-31Completed
[NCT02800447]92 participants (Actual)Interventional2016-06-30Active, not recruiting
Oral Combination Chemotherapy in the Treatment of AIDS-Associated Hodgkin's Disease [NCT00003114]Phase 25 participants (Actual)Interventional1997-07-31Completed
Phase III Randomized Evaluation of 13-Cis-Retinoic Acid (cRA) Plus Procarbazine Versus Procarbazine Alone in the Treatment of Patients With Recurrent Primary Malignant Gliomas [NCT00003564]Phase 30 participants (Actual)InterventionalWithdrawn(stopped due to Study withdrawn.)
A Comprehensive Study of Clinically Staged Pediatric Hodgkin's Disease: Chemotherapy for All Patients; Supplementary Low Dose Involved Field Irradiation for Selected Patients (CCG 5942) [NCT00592111]Phase 221 participants (Actual)Interventional1996-03-31Completed
Multicenter Randomized Phase II Study of Methotrexate (MTX) and Temozolomide Versus MTX, Procarbazine, Vincristine and Cytarabine for Primary CNS Lymphoma (PCNSL) in the Elderly [NCT00503594]Phase 292 participants (Anticipated)Interventional2007-07-31Recruiting
A Pilot Study of Dose-Intensified Procarbazine, CCNU, Vincristine (PCV) for Poor Prognosis Pediatric and Adult Brain Tumors Utilizing Fibronectin-Assisted, Retroviral-Mediated Modification of CD34+ Peripheral Blood Cells With O6-Methylguanine DNA Methyltr [NCT00005796]Phase 110 participants (Actual)Interventional2000-02-29Completed
A Phase I/II Trial of the Bruton's Tyrosine Kinase (BTK) Inhibitor, Ibrutinib, in Patients With Newly Diagnosed or Refractory/Recurrent Primary Central Nervous System Lymphoma (PCNSL) and Refractory/Recurrent Secondary Central Nervous System Lymphoma (SCN [NCT02315326]Phase 1/Phase 2109 participants (Anticipated)Interventional2014-12-31Recruiting
Hodgkin's Disease Study [NCT00416377]353 participants (Anticipated)InterventionalActive, not recruiting
First International Inter-Group Study for Classical Hodgkin's Lymphoma in Children and Adolescents [NCT00433459]Phase 32,134 participants (Actual)Interventional2007-01-31Completed
A Phase III Randomized Study of SU101 Versus Procarbazine for Patients With Glioblastoma Multiforme in First Relapse [NCT00003293]Phase 30 participants Interventional1998-02-28Completed
HD21 for Advanced Stages Treatment Optimization Trial in the First-line Treatment of Advanced Stage Hodgkin Lymphoma; Comparison of 6 Cycles of Escalated BEACOPP With 6 Cycles of BrECADD [NCT02661503]Phase 31,500 participants (Anticipated)Interventional2016-07-31Recruiting
Combination Chemotherapy (Methotrexate, Procarbazine And CCNU), Intraventricular Cytarabine And Methotrexate, +/- Intra-Ocular Chemotherapy For Patients With Primary Central Nervous System Lymphoma [NCT00074191]Phase 21 participants (Actual)Interventional2000-01-31Completed
A Phase II Study VEPEMB In Patients With Hodgkin's Lymphoma Aged ≥ 60 Years; Vinblastine, Cyclophosphamide, Procarbazine, Prednisolone, Etoposide, Mitoxantrone, and Bleomycin in Treating Older Patients With Hodgkin's Lymphoma [NCT00079105]Phase 2175 participants (Actual)Interventional2004-01-31Completed
A Prospective Randomised Trial Comparing Temozolomide With PCV In The Treatment Of Recurrent WHO Astrocytic Tumours Grades III And IV [NCT00052455]Phase 3500 participants (Anticipated)Interventional2002-10-31Completed
Protocol For The Treatment Of Children And Adolescents With Hodgkin's Disease [NCT00025064]Phase 2260 participants (Anticipated)Interventional2000-01-31Active, not recruiting
A Phase II Trial Of Thalidomide And Procarbazine In Adults With Recurrent/Progressive Gliomas [NCT00079092]Phase 218 participants (Anticipated)Interventional2004-01-01Completed
Dose-Modified Oral Combination Chemotherapy In Patients With Aids-Related Non-Hodgkin's Lymphoma In The United States And Africa [NCT00049439]Phase 254 participants (Actual)Interventional1998-03-31Completed
Pilot Study I for Treatment of Cancer in Children With Ataxia-Telangiectasia [NCT00187057]6 participants (Actual)Interventional2002-09-30Completed
Rituximab, Methotrexate, Procarbazine and Vincristine Followed by High-dose Chemotherapy With Autologous Stem-cell Rescue in Newly-diagnosed Primary CNS Lymphoma (PCNSL) [NCT00596154]Phase 233 participants (Actual)Interventional2004-12-31Completed
Optimising Therapy for Boys With Hodgkin's Lymphoma and Quality Assurance of Therapy for Girls With Hodgkin's Lymphoma Until Start of a New Prospective Trial for Hodgkin's Lymphoma in Childhood and Adolescence [NCT00416832]Phase 2648 participants (Anticipated)Interventional2002-11-30Completed
[NCT00264953]Phase 31,395 participants (Actual)Interventional1998-05-31Completed
[NCT00265031]Phase 30 participants Interventional1999-01-31Completed
Hodgkins Disease Study [NCT00417014]358 participants (Anticipated)InterventionalActive, not recruiting
Phase 2 Clinical Trial of PC(Procarbazine-CCNU) Chemotherapy in Patients With Recurrent or Resistant Glioblastoma With Methylated MGMT [NCT01737346]Phase 252 participants (Anticipated)Interventional2012-10-31Recruiting
Phase II Study of Methotrexate, Mechlorethamine, Vincristine, Prednisone, and Procarbazine (MMOPP) as Primary Therapy in Infants or Young Children With Primitive Neuroectodermal Tumors or High-Grade Astrocytoma [NCT00002463]Phase 24 participants (Actual)Interventional1989-02-28Completed
A Prospective Multicenter Study on HIV-associated Hodgkin Lymphoma [NCT01468740]Phase 2130 participants (Anticipated)Interventional2004-03-31Recruiting
Chemotherapy for Progressive Low Grade Astrocytoma in Children Less Than Ten Years Old [NCT00002944]Phase 3428 participants (Actual)Interventional1997-04-30Completed
PHASE II STUDY OF PREIRRADIATION PCV CHEMOTHERAPY IN PATIENTS WITH SUPRATENTORIAL LOW-GRADE GLIOMAS [NCT00002806]Phase 243 participants (Actual)Interventional1996-07-31Completed
A Randomized Phase III Trial to Assess Response Adapted Therapy Using FDG-PET Imaging in Patients With Newly Diagnosed, Advanced Hodgkin Lymphoma [NCT00678327]Phase 31,202 participants (Actual)Interventional2008-08-29Active, not recruiting
Phase III Intergroup Randomized Comparison of Radiation Alone vs. Pre-Radiation Chemotherapy for Pure and Mixed Anaplastic Oligodendrogliomas [NCT00002569]Phase 3299 participants (Actual)Interventional1994-07-31Completed
PHASE III STUDY OF ADJUVANT PROCARBAZINE, CCNU AND VINCRISTINE CHEMOTHERAPY IN PATIENTS WITH HIGHLY ANAPLASTIC OLIGODENDROGLIOMA [NCT00002840]Phase 3350 participants (Anticipated)Interventional1996-08-31Completed
A Phase I/II Study of Oral Procarbazine in the Treatment of Recurrent High Grade Astrocytomas [NCT00004004]Phase 1/Phase 20 participants Interventional1999-07-31Completed
Pilot Study for the Treatment of Children With Newly Diagnosed Advanced Stage Hodgkin's Disease: Upfront Dose Intensive Chemotherapy [NCT00004010]Phase 299 participants (Actual)Interventional1999-10-31Completed
Prospective Clinical Trials in the Use of Photodynamic Therapy (PDT) for the Treatment of Malignant Supratentorial Brain Tumors [NCT00003788]Phase 3270 participants (Anticipated)Interventional1998-04-30Active, not recruiting
A UKLG Randomised Trial of Initial Chemotherapy for Advanced Stage Hodgkins Disease [NCT00003421]Phase 3800 participants (Anticipated)Interventional1998-06-30Completed
Phase II Trial of Response-Adapted Therapy Based on Positron Emission Tomography (PET) for Bulky Stage I and II Classical Hodgkin Lymphoma (HL) [NCT01390584]Phase 26 participants (Actual)Interventional2013-05-24Terminated(stopped due to slow accrual)
A Phase II Study of Observation in Favorable Low-Grade Glioma and a Phase II Study of Radiation With or Without PCV Chemotherapy in Unfavorable Low-Grade Glioma [NCT00003375]Phase 2/Phase 3370 participants (Actual)Interventional1998-10-31Completed
Protocol H8 for a Prospective Controlled Trial in Clinical Stage I-II Supradiaphragmatic Hodgkin's Disease. Evaluation of Treatment Efficacy and (Long Term) Toxicity in Three Different Prognostic Subgroups [H8 Trial] [NCT00379041]Phase 31,158 participants (Anticipated)Interventional1993-09-01Active, not recruiting
A Study to Evaluate the Safety and Effectiveness of PCV Chemotherapy in Patients With Recurrent High-grade Glioma With IDH1/2 Mutation [NCT02333513]100 participants (Anticipated)Interventional2015-02-28Not yet recruiting
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
BEACOPP (4 Cycles Escalated + 4 Cycles Baseline) Versus ABVD (8 Cycles) In Stage III & IV Hodgkin's Lymphoma [NCT00049595]Phase 3552 participants (Actual)Interventional2002-08-31Completed
A Phase II Trial of Intensive Chemotherapy and Autotransplantation for Patients With Newly Diagnosed Anaplastic Oligodendroglioma [NCT00003101]Phase 260 participants (Anticipated)Interventional1997-08-31Completed
Oral Combination Chemotherapy in Conjunction With G-CSF in the Treatment of Elderly Patients With Intermediate and High Grade Non-Hodgkin's Lymphoma [NCT00003113]Phase 26 participants (Actual)Interventional1997-07-31Terminated
Combined Modality Therapy of AIDS-Related and Immunocompetent Primary CNS Lymphoma (PCL) Using Filgrastim (G-CSF) [NCT00003929]Phase 20 participants (Actual)Interventional1998-06-30Withdrawn
Randomized, Phase II Trial of CHOP vs. Oral Chemotherapy With Concomitant Antiretroviral Therapy in Patients With HIV-Associated Lymphoma in Sub-Saharan Africa [NCT01775475]Phase 27 participants (Actual)Interventional2016-09-15Completed
Phase III Intergroup Study of Radiotherapy With Concomitant and Adjuvant Temozolomide Versus Radiotherapy With Adjuvant PCV Chemotherapy in Patients With 1p/19q Co-deleted Anaplastic Glioma or Low Grade Glioma [NCT00887146]Phase 3360 participants (Anticipated)Interventional2009-09-30Recruiting
Brentuximab Vedotin as Consolidation Treatment in Patients With Stage I/II Hodgkin's Lymphoma and FDG-PET Positivity After 2 Cycles of ABVD [NCT02298283]Phase 240 participants (Actual)Interventional2015-04-30Completed
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

TrialOutcome
NCT00151281 (4) [back to overview]Dynamic Levels of Plasma VEGF
NCT00151281 (4) [back to overview]Overall Survival and Progression Free Survival
NCT00151281 (4) [back to overview]Asses the Toxicity Profiles
NCT00151281 (4) [back to overview]The Quality of Life (QoL) of Patients Receiving RT-PEPC Treatment
NCT00335140 (1) [back to overview]Complete Response Rate - Locally Reviewed
NCT00574496 (3) [back to overview]Disease Relapse or Progression as Measured by CT Scan or PET
NCT00574496 (3) [back to overview]Overall Survival
NCT00574496 (3) [back to overview]Progression-free Survival at 1 Year
NCT00577993 (2) [back to overview]Number of Participants With Overall Survival (10 Years) by Treatment
NCT00577993 (2) [back to overview]Number of Participants With Progression Free Survival (10 Years) by Treatment
NCT00594815 (2) [back to overview]Progression Free Survival
NCT00594815 (2) [back to overview]Total Number of Participants Who Experienced Acute Treatment Related Adverse Events
NCT00822120 (8) [back to overview]Complete and Partial Response Rates for HIV-negative Patients Treated With Response- Adapted Therapy Based on FDG-PET Imaging After 2 Cycles of ABVD
NCT00822120 (8) [back to overview]Percentage of HIV-negative Patients Who Are PET-positive After 2 Cycles of ABVD With 2-year PFS
NCT00822120 (8) [back to overview]Percentage of HIV-negative Patients With 2-year Overall Survival (OS) Treated With 2 Initial Cycles of ABVD Followed by Response-Adapted Therapy Based on Interim FDG-PET Imaging
NCT00822120 (8) [back to overview]Percentage of HIV-negative Patients With 2-year Progression-free Survival (PFS) Treated With 2 Initial Cycles of Adriamycin, Bleomycin, Vnblastine, and Dacarbazine (ABVD) Followed by Response-adapted Therapy Based on Interim FDG-PET Imaging.
NCT00822120 (8) [back to overview]Percentage of HIV-positive Patients With 2-year Progression-free Survival (PFS) Treated With Initial 2 Cycles of Adriamycin, Bleomycin, Vnblastine, and Dacarbazine (ABVD) Followed by Response-adapted Therapy Based on Interim FDG-PET Imaging.
NCT00822120 (8) [back to overview]Percentage of HIV-positive Patients With 5-year Overall Survival (OS) Treated With 2 Initial Cycles of ABVD Followed by Response-Adapted Therapy Based on Interim FDG-PET Imaging.
NCT00822120 (8) [back to overview]Number of HIV-negative Patients With Grade 3 Through Grade 5 Adverse Events That Are Related to Study Drug
NCT00822120 (8) [back to overview]Number of HIV-positive Patients With Grade 3 Through Grade 5 Adverse Events That Are Related to Study Drug
NCT01132807 (3) [back to overview]36 Month Progression Free Survival Rate of Patients Receiving 4 Cycles of ABVD Versus Patients Receiving 2 Cycles of ABVD and 2 Cycles of BEACOPP and Radiation.
NCT01132807 (3) [back to overview]Complete Response Rate
NCT01132807 (3) [back to overview]Progression-Free Survival (PFS) at 36-Months for Patients Who Received 4 Cycles of ABVD
NCT01390584 (5) [back to overview]Complete Response (CR) Rate After Induction Treatment
NCT01390584 (5) [back to overview]Overall Survival
NCT01390584 (5) [back to overview]Progression-free Survival at 36 Months Among Patients Who Are PET Positive After Induction Treatment
NCT01390584 (5) [back to overview]Progression-free Survival Rate
NCT01390584 (5) [back to overview]Proportion of Patients Who Are PET Negative After Induction Treatment
NCT01399372 (5) [back to overview]Percentage of Participants With Neurocognitive Failure
NCT01399372 (5) [back to overview]Progression-free Survival
NCT01399372 (5) [back to overview]Global Heath Status (GHS) Score of the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire (EORTC QLQ-C30)
NCT01399372 (5) [back to overview]Overall Survival
NCT01399372 (5) [back to overview]Percentage of Participants Experiencing Partial Response or Complete Response
NCT01775475 (8) [back to overview]Change in Absolute CD4 Count From Baseline to Post-treatment
NCT01775475 (8) [back to overview]Number of Patients Who Complete Treatment
NCT01775475 (8) [back to overview]Overall Response Rate
NCT01775475 (8) [back to overview]Overall Survival
NCT01775475 (8) [back to overview]Participants Who Experienced an Adverse Event
NCT01775475 (8) [back to overview]Progression-free Survival
NCT01775475 (8) [back to overview]Proportion of Patients Who Are Adherent to Antiretroviral Therapy
NCT01775475 (8) [back to overview]Proportion of Patients Who Are Adherent to Chemotherapy

Dynamic Levels of Plasma VEGF

Stromal angiogenesis was assessed using blood vascular and perivascular markers, including VEGFR-1, VEGFR-2, CD34, and a-SMA, as well as lymphatic vascular markers ofVEGFR-3, podoplanin, and Lyve-1. (NCT00151281)
Timeframe: 38 months

Interventionpg/mL (Median)
RT-PEPC Drug Therapy109.5

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Overall Survival and Progression Free Survival

measured by overall Response Rate (ORR), which includes Complete response and partial response. (NCT00151281)
Timeframe: 38 months

Interventionpercentage of patients (Number)
Study Treatment Arm73

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Asses the Toxicity Profiles

Toxicities were graded according to the National Cancer Institute Common Terminology Criteria for Adverse Events, version 3.0. (NCT00151281)
Timeframe: 38 months

InterventionParticipants (Count of Participants)
Grade 3 or 4 neutropeniaAnemiaThrombocytopeniaFatigueConstipationCoughNauseaNeuropathyDyspneaRash
RT-PEPC Drug Therapy141422141413131110

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The Quality of Life (QoL) of Patients Receiving RT-PEPC Treatment

"QoL assessments were obtained with version 3 of the Functional Assessment of Cancer Therapy-General (FACT-G) instrument. The FACT-G is comprised of four subscales: physical well-being (7-items, score range 0-28), social/family well-being (7-items, score range 0-28), emotional well-being (6-items, score range 0-24), and functional well-being (7-items, score range 0-28). Users of the FACT-G are able to generate an overall score and four subscale scores with ranges and distributions that are sample-specific. All questions in the FACT-G use a 5-point rating scale (0 = Not at all to 4 = Very much) A higher number indicates a better Quality of Life, and has a possible range of 0-108 points.~ANOVA was used to compare the difference in the means of total score among the different time points (baseline, every 2M until 6M, and every 6M until PD). The mean of the total FACT-G scores at baseline and mean of total score at all timepoints (using ANOVA) are reported below." (NCT00151281)
Timeframe: baseline, every 2 months until Month 6, and every 6 months until disease progression

InterventionFACT-G score (Mean)
Mean FACT-G Score at baselineMean Total FACT-G Score between all time points
RT-PEPC Drug Therapy83.389.4

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Complete Response Rate - Locally Reviewed

"Assessed by the ECOG-ACRIN data manager based upon local review of images and data sent by the local sites.~Treatment response was determined by calculating the sum of the maximal cross section in 2 separate axes using enhancing lesion(s) on CT or MRI imaging. The same imaging modality was to be used throughout assessment. Complete response was defined as the disappearance of all contrast enhancing tumor size on CT or MRI, patient was off all glucocorticoids, and resolution of all meningeal and vitreous involvement if present. Response must have lasted at least 4 weeks." (NCT00335140)
Timeframe: For the primary endpoint, complete response will be based on disease status at three weeks post the end of therapy (week 17).

Interventionpercentage of participants (Number)
Rituximab + Standard Chemotherapy64

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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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Overall Survival

(NCT00574496)
Timeframe: up to 8 years

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

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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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Number of Participants With Overall Survival (10 Years) by Treatment

Overall Survival is the time from date of treatment start until date of death due to any cause or last Follow-up within 10 years. (NCT00577993)
Timeframe: 10 Years

InterventionParticipants (Count of Participants)
Fludarabine,Mitoxantrone, and Dexamethasone (FND)-Rituximab59
Rituximab- Fludarabine,Mitoxantrone, and Dexamethasone (FND)58

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Number of Participants With Progression Free Survival (10 Years) by Treatment

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. (NCT00577993)
Timeframe: 10 years

InterventionParticipants (Count of Participants)
Fludarabine,Mitoxantrone, and Dexamethasone (FND)-Rituximab59
Rituximab- Fludarabine,Mitoxantrone, and Dexamethasone (FND)58

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Progression Free Survival

Overall Progression Free Survival at 2 years (NCT00594815)
Timeframe: 2 Years

Interventionpercentage of participants (Number)
Immunocompetent Pts With Newly Diagnosed Primary CNS Lymphoma57

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Complete and Partial Response Rates for HIV-negative Patients Treated With Response- Adapted Therapy Based on FDG-PET Imaging After 2 Cycles of ABVD

Complete Response (CR) is a complete disappearance of all disease with the exception of the following. If no PET scan or when the PET scan was positive before therapy, a post-treatment residual mass of any size is permitted if it is PET negative. If the PET scan was negative before therapy, all nodal masses at baseline must have regressed. No new lesions. Previously enlarged organs must have regressed and not be palpable. Bone marrow (BM) must be negative if positive at baseline. Normalization of markers. Partial Response (PR) is a 50% decrease in the sum of products of greatest diameters (SPD) for up to 6 identified dominant lesions, including spleenic and hepatic nodules from baseline. No new lesions and no increase in the size of liver, spleen or other nodes. If PET scan or when the PET scan was positive before therapy, PET should be positive in at least one previously involved site. (NCT00822120)
Timeframe: 7 months after registration

Interventionpercentage of patients (Number)
PET-negative: Continued ABVD After 2 Cycles of ABVD100
PET-positive: BEACOPP Escalated After 2 Cycles of ABVD93

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Percentage of HIV-negative Patients Who Are PET-positive After 2 Cycles of ABVD With 2-year PFS

Disease progression is defined using the 2007 revised Cheson et al. criteria that is at least 50% increase in sum of the product of the diameters (SPD) of target measurable nodal lesions over the smallest sum observed, or >= 50% increase in greatest transverse diameter (GTD) of any nodal > 1 cm in shortest axis, or >= 50% increase in the SPD of other target measurable lesions over the smallest sum observed, any new bone marrow involvement, any new lesion, lymph node with long axis is > 1.5 cm or if both long and short axes are > 1 cm, PET positive if patients with no pretreatment PET scan or when PET scan was positive before therapy. Progression-free survival is measured from date of registration to date of first observation of progressive disease, or death due to any cause. Patients last known to be alive and progression-free are censored at date of last contact. (NCT00822120)
Timeframe: 2 years

Interventionpercentage of participants (Number)
HIV-negative: 2 Cycles of ABVD Followed by Escalated BEACOPP64

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Percentage of HIV-negative Patients With 2-year Overall Survival (OS) Treated With 2 Initial Cycles of ABVD Followed by Response-Adapted Therapy Based on Interim FDG-PET Imaging

Measured from date of registration to date of death due to any cause. Patients last known to be alive and are censored at date of last contact. (NCT00822120)
Timeframe: 2 years

Interventionpercentage of participants (Number)
HIV-negative:2 Cycles of ABVD Followed by PET-directed Therapy98

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Percentage of HIV-negative Patients With 2-year Progression-free Survival (PFS) Treated With 2 Initial Cycles of Adriamycin, Bleomycin, Vnblastine, and Dacarbazine (ABVD) Followed by Response-adapted Therapy Based on Interim FDG-PET Imaging.

Disease progression is defined using the 2007 revised Cheson et al. criteria that is at least 50% increase in sum of the product of the diameters (SPD) of target measurable nodal lesions over the smallest sum observed, or >= 50% increase in greatest transverse diameter (GTD) of any nodal > 1 cm in shortest axis, or >= 50% increase in the SPD of other target measurable lesions over the smallest sum observed, any new bone marrow involvement, any new lesion, lymph node with long axis is > 1.5 cm or if both long and short axes are > 1 cm, PET positive if patients with no pretreatment PET scan or when PET scan was positive before therapy. Progression-free survival is measured from date of registration to date of first observation of progressive disease, or death due to any cause. Patients last known to be alive and progression-free are censored at date of last contact. (NCT00822120)
Timeframe: 2 years

Interventionpercentage of participants (Number)
HIV-negative: 2 Cycles of ABVD Followed by PET-directed Therap79

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Percentage of HIV-positive Patients With 2-year Progression-free Survival (PFS) Treated With Initial 2 Cycles of Adriamycin, Bleomycin, Vnblastine, and Dacarbazine (ABVD) Followed by Response-adapted Therapy Based on Interim FDG-PET Imaging.

Disease progression is defined using the 2007 revised Cheson et al. criteria that is at least 50% increase in sum of the product of the diameters (SPD) of target measurable nodal lesions over the smallest sum observed, or >= 50% increase in greatest transverse diameter (GTD) of any nodal > 1 cm in shortest axis, or >= 50% increase in the SPD of other target measurable lesions over the smallest sum observed, any new bone marrow involvement, any new lesion, lymph node with long axis is >1.5 cm or if both long and short axes are > 1 cm, PET positive if patients with no pretreatment PET scan or when PET scan was positive before therapy. progression-free survival is measured from date of registration to date of first observation of progressive disease, or death due to any cause. Patients last known to be alive and progression-free are censored at date of last contact. (NCT00822120)
Timeframe: 2 years

Interventionpercentage of patients (Number)
HIV-positive: 2 Cycles of ABVD Followed by PET-directed Therap83

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Percentage of HIV-positive Patients With 5-year Overall Survival (OS) Treated With 2 Initial Cycles of ABVD Followed by Response-Adapted Therapy Based on Interim FDG-PET Imaging.

Measured from date of registration to date of death due to any cause. Patients last known to be alive and are censored at date of last contact. (NCT00822120)
Timeframe: 5 years

Interventionpercentage of participants (Number)
HIV-positive: 2 Cycles of ABVD Followed by PET-directed Therap89

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36 Month Progression Free Survival Rate of Patients Receiving 4 Cycles of ABVD Versus Patients Receiving 2 Cycles of ABVD and 2 Cycles of BEACOPP and Radiation.

All patients received an initial 2-28 day cycles of doxorubicin, bleomycin, vinblastine, and dacarbazine (ABVD) on Days 1 and 15. After the first 2 cycles of ABVD, PET/CT was performed and submitted for central review (cycle 2, days 23-25) and determined whether patients would receive 2 cycles of escalated BEACOPP and involved-field RT (IFRT) or an additional 2 cycles of ABVD. PFS for each patient is measured as the time from registration on trial to the first incident of death or progression. The PFS rate at 36 months is calculated as the number of patients who have a progression-free survival time greater than 36 months divided by the total number of patients that started treatment. For this endpoint, we compare the PFS rate between patients who received 4 cycles of ABVD and patients who received 2 cycles of ABVD and 2 cycles of IFRT. (NCT01132807)
Timeframe: at 36 months

Interventionproportion of participants (Number)
Treatment (ABVD:4 Cycles).91
Escalated BEACOPP and Involved Field Radiation Therapy.67

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Complete Response Rate

A Complete Response (CR) was defined as having the following conditions: 1. A complete disappearance of all detectable clinical evidence of disease and disease-related symptoms if present before therapy. 2. In patients with a PET scan that was positive before therapy, a post-treatment residual mass of any size is permitted as long as it is PET-negative. A Complete Response rate was defined as the number of patients who achieved a CR divided by the number of patients that were eligible for analysis in each group. The CR rate was calculated for patients that completed 4 cycles of ABVD and for patients that completed 2 cycles of ABVD and 2 cycles of BEACOPP and IFRT. (NCT01132807)
Timeframe: Up to 5 years

Interventionproportion of participants (Number)
Treatment (ABVD: 4 Cycles).97
Escalated BEACOPP and Involved Field Radiation Therapy.85

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Progression-Free Survival (PFS) at 36-Months for Patients Who Received 4 Cycles of ABVD

The primary objective of this trial is to estimate the 3 year PFS in patients who received 4 cycles of ABVD. PFS for each patient is measured as the time from registration on trial to the first incident of death or progression. The PFS at 36 months is calculated as the number of patients who have a progression-free survival time greater than 36 months divided by the total number of patients that started treatment. For this endpoint, all patients that received 4 cycles of doxorubicin, bleomycin, vinblastine, and dacarbazine (ABVD) are included. (NCT01132807)
Timeframe: 36 Months

Interventionproportion of patients (Number)
Treatment (ABVD: 4 Cycles).91

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Complete Response (CR) Rate After Induction Treatment

Complete response (CR) is defined as complete disappearance of all detectable clinical evidence of disease and disease-related symptoms if present prior to therapy. (NCT01390584)
Timeframe: Assessed at end of Cycle 2

Interventionproportion of participants (Number)
Step 1: Induction Tx1.0

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Overall Survival

Overall survival is defined as the time from study entry to death or date last known alive. (NCT01390584)
Timeframe: Assessed at 36 months

Interventionmonths (Median)
ABVD + INRTNA
ABVD + BEACOPP + INRTNA

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Progression-free Survival at 36 Months Among Patients Who Are PET Positive After Induction Treatment

Progression-free survival is defined as the time from study entry to lymphoma progression or death from any cause. Proportion of patients who are progression-free and alive at 36 months will be reported. Progression is defined as appearance of any new lesions more than 1.5 cm in any axis, at least a 50% increase from nadir in sum of the product of the diameters (SPD) of any previously involved nodes or extranodal masses or the size of other lesions, or at least 50% increase in the longest diameter of any single previously identified node or extranodal mass more than 1 cm in its short axis. (NCT01390584)
Timeframe: Assessed at 36 months

Interventionproportion of participants (Number)
ABVD + BEACOPP + INRTNA

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Progression-free Survival Rate

Progression-free survival is defined as the time from study entry to lymphoma progression or death from any cause. Proportion of patients who are progression-free and alive at 36 months will be reported. Progression is defined as appearance of any new lesions more than 1.5 cm in any axis, at least a 50% increase from nadir in sum of the product of the diameters (SPD) of any previously involved nodes or extranodal masses or the size of other lesions, or at least 50% increase in the longest diameter of any single previously identified node or extranodal mass more than 1 cm in its short axis. (NCT01390584)
Timeframe: Assessed at 36 months

Interventionproportion of participants (Number)
ABVD + INRTNA
ABVD + BEACOPP + INRTNA

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Proportion of Patients Who Are PET Negative After Induction Treatment

(NCT01390584)
Timeframe: Assessed at end of Cycle 2

Interventionproportion of participants (Number)
Step 1: Induction Tx0.8

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Percentage of Participants With Neurocognitive Failure

Neurocognitive failure is defined as cognitive failure on two or more of the following tests: Hopkins Verbal Learning Test - Revised (HVLT-R) Free Recall, HVLT-R Delayed Recall, HVLT-R Delayed Recognition, Trail Making Test Part A, Trail Making Test Part B, and Controlled Oral Word Association. Cognitive failure for each test is defined as a change from baseline in raw score (post baseline score - baseline score) at or exceeding the minimally important difference reported in the literature [determined by the reliable change index (RCI) method] of -5, -3, -2,12, 26, and -12, respectively, indicating a worsening of neurocognitive function. Time to neurocognitive failure is defined as time from randomization to date of first failure, last known follow-up (censored), or death without failure (competing risk). Failure rates are estimated using the cumulative incidence method and the distributions of failure times are compared between the arms. Two-year estimates are provided here. (NCT01399372)
Timeframe: Neurocognitive function tests were administered at baseline, after cycle 4 of treatment (4 months), then every six months after end of treatment (7 months) for five years. Two-year rates are provided here.

Interventionpercentage of participants (Number)
Chemotherapy31.6
Chemotherapy + Low-Dose WBRT17.9

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Progression-free Survival

Progression is defined as any of the following: more than 25% increase in the contrast-enhancing lesion seen on magnetic resonance imaging (MRI) compared with baseline or best response; new site of disease (central nervous system or systemic); recurrent or new ocular disease; recurrent or positive cerebrospinal fluid (CSF) cytology. Progression-free survival time is defined as time from randomization to the date of first progression, death, or last known follow-up (censored). Progression-free survival rates are estimated using the Kaplan-Meier method. (NCT01399372)
Timeframe: From randomization to last follow-up. Maximum follow-up at time of analysis was 7.3 years.

Interventionyears (Median)
Chemotherapy2.1
Chemotherapy + Low-Dose WBRTNA

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Global Heath Status (GHS) Score of the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire (EORTC QLQ-C30)

"Global Health Status is calculated from two questions on the EORTC QLQ-C30. The question responses range from 1 very poor to 7 excellent such that a higher response indicates better quality of life (QOL). The mean of these responses is linearly transformed to a range of 0 (worst) to 100 (best). Data through five years after end of protocol treatment is included in the analysis, while summary data is provided only through three years due to very few participants after that timepoint." (NCT01399372)
Timeframe: EORTC QLQ-C30 was administered at baseline, after cycle 4 of treatment (4 months), then every six months after end of treatment (7 months) for five years.

,
Interventionscore on a scale (Mean)
BaselineEnd of cycle 46 Months Post-Treatment12 Months Post-Treatment18 Months Post-Treatment24 Months Post-Treatment30 Months Post-Treatment36 Months Post-Treatment42 Months Post-Treatment48 Months Post-Treatment54 Months Post-Treatment60 Months Post-Treatment
Chemotherapy62.7867.6774.5478.4776.7970.8377.0875.0075.0079.7670.2480.56
Chemotherapy + Low-Dose WBRT54.9064.5875.3578.9976.6783.3379.6385.0077.5684.3891.6783.33

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Overall Survival

Overall survival time is defined as time from randomization to the date of death from any cause or last known follow-up (censored). Overall survival rates are estimated by the Kaplan-Meier method. (NCT01399372)
Timeframe: From randomization to last follow-up. Maximum follow-up at time of analysis was 7.3 years.

Interventionyears (Median)
ChemotherapyNA
Chemotherapy + Low-Dose WBRTNA

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Percentage of Participants Experiencing Partial Response or Complete Response

Response was evaluated using the international criteria proposed by the International Primary Central Nervous System Lymphoma (PCNSL) Study Group criteria. Complete Response was defined as no contrast brain enhancement on magnetic resonance imaging (MRI), no corticosteroid use for at least 2 weeks, a normal eye exam, and negative CSF cytology. Partial response was defined as at least 50% decrease in enhancing tumor on MRI compared with baseline imaging, no or minor retinal pigment epithelium (RPE) abnormality, and negative CSF cytology. (NCT01399372)
Timeframe: After 4th cycle of chemotherapy, approximately 4 months after randomization.

Interventionpercentage of participants (Number)
Chemotherapy83.3
Chemotherapy + Low-Dose WBRT80.6

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Change in Absolute CD4 Count From Baseline to Post-treatment

Change in absolute CD4 count from baseline to post-treatment (visit 6) (NCT01775475)
Timeframe: From baseline to 18 weeks

Interventioncells per mm^3 (Mean)
Arm I (CHOP)-41.3
Arm II (Oral Chemotherapy)203.3

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Number of Patients Who Complete Treatment

Number of patients who complete chemotherapy treatment. (NCT01775475)
Timeframe: Up to 18 weeks

InterventionParticipants (Count of Participants)
Arm I (CHOP)3
Arm II (Oral Chemotherapy)1

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Overall Response Rate

Overall response is complete or partial response as defined by response definitions of the 2014 International Conference on Malignant Lymphoma Imaging Working Group (i.e. Lugano classification). Complete response is the disappearance of all lesions with no new lesions detected. Partial response is >=50% decrease in the sum of the perpendicular diameters of up to 6 target measurable nodes and extranodal sites and no new sites of disease. (NCT01775475)
Timeframe: Up to 24 months

InterventionParticipants (Count of Participants)
Arm I (CHOP)3
Arm II (Oral Chemotherapy)1

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Overall Survival

Proportion of participants who survived 2 years (NCT01775475)
Timeframe: Up to 24 months

InterventionProportion of participants (Number)
Arm I (CHOP)0
Arm II (Oral Chemotherapy)0

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Participants Who Experienced an Adverse Event

Number of participants who experienced an adverse event (NCT01775475)
Timeframe: Up to 24 months

InterventionParticipants (Count of Participants)
Arm I (CHOP)4
Arm II (Oral Chemotherapy)3

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Progression-free Survival

Proportion of participants who survived without disease progression at 2 years (NCT01775475)
Timeframe: Up to 24 months

Interventionproportion (Number)
Arm I (CHOP)0
Arm II (Oral Chemotherapy)0

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Proportion of Patients Who Are Adherent to Antiretroviral Therapy

Number of patients who did not miss any of their doses of antiretroviral therapy (NCT01775475)
Timeframe: Up to 24 months

InterventionParticipants (Count of Participants)
Arm I (CHOP)3
Arm II (Oral Chemotherapy)3

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Proportion of Patients Who Are Adherent to Chemotherapy

Patients who did not miss any doses of chemotherapy (NCT01775475)
Timeframe: Up to 18 weeks

InterventionParticipants (Count of Participants)
Arm I (CHOP)4
Arm II (Oral Chemotherapy)3

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