niacinamide and Adenocarcinoma studies

nicotinamide : A pyridinecarboxamide that is pyridine in which the hydrogen at position 3 is replaced by a carboxamide group.

Research Excerpts

Excerpt	Relevance	Reference
"Patients with biopsy-proven, unresectable pancreatic adenocarcinoma (based on vascular invasion detected by computed tomography) were treated with gemcitabine (300 mg/m2 i."	9.19	A phase I, dose-finding study of sorafenib in combination with gemcitabine and radiation therapy in patients with unresectable pancreatic adenocarcinoma: a Grupo Español Multidisciplinario en Cáncer Digestivo (GEMCAD) study. ( Aparicio, J; Ayuso, JR; Conill, C; Feliu, J; Fuster, D; García-Mora, C; Martín, M; Maurel, J; Petriz, ML; Sánchez-Santos, ME, 2014)
"Aim of the study was to investigate efficacy and safety of sorafenib in patients with advanced lung adenocarcinoma after failure of epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) therapy."	9.19	A multicenter phase II study of sorafenib monotherapy in clinically selected patients with advanced lung adenocarcinoma after failure of EGFR-TKI therapy (Chinese Thoracic Oncology Group, CTONG 0805). ( Chen, GY; Cheng, Y; Huang, C; Li, AW; Su, J; Wu, YL; Xu, CR; Yan, HH; Yang, JJ; Zhang, L; Zhang, XC; Zhou, CC; Zhou, Q, 2014)
"This randomized, double-blind, placebo-controlled, phase IIb study evaluated adding sorafenib to first-line modified FOLFOX6 (mFOLFOX6) for metastatic colorectal cancer (mCRC)."	9.17	Sorafenib in combination with oxaliplatin, leucovorin, and fluorouracil (modified FOLFOX6) as first-line treatment of metastatic colorectal cancer: the RESPECT trial. ( Bulavina, I; Burdaeva, O; Cassidy, J; Chang, YL; Cheporov, S; Davidenko, I; Garcia-Carbonero, R; Gladkov, O; Köhne, CH; Lokker, NA; O'Dwyer, PJ; Potter, V; Rivera, F; Salazar, R; Samuel, L; Sobrero, A; Tabernero, J; Tejpar, S; Van Cutsem, E; Vladimirova, L, 2013)
"This study evaluated the addition of sorafenib to gemcitabine and cisplatin in biliary adenocarcinoma first-line therapy."	9.17	A phase II study of gemcitabine and cisplatin plus sorafenib in patients with advanced biliary adenocarcinomas. ( Abou-Alfa, GK; Capanu, M; Chou, JF; Chung, KY; Gansukh, B; Katz, SS; Lee, JK; Ma, J; O'Reilly, EM; Reidy-Lagunes, D; Saltz, LB; Segal, NH; Shia, J; Yu, KH, 2013)
" One patient with advanced-stage lung adenocarcinoma, who was treated with oral sorafenib, demonstrated a near-complete clinical and radiographic remission for 5 years."	7.80	Oncogenic and sorafenib-sensitive ARAF mutations in lung adenocarcinoma. ( Amann, J; Araujo, L; Carbone, DP; Greulich, H; Horn, L; Imielinski, M; Kaplan, B; Meyerson, M; Schiller, J; Villalona-Calero, MA, 2014)
"The aim of the present study was to observe the effects of sorafenib on the proliferation, apoptosis and invasion of A549/DDP cisplatin-resistant lung adenocarcinoma cells cultured in vitro."	7.80	Therapeutic effects of sorafenib on the A549/DDP human lung adenocarcinoma cell line in vitro. ( Chen, XQ; Li, ZY; Lin, TY; Wang, YL, 2014)
"To evaluate Sorafenib's efficacy (60 mg/kg/d per os) in preventing the transformation of high grade prostate intraepithelial neoplasia (HGPIN) into adenocarcinoma (ADC) and in inhibiting the onset and progression of poorly differentiated carcinoma (PDC) in transgenic adenocarcinoma mouse prostate (TRAMP) mice."	7.76	Sorafenib's inhibition of prostate cancer growth in transgenic adenocarcinoma mouse prostate mice and its differential effects on endothelial and pericyte growth during tumor angiogenesis. ( Bono, AV; Cheng, L; Cunico, SC; Iezzi, M; Liberatore, M; Montironi, R; Musiani, P; Pannellini, T; Sasso, F, 2010)
"HT29 and SW48 colorectal cancer cells were studied in vitro using MTT assays to establish the optimal timing of radiation and sorafenib."	7.76	Sorafenib and radiation: a promising combination in colorectal cancer. ( Downing, L; Galoforo, S; Marples, B; Martinez, AA; McGonagle, M; Robertson, JM; Suen, AW; Wilson, GD, 2010)
"These results support a rational basis for future clinical studies to assess the therapeutic benefit of Sorafenib in esophageal adenocarcinoma."	7.74	Sorafenib triggers antiproliferative and pro-apoptotic signals in human esophageal adenocarcinoma cells. ( Bissonnette, M; Cerda, S; Chumsangsri, A; Delgado, JS; Dougherty, U; Fichera, A; Lichtenstein, L; Mustafi, R; Yee, J, 2008)
"Median neoadjuvant rectal cancer score was 8."	6.82	Phase I study of pre-operative continuous 5-FU and sorafenib with external radiation therapy in locally advanced rectal adenocarcinoma. ( Almhanna, K; Campos, T; Chen, DT; Hoffe, SE; Jiang, K; Kim, R; Prithviraj, GK; Shibata, D; Shridhar, R; Strosberg, J; Zhao, X, 2016)
"Sorafenib is a small molecule that blocks the activation of C-RAF, B-RAF, c-KIT, FLT-3, RET, VEGFR-2, VEGFR-3 and PDGFR approved for advanced renal cell and hepatocellular carcinoma (b, c)."	5.42	A significant response to sorafenib in a woman with advanced lung adenocarcinoma and a BRAF non-V600 mutation. ( Casado Sáenz, E; Falagan, S; García Sánchez, S; Gómez-Raposo, C; Hernández Jusdado, R; Moreno Rubio, J; Moreno, V; Sereno, M; Zambrana Tébar, F, 2015)
"Sorafenib has been approved for use in the treatment of metastatic renal cell carcinoma."	5.35	[Sorafenib-induced multiple eruptive keratoacanthomas]. ( Dupre-Goetghebeur, D; Jantzem, H; Merrer, J; Spindler, P, 2009)
"Sorafenib is the first anti-angiogenic agent to demonstrate activity in RMSGC patients, particularly in some histotypes such as HG-MEC, SDC and adenocarcinoma, NOS."	5.22	A phase II study of sorafenib in recurrent and/or metastatic salivary gland carcinomas: Translational analyses and clinical impact. ( Alfieri, S; Bergamini, C; Bossi, P; Civelli, E; Cortelazzi, B; Dagrada, GP; Granata, R; Imbimbo, M; Licitra, L; Lo Vullo, S; Locati, LD; Mariani, L; Mirabile, A; Morosi, C; Orlandi, E; Perrone, F; Pilotti, S; Quattrone, P; Resteghini, C; Saibene, G, 2016)
"We performed a multicenter phase II study of sorafenib 200 mg orally twice daily along with oxaliplatin 85 mg/m(2) IV on days 1 and 15, followed by capecitabine 2250 mg/m(2) orally every 8 h for six doses starting on days 1 and 15 of a 28-day cycle in patients who had no more than one previous chemotherapy regimen for their pancreatic adenocarcinoma."	5.20	A phase II study of sorafenib, oxaliplatin, and 2 days of high-dose capecitabine in advanced pancreas cancer. ( Eickhoff, J; Groteluschen, D; LoConte, NK; Lubner, SJ; Makielski, RJ; Mulkerin, DL; Traynor, AM, 2015)
"Locally advanced or metastatic pancreatic adenocarcinoma patients were randomized in a 1:1 ratio to receive cisplatin plus gemcitabine with sorafenib 400mg bid (arm A) or without sorafenib (arm B)."	5.19	Sorafenib does not improve efficacy of chemotherapy in advanced pancreatic cancer: A GISCAD randomized phase II study. ( Aitini, E; Barni, S; Berardi, R; Bidoli, P; Boni, C; Caprioni, F; Cascinu, S; Cinquini, M; Conte, P; Di Costanzo, F; Faloppi, L; Ferrari, D; Labianca, R; Mosconi, S; Siena, S; Sobrero, A; Tonini, G; Villa, F; Zagonel, V, 2014)
"Patients with biopsy-proven, unresectable pancreatic adenocarcinoma (based on vascular invasion detected by computed tomography) were treated with gemcitabine (300 mg/m2 i."	5.19	A phase I, dose-finding study of sorafenib in combination with gemcitabine and radiation therapy in patients with unresectable pancreatic adenocarcinoma: a Grupo Español Multidisciplinario en Cáncer Digestivo (GEMCAD) study. ( Aparicio, J; Ayuso, JR; Conill, C; Feliu, J; Fuster, D; García-Mora, C; Martín, M; Maurel, J; Petriz, ML; Sánchez-Santos, ME, 2014)
"Aim of the study was to investigate efficacy and safety of sorafenib in patients with advanced lung adenocarcinoma after failure of epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) therapy."	5.19	A multicenter phase II study of sorafenib monotherapy in clinically selected patients with advanced lung adenocarcinoma after failure of EGFR-TKI therapy (Chinese Thoracic Oncology Group, CTONG 0805). ( Chen, GY; Cheng, Y; Huang, C; Li, AW; Su, J; Wu, YL; Xu, CR; Yan, HH; Yang, JJ; Zhang, L; Zhang, XC; Zhou, CC; Zhou, Q, 2014)
"This randomized, double-blind, placebo-controlled, phase IIb study evaluated adding sorafenib to first-line modified FOLFOX6 (mFOLFOX6) for metastatic colorectal cancer (mCRC)."	5.17	Sorafenib in combination with oxaliplatin, leucovorin, and fluorouracil (modified FOLFOX6) as first-line treatment of metastatic colorectal cancer: the RESPECT trial. ( Bulavina, I; Burdaeva, O; Cassidy, J; Chang, YL; Cheporov, S; Davidenko, I; Garcia-Carbonero, R; Gladkov, O; Köhne, CH; Lokker, NA; O'Dwyer, PJ; Potter, V; Rivera, F; Salazar, R; Samuel, L; Sobrero, A; Tabernero, J; Tejpar, S; Van Cutsem, E; Vladimirova, L, 2013)
"This study evaluated the addition of sorafenib to gemcitabine and cisplatin in biliary adenocarcinoma first-line therapy."	5.17	A phase II study of gemcitabine and cisplatin plus sorafenib in patients with advanced biliary adenocarcinomas. ( Abou-Alfa, GK; Capanu, M; Chou, JF; Chung, KY; Gansukh, B; Katz, SS; Lee, JK; Ma, J; O'Reilly, EM; Reidy-Lagunes, D; Saltz, LB; Segal, NH; Shia, J; Yu, KH, 2013)
"Motesanib plus carboplatin/paclitaxel did not significantly improve OS over carboplatin/paclitaxel alone in patients with advanced nonsquamous NSCLC or in the adenocarcinoma subset."	5.16	International, randomized, placebo-controlled, double-blind phase III study of motesanib plus carboplatin/paclitaxel in patients with advanced nonsquamous non-small-cell lung cancer: MONET1. ( Banaclocha, NM; Blackhall, F; Ciuleanu, TE; Dediu, M; Galimi, F; Galiulin, R; Hei, YJ; Ichinose, Y; Kubota, K; McCoy, S; Papai-Szekely, Z; Park, K; Pirker, R; Scagliotti, GV; Spigel, DR; Sydorenko, O; Vynnychenko, I; Yao, B, 2012)
"THERE WERE 62 PATIENTS (37 MEN, MEAN AGE: 61 years) treated with sorafenib (62%), sunitinib (22%), and vandetanib (16%) outside of clinical trials; 22 had papillary, five had follicular, five had Hürthle cell, 13 had poorly differentiated, and 17 had medullary thyroid carcinoma (MTC)."	3.80	Tyrosine kinase inhibitor treatments in patients with metastatic thyroid carcinomas: a retrospective study of the TUTHYREF network. ( Baudin, E; Bonichon, F; Borget, I; Brassard, M; Chougnet, CN; Claude-Desroches, M; de la Fouchardière, C; Do Cao, C; Giraudet, AL; Leboulleux, S; Massicotte, MH; Schlumberger, M, 2014)
" One patient with advanced-stage lung adenocarcinoma, who was treated with oral sorafenib, demonstrated a near-complete clinical and radiographic remission for 5 years."	3.80	Oncogenic and sorafenib-sensitive ARAF mutations in lung adenocarcinoma. ( Amann, J; Araujo, L; Carbone, DP; Greulich, H; Horn, L; Imielinski, M; Kaplan, B; Meyerson, M; Schiller, J; Villalona-Calero, MA, 2014)
"The aim of the present study was to observe the effects of sorafenib on the proliferation, apoptosis and invasion of A549/DDP cisplatin-resistant lung adenocarcinoma cells cultured in vitro."	3.80	Therapeutic effects of sorafenib on the A549/DDP human lung adenocarcinoma cell line in vitro. ( Chen, XQ; Li, ZY; Lin, TY; Wang, YL, 2014)
"Single and multiple oral doses of everolimus and sorafenib were administered alone and in combination in immunocompetent male mice and to severe combined immune-deficient (SCID) mice bearing low-passage, patient-derived pancreatic adenocarcinoma in seven different studies."	3.79	Physiologically based pharmacokinetic models for everolimus and sorafenib in mice. ( Fetterly, GJ; Hylander, BH; Jusko, WJ; Ma, WW; Pawaskar, DK; Repasky, EA; Straubinger, RM, 2013)
"To evaluate Sorafenib's efficacy (60 mg/kg/d per os) in preventing the transformation of high grade prostate intraepithelial neoplasia (HGPIN) into adenocarcinoma (ADC) and in inhibiting the onset and progression of poorly differentiated carcinoma (PDC) in transgenic adenocarcinoma mouse prostate (TRAMP) mice."	3.76	Sorafenib's inhibition of prostate cancer growth in transgenic adenocarcinoma mouse prostate mice and its differential effects on endothelial and pericyte growth during tumor angiogenesis. ( Bono, AV; Cheng, L; Cunico, SC; Iezzi, M; Liberatore, M; Montironi, R; Musiani, P; Pannellini, T; Sasso, F, 2010)
"HT29 and SW48 colorectal cancer cells were studied in vitro using MTT assays to establish the optimal timing of radiation and sorafenib."	3.76	Sorafenib and radiation: a promising combination in colorectal cancer. ( Downing, L; Galoforo, S; Marples, B; Martinez, AA; McGonagle, M; Robertson, JM; Suen, AW; Wilson, GD, 2010)
"These results support a rational basis for future clinical studies to assess the therapeutic benefit of Sorafenib in esophageal adenocarcinoma."	3.74	Sorafenib triggers antiproliferative and pro-apoptotic signals in human esophageal adenocarcinoma cells. ( Bissonnette, M; Cerda, S; Chumsangsri, A; Delgado, JS; Dougherty, U; Fichera, A; Lichtenstein, L; Mustafi, R; Yee, J, 2008)
" nicotinamide, isonicotinamide or nicotinic acid, as extra (axial) ligands, were tested in vivo on transplanted mice tumors, namely Lewis lung carcinoma (3LL), melanoma B16, and mammary adenocarcinoma Ca755."	3.72	Selectivity of effects of redox-active cobalt(III) complexes on tumor tissue. ( Bubnovskaya, L; Campanella, L; Ganusevich, I; Kovelskaya, A; Levitin, I; Osinsky, S; Sigan, A; Valkovskaya, N; Wardman, P, 2004)
"10 mmol/kg) and carbogen breathing, administered alone or in combination, were investigated on two tumour cell lines: EMT6 (a rodent mammary carcinoma) and HRT18 (a human rectal adenocarcinoma) using a clonogenic assay."	3.69	Efficacy of agents counteracting hypoxia in fractionated radiation regimes. ( Guichard, M; Stern, S, 1996)
"Median neoadjuvant rectal cancer score was 8."	2.82	Phase I study of pre-operative continuous 5-FU and sorafenib with external radiation therapy in locally advanced rectal adenocarcinoma. ( Almhanna, K; Campos, T; Chen, DT; Hoffe, SE; Jiang, K; Kim, R; Prithviraj, GK; Shibata, D; Shridhar, R; Strosberg, J; Zhao, X, 2016)
"To define the safety, efficacy, and pharmacogenetic and pharmacodynamic effects of sorafenib with gemcitabine-based chemoradiotherapy (CRT) in locally advanced pancreatic cancer."	2.79	Phase 1 pharmacogenetic and pharmacodynamic study of sorafenib with concurrent radiation therapy and gemcitabine in locally advanced unresectable pancreatic cancer. ( Akisik, FM; Anderson, S; Bu, G; Cardenes, HR; Chiorean, EG; Clark, R; Deluca, J; DeWitt, J; Helft, P; Johnson, CS; Johnston, EL; Loehrer, PJ; Perkins, SM; Sandrasegaran, K; Schneider, BP; Shahda, S; Spittler, AJ, 2014)
"Patients with advanced or metastatic renal cell carcinoma (RCC) with predominant clear cell histology were treated with oral dovitinib 500 or 600 mg/day (5-days-on/2-days-off schedule)."	2.78	Phase I study of dovitinib (TKI258), an oral FGFR, VEGFR, and PDGFR inhibitor, in advanced or metastatic renal cell carcinoma. ( Angevin, E; Castellano, D; Chang, J; Escudier, B; Gschwend, JE; Harzstark, A; Kay, A; Lin, CC; Lopez-Martin, JA; Sen, P; Shi, M; Soria, JC, 2013)
"Sorafenib is a raf kinase and angiogenesis inhibitor with activity in multiple cancers."	2.77	A double-blind randomized discontinuation phase-II study of sorafenib (BAY 43-9006) in previously treated non-small-cell lung cancer patients: eastern cooperative oncology group study E2501. ( Carbone, DP; Hanna, NH; Lee, JW; Schiller, JH; Traynor, AM; Wakelee, HA, 2012)
"Sorafenib is a small-molecule multitargeted kinase inhibitor that blocks the activation of C-RAF, B-RAF, c-KIT, FLT-3, RET, vascular endothelial growth factor receptor 2 (VEGFR-2), VEGFR-3 and platelet-derived growth factor receptor β."	2.76	Sorafenib in combination with erlotinib or with gemcitabine in elderly patients with advanced non-small-cell lung cancer: a randomized phase II study. ( Cerea, G; Chella, A; Ciardiello, F; de Marinis, F; Di Maio, M; Fasano, M; Favaretto, A; Gridelli, C; Maione, P; Mattioli, R; Morgillo, F; Pasello, G; Ricciardi, S; Rossi, A; Tortora, G, 2011)
" The majority of adverse events (AEs) were Grade 1-2 in severity."	2.76	Long-term safety and tolerability of sorafenib in patients with advanced non-small-cell lung cancer: a case-based review. ( Adjei, AA; Blumenschein, GR; Gatzemeier, U; Heigener, D; Hillman, S; Mandrekar, S, 2011)
"Sorafenib is a small molecule that blocks the activation of C-RAF, B-RAF, c-KIT, FLT-3, RET, VEGFR-2, VEGFR-3 and PDGFR approved for advanced renal cell and hepatocellular carcinoma (b, c)."	1.42	A significant response to sorafenib in a woman with advanced lung adenocarcinoma and a BRAF non-V600 mutation. ( Casado Sáenz, E; Falagan, S; García Sánchez, S; Gómez-Raposo, C; Hernández Jusdado, R; Moreno Rubio, J; Moreno, V; Sereno, M; Zambrana Tébar, F, 2015)
"Kinase inhibitor therapy may be used to treat thyroid carcinoma that is symptomatic and/or progressive and not amenable to treatment with radioactive iodine."	1.40	Thyroid carcinoma, version 2.2014. ( Ball, DW; Byrd, D; Dickson, P; Duh, QY; Ehya, H; Haddad, RI; Haymart, M; Hoffmann, KG; Hoh, C; Hughes, M; Hunt, JP; Iagaru, A; Kandeel, F; Kopp, P; Lamonica, DM; Lydiatt, WM; McCaffrey, J; Moley, JF; Parks, L; Raeburn, CD; Ridge, JA; Ringel, MD; Scheri, RP; Shah, JP; Sherman, SI; Sturgeon, C; Tuttle, RM; Waguespack, SG; Wang, TN; Wirth, LJ, 2014)
"Sorafenib treatment correlated with a downregulation of both FLICE-Inhibitory Protein (FLIP) and myeloid cell leukaemia-1 (Mcl-1), caused by a proteasomal degradation of both proteins."	1.36	The multikinase inhibitor Sorafenib induces apoptosis and sensitises endometrial cancer cells to TRAIL by different mechanisms. ( Dolcet, X; Domingo, M; Eritja, N; Gonzalez-Tallada, FJ; Llobet, D; Matias-Guiu, X; Pallares, J; Santacana, M; Sorolla, A; Yeramian, A, 2010)
"Sorafenib has been approved for use in the treatment of metastatic renal cell carcinoma."	1.35	[Sorafenib-induced multiple eruptive keratoacanthomas]. ( Dupre-Goetghebeur, D; Jantzem, H; Merrer, J; Spindler, P, 2009)
" The half-life of nicotinamide increased from 1."	1.29	Pharmacokinetics of varying doses of nicotinamide and tumour radiosensitisation with carbogen and nicotinamide: clinical considerations. ( Dennis, MF; Hodgkiss, RJ; Johns, H; Rojas, A; Stratford, MR, 1993)

Research

Studies (81)

Authors

Clinical Trials (15)

Trial Overview

Trial Outcomes

Phase II: Overall Survival (OS) Time

Timeframe	Studies, this research(%)	All Research%
pre-1990	8 (9.88)	18.7374
1990's	9 (11.11)	18.2507
2000's	8 (9.88)	29.6817
2010's	54 (66.67)	24.3611
2020's	2 (2.47)	2.80

Authors	Studies
Arçay, A	1
Eiber, M	1
Langbein, T	1
Soeda, F	1
Watabe, T	1
Kato, H	1
Uemura, M	1
Nonomura, N	1
Manzo, A	1
Montanino, A	1
Carillio, G	1
Costanzo, R	1
Sandomenico, C	1
Normanno, N	1
Piccirillo, MC	1
Daniele, G	1
Perrone, F	2
Rocco, G	1
Morabito, A	1
Van Cutsem, E	2
Hidalgo, M	1
Canon, JL	1
Macarulla, T	1
Bazin, I	1
Poddubskaya, E	1
Manojlovic, N	1
Radenkovic, D	1
Verslype, C	1
Raymond, E	1
Cubillo, A	1
Schueler, A	1
Zhao, C	1
Hammel, P	1
Pawaskar, DK	1
Straubinger, RM	1
Fetterly, GJ	1
Hylander, BH	1
Repasky, EA	1
Ma, WW	1
Jusko, WJ	1
Tabernero, J	1
Garcia-Carbonero, R	1
Cassidy, J	1
Sobrero, A	2
Köhne, CH	1
Tejpar, S	1
Gladkov, O	1
Davidenko, I	1
Salazar, R	1
Vladimirova, L	1
Cheporov, S	1
Burdaeva, O	1
Rivera, F	1
Samuel, L	1
Bulavina, I	1
Potter, V	1
Chang, YL	1
Lokker, NA	1
O'Dwyer, PJ	2
Sarris, EG	1
Syrigos, KN	1
Saif, MW	2
Lee, JK	1
Capanu, M	2
O'Reilly, EM	1
Ma, J	1
Chou, JF	1
Shia, J	1
Katz, SS	1
Gansukh, B	1
Reidy-Lagunes, D	1
Segal, NH	1
Yu, KH	1
Chung, KY	1
Saltz, LB	1
Abou-Alfa, GK	1
Martin-Richard, M	1
Gallego, R	1
Pericay, C	1
Garcia Foncillas, J	1
Queralt, B	1
Casado, E	1
Barriuso, J	1
Iranzo, V	1
Juez, I	1
Visa, L	1
Saigi, E	1
Barnadas, A	1
Garcia-Albeniz, X	1
Maurel, J	2
Cascinu, S	1
Berardi, R	1
Bidoli, P	1
Labianca, R	1
Siena, S	1
Ferrari, D	1
Barni, S	1
Aitini, E	1
Zagonel, V	1
Caprioni, F	1
Villa, F	1
Mosconi, S	1
Faloppi, L	1
Tonini, G	1
Boni, C	1
Conte, P	1
Di Costanzo, F	1
Cinquini, M	1
Huang, LY	1
Lee, YS	1
Huang, JJ	1
Chang, CC	1
Chang, JM	1
Chuang, SH	1
Kao, KJ	1
Tsai, YJ	1
Tsai, PY	1
Liu, CW	1
Lin, HS	1
Lau, JY	1
Aparicio, J	1
García-Mora, C	1
Martín, M	2
Petriz, ML	1
Feliu, J	1
Sánchez-Santos, ME	1
Ayuso, JR	1
Fuster, D	1
Conill, C	1
Massicotte, MH	1
Brassard, M	1
Claude-Desroches, M	1
Borget, I	1
Bonichon, F	1
Giraudet, AL	1
Do Cao, C	1
Chougnet, CN	1
Leboulleux, S	1
Baudin, E	1
Schlumberger, M	1
de la Fouchardière, C	1
Zhou, Q	1
Zhou, CC	1
Chen, GY	1
Cheng, Y	1
Huang, C	1
Zhang, L	1
Xu, CR	1
Li, AW	1
Yan, HH	1
Su, J	1
Zhang, XC	1
Yang, JJ	1
Wu, YL	1
Imielinski, M	1
Greulich, H	1
Kaplan, B	1
Araujo, L	1
Amann, J	1
Horn, L	1
Schiller, J	1
Villalona-Calero, MA	1
Meyerson, M	1
Carbone, DP	2
Karashima, T	1
Komatsu, T	1
Niimura, M	1
Kawada, C	1
Kamada, M	1
Inoue, K	1
Udaka, K	1
Kuroda, N	1
Shuin, T	1
Chiorean, EG	1
Schneider, BP	1
Akisik, FM	1
Perkins, SM	1
Anderson, S	1
Johnson, CS	1
DeWitt, J	1
Helft, P	1
Clark, R	1
Johnston, EL	1
Spittler, AJ	1
Deluca, J	1
Bu, G	1
Shahda, S	1
Loehrer, PJ	1
Sandrasegaran, K	1
Cardenes, HR	1
Masri, SC	1
Misselt, AJ	1
Dudek, A	1
Konety, SH	1
Chen, XQ	1
Wang, YL	1
Li, ZY	1
Lin, TY	1
Tuttle, RM	1
Haddad, RI	1
Ball, DW	1
Byrd, D	1
Dickson, P	1
Duh, QY	1
Ehya, H	1
Haymart, M	1
Hoh, C	1
Hunt, JP	1
Iagaru, A	1
Kandeel, F	1
Kopp, P	1
Lamonica, DM	1
Lydiatt, WM	1
McCaffrey, J	1
Moley, JF	1
Parks, L	1
Raeburn, CD	1
Ridge, JA	1
Ringel, MD	1
Scheri, RP	1
Shah, JP	1
Sherman, SI	1
Sturgeon, C	1
Waguespack, SG	1
Wang, TN	1
Wirth, LJ	1
Hoffmann, KG	1
Hughes, M	1
Huang, YS	1
Xue, Z	1
Zhang, H	1
Gavrancic, T	1
Park, YH	1
Makielski, RJ	1
Lubner, SJ	1
Mulkerin, DL	1
Traynor, AM	2
Groteluschen, D	1
Eickhoff, J	1
LoConte, NK	1
Sereno, M	1
Moreno, V	1
Moreno Rubio, J	1
Gómez-Raposo, C	1
García Sánchez, S	1
Hernández Jusdado, R	1
Falagan, S	1
Zambrana Tébar, F	1
Casado Sáenz, E	1
Janjigian, YY	1
Vakiani, E	1
Ku, GY	1
Herrera, JM	1
Tang, LH	2
Bouvier, N	1
Viale, A	1
Socci, ND	1
Berger, M	1
Ilson, DH	1
Kim, R	1
Prithviraj, GK	1
Shridhar, R	1
Hoffe, SE	1
Jiang, K	1
Zhao, X	1
Chen, DT	1
Almhanna, K	1
Strosberg, J	1
Campos, T	1
Shibata, D	1
Dang, RP	1
McFarland, D	1
Le, VH	1
Camille, N	1
Miles, BA	1
Teng, MS	1
Genden, EM	1
Misiukiewicz, KJ	1
Locati, LD	1
Cortelazzi, B	1
Bergamini, C	1
Bossi, P	1
Civelli, E	1
Morosi, C	1
Lo Vullo, S	1
Imbimbo, M	1
Quattrone, P	1
Dagrada, GP	1
Granata, R	1
Resteghini, C	1
Mirabile, A	1
Alfieri, S	1
Orlandi, E	1
Mariani, L	1
Saibene, G	1
Pilotti, S	1
Licitra, L	1
Chang, H	1
Sung, JH	1
Moon, SU	1
Kim, HS	1
Kim, JW	1
Lee, JS	1
Delgado, JS	1
Mustafi, R	2
Yee, J	2
Cerda, S	1
Chumsangsri, A	2
Dougherty, U	1
Lichtenstein, L	1
Fichera, A	1
Bissonnette, M	2
Keswani, RN	1
Delgado, J	1
Cohen, EE	1
Diaz, O	1
Mazeron, R	1
Martin, E	1
Carrie, C	1
Beauparlant, P	1
Bédard, D	1
Bernier, C	1
Chan, H	1
Gilbert, K	1
Goulet, D	1
Gratton, MO	1
Lavoie, M	1
Roulston, A	1
Turcotte, E	1
Watson, M	1
Jantzem, H	1
Dupre-Goetghebeur, D	1
Spindler, P	1
Merrer, J	1
Xie, XD	1
Piao, Y	1
Liu, ZZ	1
Llobet, D	1
Eritja, N	1
Yeramian, A	1
Pallares, J	1
Sorolla, A	1
Domingo, M	1
Santacana, M	1
Gonzalez-Tallada, FJ	1
Matias-Guiu, X	1
Dolcet, X	1
Shoemaker, RH	1
Boonstra, JJ	1
van Marion, R	1
Beer, DG	1
Lin, L	1
Chaves, P	1
Ribeiro, C	1
Pereira, AD	1
Roque, L	1
Darnton, SJ	1
Altorki, NK	1
Schrump, DS	1
Klimstra, DS	1
Eshleman, JR	1
Alvarez, H	1
Shimada, Y	1
van Dekken, H	1
Tilanus, HW	1
Dinjens, WN	1
Scagliotti, G	1
Novello, S	1
von Pawel, J	1
Reck, M	1
Pereira, JR	1
Thomas, M	1
Abrão Miziara, JE	1
Balint, B	1
De Marinis, F	2
Keller, A	1
Arén, O	1
Csollak, M	1
Albert, I	1
Barrios, CH	1
Grossi, F	1
Krzakowski, M	1
Cupit, L	1
Cihon, F	1
Dimatteo, S	1
Hanna, N	1
Smit, EF	1
Dingemans, AM	1
Thunnissen, FB	1
Hochstenbach, MM	1
van Suylen, RJ	1
Postmus, PE	1
Sun, W	1
Powell, M	1
Catalano, P	1
Ansari, RH	1
Benson, AB	1
Beljanski, V	1
Knaak, C	1
Zhuang, Y	1
Smith, CD	1
Metzgeroth, G	1
Ströbel, P	1
Baumbusch, T	1
Reiter, A	1
Hastka, J	1
Jones, SJ	1
Laskin, J	1
Li, YY	1
Griffith, OL	1
An, J	1
Bilenky, M	1
Butterfield, YS	1
Cezard, T	1
Chuah, E	1
Corbett, R	1
Fejes, AP	1
Griffith, M	1
Mayo, M	1
Melnyk, N	1
Morin, RD	1
Pugh, TJ	1
Severson, T	1
Shah, SP	1
Sutcliffe, M	1
Tam, A	1
Terry, J	1
Thiessen, N	1
Thomson, T	1
Varhol, R	1
Zeng, T	1
Zhao, Y	1
Moore, RA	1
Huntsman, DG	1
Birol, I	1
Hirst, M	1
Holt, RA	1
Marra, MA	1
Bono, AV	1
Pannellini, T	1
Liberatore, M	1
Montironi, R	1
Cunico, SC	1
Cheng, L	1
Sasso, F	1
Musiani, P	1
Iezzi, M	1
Suen, AW	1
Galoforo, S	1
Marples, B	1
McGonagle, M	1
Downing, L	1
Martinez, AA	1
Robertson, JM	1
Wilson, GD	1
Kindler, HL	1
Wroblewski, K	1
Wallace, JA	1
Hall, MJ	1
Locker, G	1
Nattam, S	1
Agamah, E	1
Stadler, WM	1
Vokes, EE	1
Sulkes, A	1
Gridelli, C	1
Morgillo, F	2
Favaretto, A	1
Chella, A	1
Cerea, G	1
Mattioli, R	1
Tortora, G	1
Rossi, A	1
Fasano, M	1
Pasello, G	1
Ricciardi, S	1
Maione, P	1
Di Maio, M	1
Ciardiello, F	2
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Rajan, A	1
Dombi, E	1
Steinberg, SM	1
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Okines, AF	1
Reynolds, AR	1
Cunningham, D	1
Adjei, AA	1
Blumenschein, GR	1
Mandrekar, S	1
Hillman, S	1
Gatzemeier, U	1
Heigener, D	1
Cascone, T	1
D'Aiuto, E	1
Martinelli, E	1
Troiani, T	1
Saintigny, P	1
De Palma, R	1
Heymach, JV	1

Trial	Phase	Enrollment	Study Type	Start Date	Status
Phase II Randomized Trial of MEK Inhibitor MSC1936369B or Placebo Combined With Gemcitabine in Metastatic Pancreas Cancer Subjects[NCT01016483]	Phase 1/Phase 2	141 participants (Actual)	Interventional	2009-11-30	Completed
Phase 2b, DB, Randomized Study Evaluating Efficacy & Safety of Sorafenib Compared With Placebo When Administered in Combination With Modified FOLFOX6 for the Treatment of Metastatic CRC Subjects Previously Untreated for Stage IV Disease[NCT00865709]	Phase 2	198 participants (Actual)	Interventional	2009-03-31	Completed
Open-label, Multicentric Phase I-II Trial to Evaluate the Efficacy and Safety of the Combination of Sorafenib (BAY 43-9006), Gemcitabine and Concurrent Radiotherapy, in Locally Advanced Pancreatic Carcinoma[NCT00789763]	Phase 1	12 participants (Actual)	Interventional	2007-12-31	Completed
A Phase II Study of Sorafenib (BAY 43-9006®) in Patients With Relapsed Advanced Non-Small Cell Lung Cancer(NSCLC) After Failure of Epidermal Growth Factor Receptor-tyrosine Kinase Inhibitor (EGFR-TKI)Treatment[NCT00922584]	Phase 2	65 participants (Actual)	Interventional	2008-12-31	Completed
Phase II Trial of Sorafenib for Patients With Metastatic or Recurrent Esophageal and Gastroesophageal Junction Cancer[NCT00917462]	Phase 2	35 participants (Actual)	Interventional	2009-06-30	Completed
Phase I Study of Pre-operative Continuous 5-FU, and Sorafenib With External Radiation Therapy in Locally Advanced Rectal Adenocarcinoma[NCT01376453]	Phase 1	18 participants (Actual)	Interventional	2011-06-30	Completed
Safety and Efficacy of Sequential Stereotactic Radiotherapy With S1 Combined With Endostar in the Treatment of Stage IV Lung Squamous Cell Carcinoma: Prospective, Multicenter, Exploratory Study[NCT04274270]		60 participants (Anticipated)	Interventional	2020-04-01	Not yet recruiting
A Randomized Controlled Trial Comparing Safety and Efficacy of Carboplatin and Paclitaxel Plus or Minus Sorafenib (BAY 43-9006) in Chemonaive Patients With Stage IIIB-IV Non-Small Cell Lung Cancer (NSCLC)[NCT00300885]	Phase 3	926 participants (Actual)	Interventional	2006-02-28	Terminated (stopped due to Based on the results of the interim analysis, it was determined that the study would not meet its primary efficacy endpoint and the study was terminated early.)
A Phase II Study to Evaluate Overall Response Rate of BAY 43-9006 (Sorafenib) Combined With Docetaxel and Cisplatin or Oxaliplatin in the Treatment of Metastatic or Advanced Unresectable Gastric and Gastroesophageal Junction (GEJ) Adenocarcinoma[NCT00253370]	Phase 2	44 participants (Actual)	Interventional	2005-10-31	Completed
Pazopanib With 5-Fluorouracil, Leucovorin and Oxaliplatin (FLO) as 1st-line Treatment in Advanced Gastric Cancer; a Randomized Phase-II-study of the Arbeitsgemeinschaft Internistische Onkologie[NCT01503372]	Phase 2	75 participants (Actual)	Interventional	2011-11-30	Completed
Personalized OncoGenomics (POG) Program of British Columbia: Connecting Cancer Genomics to Cancer Care[NCT02155621]		5,000 participants (Anticipated)	Interventional	2014-07-31	Recruiting
Canadian Atezolizumab Precision Targeting for Immunotherapy Intervention[NCT04273061]	Phase 2	200 participants (Anticipated)	Interventional	2020-06-17	Recruiting
Prospective Clinical Validation of Next Generation Sequencing (NGS) and Patient-Derived Tumor Organoids (PDO) Guided Therapy in Patients With Advanced/ Inoperable Solid Tumors[NCT06077591]		40 participants (Anticipated)	Interventional	2024-02-01	Not yet recruiting
Drug Response in Patient-derived Organoids Models of Advanced or Recurrent Ovarian Cancer, an Exploratory Research[NCT05290961]		30 participants (Anticipated)	Observational [Patient Registry]	2022-03-09	Recruiting
A Phase 3, Multicenter, Randomized, Placebo-Controlled, Double-Blind Trial of AMG 706 in Combination With Paclitaxel and Carboplatin for Advanced Non-small Cell Lung Cancer.[NCT00460317]	Phase 3	1,450 participants (Actual)	Interventional	2007-07-31	Terminated (stopped due to Amgen discontinued the development of AMG706 because 20050201 did not meet its primary objective.)
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Overall survival (OS) time is defined as the time (in months) from randomization to death. (NCT01016483)
Timeframe: Baseline, every 8 weeks up to EOT (6 years)

Phase II: Percentage of Subjects With Clinical Benefit

Intervention	months (Median)
Phase II: Arm 1	6.64
Phase II: Arm 2	9.33

Clinical Benefit was defined as the presence of at least one CR, PR or Stable Disease (SD) (using RECIST v1.0) during treatment. CR: Disappearance of all target lesions, PR: At least 30% decrease in the sum of the longest diameter of target lesions, taking as reference the sum of the longest diameter at baseline and SD: Neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD, taking as reference the smallest sum of the longest diameter since treatment started. (NCT01016483)
Timeframe: Baseline, every 8 weeks up to end of treatment (EOT i.e. 6 years)

Phase II: Progression-Free Survival (PFS) Time

Intervention	percentage of subjects (Number)
Phase II: Arm 1	45.5
Phase II: Arm 2	59.1

PFS was defined as the time from randomization to the first documentation of objective tumor progression (Complete Response (CR): Disappearance of all target lesions, Partial Response (PR): At least 30% decrease in the sum of the longest diameter of target lesions, taking as reference the sum of the longest diameter at baseline, Progressive Disease (PD): At least 20% increase in the sum of the longest diameter of target lesions, taking as reference the smallest sum of the longest diameter recorded since treatment started, or the appearance of 1 or more new lesions and stable disease: Neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD, taking as reference the smallest sum of the longest diameter since treatment started) or to death due to any cause, whichever occurred first. PFS calculated as (Months) = Date of first PD or death or censoring date minus date of randomization plus 1) divided by 30.4375. (NCT01016483)
Timeframe: From the time of randomization to every 8 weeks up to end of treatment (EOT) (6 years)

Phase II: Time to Progression (TTP)

Intervention	months (Median)
Phase II: Arm 1	2.83
Phase II: Arm 2	3.75

Time to progression (TTP) is defined as the time (in months) from the randomization date to the date of progression prior to the start of any subsequent therapy for the primary disease, as reported and documented by the Investigator (i.e. radiological progression per RECIST). (NCT01016483)
Timeframe: From randomization every 8 weeks up to EOT (6 years)

Safety Run-In Part: Number of Subjects With Dose Limiting Toxicities (DLTs)

Intervention	months (Median)
Phase II: Arm 1	3.78
Phase II: Arm 2	5.09

DLT using the National Cancer Institute Common Terminology Criteria for Adverse Events(CTCAE) v3.0,was defined as any of the following toxicities at any dose level and judged to be possibly or probably related to trial medication by the Investigator and/or the Sponsor and relevant for the combination treatment: Grade 3/more non-hematological toxicity excluding: Subjects with liver involvement: Grade 4 asymptomatic increases in liver function tests and subject without liver involvement: Grade 3 asymptomatic increases in liver function tests reversible within 7 days. Grade 3 vomiting encountered despite adequate therapy. Grade 3 diarrhea encountered despite adequate anti diarrhea therapy. Grade 4 neutropenia greater (>) 5 days duration or febrile neutropenia lasting for more than 1 day. Grade 4 thrombocytopenia > 1 day/Grade 3 with bleeding. Grade 4 anemia: Any treatment delay > 2 weeks due to drug-related adverse effects. (NCT01016483)
Timeframe: Up to 28 days in Cycle 1

Phase II: Number of Subjects With Treatment-Emergent Adverse Events (TEAEs), Serious TEAEs, and TEAEs Leading to Permanent Treatment Discontinuation

Intervention	subjects (Number)
Safety Run-in Part Regimen 1: 15 mg	0
Safety Run-in Part Regimen 1: 30 mg	0
Safety Run-in Part Regimen 1: 45 mg	0
Safety Run-in Part Regimen 1: 68 mg	0
Safety Run-in Part Regimen 1: 90 mg	0
Safety Run-in Part Regimen 1: 120 mg	0
Safety Run-in Part Regimen 2: 60 mg	1
Safety Run-in Part Regimen 2: 75 mg	2

An AE was any untoward medical occurrence in a subject who received study drug without regard to possibility of causal relationship. An SAE was an AE resulting in any of the following outcomes or deemed significant for any other reason: death; initial or prolonged inpatient hospitalization; life-threatening experience (immediate risk of dying); persistent or significant disability/incapacity; congenital anomaly. All AEs (serious and non-serious) except AEs recorded with an onset date prior to the first day of drug administration unless a worsening of the event was recorded after the first dosing date, in which case the event was counted as a TEAE. TEAEs include both SAEs and non-SAEs. (NCT01016483)
Timeframe: From the first dose of study drug administration until EOT (6 years)

Phase II: Percentage of Subjects With Best Overall Response (BOR)

Intervention	subjects (Number)
	TEAEs	Serious TEAEs	TEAEs Leading to Treatment Discontinuation
Phase II: Arm 1	40	28	10
Phase II: Arm 2	45	35	21

Best overall response was defined as the presence of at least one complete response (CR), partial response (PR) or Stable Disease (SD) (using RECIST v1.0) during treatment. CR: Disappearance of all target lesions, PR: At least 30% decrease in the sum of the longest diameter of target lesions, taking as reference the sum of the longest diameter at baseline and SD: Neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD, taking as reference the smallest sum of the longest diameter since treatment started. (NCT01016483)
Timeframe: Baseline, every 8 weeks up to end of treatment (EOT i.e. 6 years)

Safety Run-In Part: Apparent Oral Clearance (CL/f) of Pimasertib (MSC1936369B): Regimen 1

Intervention	percentage of subjects (Number)
	CR	PR	SD	PD	Missing
Phase II: Arm 1	0	9.1	36.4	29.5	25
Phase II: Arm 2	0	9.1	50.0	20.5	20.5

Clearance of a drug was a measure of the rate at which a drug is metabolized or eliminated by normal biological processes. Clearance obtained after oral dose (apparent oral clearance) was influenced by the fraction of the dose absorbed. (NCT01016483)
Timeframe: 0 hour (pre-dose), 0.5, 1, 1.5, 2, 2.5, 4, 8, 12, 24 (post-dose) on Day 1, 22 of Cycle 1

Safety Run-In Part: Apparent Oral Clearance (CL/f) of Pimasertib (MSC1936369B): Regimen 2

Intervention	Liter per hour (L/h) (Geometric Mean)
	CL/f: MSC1936369B on Day 1 (n=4,3,3,2,3,11)	CL/f: MSC1936369B on Day 22 (n=2,2,3,2,3,9)
Regimen 1: 120 mg	55.171	55.723
Regimen 1: 30 mg	58.104	42.484
Regimen 1: 45 mg	51.072	44.579
Regimen 1: 68 mg	87.765	56.502
Regimen 1: 90 mg	52.025	50.873
Regimen 1:15 mg	92.152	74.143

Clearance of a drug is a measure of the rate at which a drug is metabolized or eliminated by normal biological processes. Clearance obtained after oral dose (apparent oral clearance) is influenced by the fraction of the dose absorbed. (NCT01016483)
Timeframe: 0 hour (pre-dose), 0.5, 1, 1.5, 2, 2.5, 4, 8, 12, 24 (post-dose) on Day 1, 22 of Cycle 1

Safety Run-In Part: Apparent Volume of Distribution (V) of Gemcitabine: Regimen 1

Intervention	Liter per hour (L/H) (Geometric Mean)
	CL/f: MSC1936369B on Day 1 (n=10,11)	CL/f: MSC1936369B on Day 22 (n=8,5)
Regimen 2: 60 mg	85.186	70.163
Regimen 2: 75 mg	52.558	68.312

Apparent volume of distribution was defined as the theoretical volume in which the total amount of drug would need to be uniformly distributed to produce the desired plasma concentration of a drug. (NCT01016483)
Timeframe: 0 hour (pre-dose), 0.5, 1, 1.5, 2, 2.5, 4, 8, 12, 24 (post-dose) on Day 1, 22 of Cycle 1

Safety Run-In Part: Apparent Volume of Distribution (V) of Gemcitabine: Regimen 2

Intervention	liter (Geometric Mean)
	V: Gemcitabine (dFdC) on Day 1 (n= 4,3,3,3,3,11)	V: Gemcitabine (dFdC) on Day 22 (n=2,2,1,2,2,9)
Regimen 1: 120 mg	1270.1	805.15
Regimen 1: 15 mg	359.55	1723.6
Regimen 1: 30 mg	531.23	908.50
Regimen 1: 45 mg	587.64	251.79
Regimen 1: 68 mg	729.65	149.65
Regimen 1: 90 mg	2402.1	2140.8

Volume of distribution is defined as the theoretical volume in which the total amount of drug would need to be uniformly distributed to produce the desired plasma concentration of a drug. (NCT01016483)
Timeframe: 0 hour (pre-dose), 0.5, 1, 1.5, 2, 2.5, 4, 8, 12, 24 (post-dose) on Day 1, 22 of Cycle 1

Safety Run-In Part: Area Under Curve (AUC: 0 to Infinity) of Pimasertib (MSC1936369B), Gemcitabine (dFdC), and Gemcitabine Inactive Metabolite 2',2'-Difluorodeoxyuridine (dFdU): Regimen 1

Intervention	liter (Geometric Mean)
	V: Gemcitabine on Day 1 (n=11,14)	V: Gemcitabine on Day 22 (n=9,4)
Regimen 2: 60 mg	716.12	1590.8
Regimen 2: 75 mg	1059.0	801.90

AUC:0 to infinity was a measure of the serum concentration of the drug over time. It was used to characterize drug absorption. (NCT01016483)
Timeframe: 0 hour (pre-dose), 0.5, 1, 1.5, 2, 2.5, 4, 8, 12, 24 (post-dose) on Day 1 of Cycle 1 for MSC1936369B, 0 hour (pre-dose), 0.5, 1, 1.5, 2, 2.5, 4, 8, 12, 24 (post-dose) on Day 1, 22 of Cycle 1 for Gemcitabine

Safety Run-In Part: Area Under Curve (AUC:0 to Infinity) of Pimasertib (MSC1936369B), Gemcitabine (dFdC), and Gemcitabine Inactive Metabolite 2',2'-Difluorodeoxyuridine (dFdU) Regimen 2

Intervention	hournanogram per milliliter (hng/mL) (Geometric Mean)
	AUC: MSC1936369B on Day 1 (n=4,3,3,3,3,11)	AUC: Gemcitabine (dFdC) on Day 1(n=4,3,3,3,3,11)	AUC: Gemcitabine (dFdC) on Day 22(n=2,2,1,2,2,9)	AUC: Metabolite (dFdU) on Day 1 (n=4,3,3,3,3,11)	AUC: Metabolite (dFdU) on Day 22 (n=2,2,2,2,2,10)
Regimen 1: 30 mg	516.3	13536.5	12019.6	228032.9	376280.5
Regimen 1: 45 mg	881.1	10053.3	9093.2	276968.3	217930.8
Regimen 1: 68 mg	774.8	18956.0	76448.7	259816.2	327424.8
Regimen 1: 90 mg	1729.9	8178.4	9604.8	239902.9	248496.4
Regimen 1:15 mg	162.8	29536.1	10828.0	245795.5	190952.6
Regimen1: 120 mg	2175.1	11680.1	10598.0	240293.8	247430.7

AUC:0 to infinity is a measure of the serum concentration of the drug over time. It is used to characterize drug absorption. (NCT01016483)
Timeframe: 0 hour (pre-dose), 0.5, 1, 1.5, 2, 2.5, 4, 8, 12, 24 (post-dose) on Day 1 of Cycle 1 for MSC1936369B, 0 hour (pre-dose), 0.5, 1, 1.5, 2, 2.5, 4, 8, 12, 24 (post-dose) on Day 1, 22 of Cycle 1 for Gemcitabine

Safety Run-In Part: Levels of Pharmacodynamic (Pd) Markers (Phosphorylated- Extracellular Signal-Regulated Kinase (ERK) in Peripheral Blood Mononuclear Cells [PBMCs]): Regimen 1

Intervention	hournanogram per milliliter (hng/mL) (Geometric Mean)
	AUC: MSC1936369B on Day 1 (n= 10, 11)	AUC: Gemcitabine (dFdC) on Day 1 (n= 11, 14)	AUC: Gemcitabine (dFdC) on Day 22 (n= 9, 4)	AUC: Metabolite (dFdU) on Day 1 (n= 11, 13)	AUC: Metabolite (dFdU) on Day 22 (n= 10, 5)
Regimen 1: 75 mg	1427.0	8065.5	10102.3	234934.8	256714.9
Regimen 2: 60 mg	704.3	11932.0	10719.1	189007.0	177504.5

ERK phosphoprotein in peripheral blood monocytes (PBMCs) was analyzed from blood samples of all subjects in the SAF analysis set (safety-run part) only. (NCT01016483)
Timeframe: pre-dose on Day 1, 2, 22 of Cycle 1; post-dose on Day 1, 22 of Cycle 1

Safety Run-In Part: Levels of Pharmacodynamic (Pd) Markers (Phosphorylated- Extracellular Signal-Regulated Kinase (ERK) in Peripheral Blood Mononuclear Cells [PBMCs]): Regimen 2

Intervention	Fluorescence Intensity (Mean)
	Cycle 1 Day 1 Pre-dose (n=3,2,2,3,3,7)	Cycle 1 Day 1 Post-dose (n=3,2,2,3,2,6)	Cycle 1 Day 2 Pre-dose (n=3,2,1,2,2,6)	Cycle 1 Day 22 Pre-dose (n=2,1,2,1,3,5)	Cycle 1 Day 22 Post-dose (n=0,0,0,0,2)
Regimen 1: 30 mg	6.476	2.061	6.719	6.000	NA
Regimen 1: 45 mg	4.767	0.837	3.902	1.978	NA
Regimen 1: 68 mg	6.509	3.881	2.768	8.653	NA
Regimen 1: 90 mg	4.608	1.059	4.874	4.252	NA
Regimen 1:15 mg	5.389	1.611	4.818	5.242	NA
Regimen1: 120 mg	4.229	0.946	3.636	3.453	4.130

Safety Run-In Part: Maximum Concentration (Cmax) of Pimasertib (MSC1936369B), Gemcitabine (dFdC), and Gemcitabine Inactive Metabolite 2',2'-Difluorodeoxyuridine (dFdU) for Regimen 1

Intervention	Fluorescence Intensity (Mean)
	Cycle 1 Day 1 Pre-dose (n=7,4)	Cycle 1 Day 1 Post-dose (n=5,3)	Cycle 1 Day 2 Pre-dose (n=7,3)	Cycle 1 Day 22 Pre-dose (n=6,2)	Cycle 1 Day 22 Post-dose (n=3,1)
Regimen 2: 60 mg	6.081	1.520	3.877	2.728	1.443
Regimen 2: 75 mg	5.874	1.048	2.263	2.295	1.111

(NCT01016483)
Timeframe: 0 hour (pre-dose), 0.5, 1, 1.5, 2, 2.5, 4, 8, 12, 24 (post-dose) on Day 1, 22 of Cycle 1

Safety Run-In Part: Maximum Concentration (Cmax) of Pimasertib (MSC1936369B), Gemcitabine (dFdC), Gemcitabine Inactive Metabolite 2',2'-Difluorodeoxyuridine (dFdU): Regimen 2

Intervention	nanogram per milliliter (ng/mL) (Geometric Mean)
	MSC1936369B on Days 1 (n=4,3,3,3,3,11)	MSC1936369B on Days 22 (n= 3,3,3,2,3,10)	Gemcitabine (dFdC) on Day 1 (n=4,3,3,3,3,11)	Gemcitabine (dFdC) on Day 22 (n= 2,3,3,2,3,9)	Metabolite (dFdU) on Day 1 (n= 4,3,3,3,3,11)	Metabolite (dFdU) on Day 22 (n= 2,3,3,2,3,10)
Regimen 1: 120 mg	484.3	252.9	23880.7	23207.2	34038.7	21077.5
Regimen 1: 15 mg	32.3	29.6	69540.5	24115.8	29359.8	29677.6
Regimen 1: 30 mg	131.0	174.2	21207.3	11799.7	33171.6	38265.2
Regimen 1: 45 mg	205.8	261.8	17759.9	181.9	34868.9	10569.2
Regimen 1: 68 mg	151.3	212.5	29762.1	163196.2	33804.4	32869.2
Regimen 1: 90 mg	485.3	409.1	15606.3	669.5	37786.4	17135.0

(NCT01016483)
Timeframe: 0 hour (pre-dose), 0.5, 1, 1.5, 2, 2.5, 4, 8, 12, 24 (post-dose) on Day 1, 22 of Cycle 1

Safety Run-In Part: Number of Subjects With Treatment-Emergent Adverse Events (TEAEs), Serious TEAEs, and TEAEs Leading to Permanent Treatment Discontinuation

Intervention	nanogram per milliliter (ng/mL) (Geometric Mean)
	MSC1936369B on Day 1 (n= 12,13)	MSC1936369B on Day 22 (n=10,9)	Gemcitabine (dFdC) on Day 1 (n=11,14)	Gemcitabine (dFdC) on Day 22 (n=9,4)	Gemcitabine Metabolite (dFdU) on Day 1 (n=11, 10)	Gemcitabine Metabolite (dFdU) on Day 22 (n=10,5)
Regimen 2: 60 mg	175.7	228.2	27849.2	21589.7	33033.3	13455.5
Regimen 2: 75 mg	345.5	244.8	17663.9	18733.4	31623.9	18298.7

An adverse event (AE) was any untoward medical occurrence in a subjects who received study drug without regard to possibility of causal relationship. An serious adverse event (SAE) was an AE resulting in any of the following outcomes or deemed significant for any other reason: death; initial or prolonged inpatient hospitalization; life-threatening experience (immediate risk of dying); persistent or significant disability/incapacity; congenital anomaly. All AEs (serious and non-serious) except AEs recorded with an onset date prior to the first day of drug administration unless a worsening of the event was recorded after the first dosing date, in which case the event was counted as a TEAE. TEAEs include both SAEs and non-SAEs. (NCT01016483)
Timeframe: From the first dose of study drug administration until EOT (6 years)

Safety Run-In Part: Oral Volume of Distribution (V/f) of Pimasertib (MSC1936369B): Regimen 1

Intervention	subjects (Number)
	TEAEs	Serious TEAEs	Permanent treatment discontinuation of pimasertib	Permanent treatment discontinuation of gemcitabine
Safety Run-in Part: Regimen 1	27	18	12	14
Safety Run-in Part: Regimen 2	26	20	16	15

Volume of distribution was defined as the theoretical volume in which the total amount of drug would need to be uniformly distributed to produce the desired plasma concentration of a drug. (NCT01016483)
Timeframe: 0 hour (pre-dose), 0.5, 1, 1.5, 2, 2.5, 4, 8, 12, 24 (post-dose) on Day 1, 22 of Cycle 1

Safety Run-In Part: Oral Volume of Distribution (V/f) of Pimasertib (MSC1936369B): Regimen 2

Intervention	liter (Geometric Mean)
	V/f: MSC1936369B on Day 1 (n=4,3,3,2,3,11)	V/f: MSC1936369B on Day 22 (n=2,2,3,2,3,8)
Regimen 1: 120 mg	367.25	414.38
Regimen 1: 15 mg	528.62	824.33
Regimen 1: 30 mg	369.12	366.30
Regimen 1: 45 mg	329.80	264.31
Regimen 1: 68 mg	524.96	441.40
Regimen 1: 90 mg	362.29	284.42

Safety Run-In Part: Time to Reach Apparent Terminal Half-Life (t1/2) of Pimasertib (MSC1936369B), Gemcitabine (dFdC), and Gemcitabine Inactive Metabolite 2',2'-Difluorodeoxyuridine (dFdU): Regimen 1

Intervention	liter (Geometric Mean)
	V/f: MSC1936369B on Day 1 (n= 10,11)	V/f: MSC1936369B on Day 22 (n=8,5)
Regimen 2: 60 mg	335.56	389.56
Regimen 2: 75 mg	213.24	319.02

Plasma decay half-life was the time measured for the plasma concentration to decrease by one half. (NCT01016483)
Timeframe: 0 hour (pre-dose), 0.5, 1, 1.5, 2, 2.5, 4, 8, 12, 24 (post-dose) on Day 1, 22 of Cycle 1

Safety Run-In Part: Time to Reach Apparent Terminal Half-Life (t1/2) of Pimasertib (MSC1936369B), Gemcitabine (dFdC), and Gemcitabine Inactive Metabolite 2',2'-Difluorodeoxyuridine (dFdU): Regimen 2

Intervention	hours (Median)
	t1/2: MSC1936369B on Day 1 (n=4,3,3,2,3,11)	t1/2: MSC1936369B on Day 22 (n=2,2,3,2,3,8)	t1/2: Gemcitabine (dFdC) on Day 1 (n=4,3,3,3,3,11)	t1/2: Gemcitabine (dFdC) on Day 22 (n=2,2,1,2,2,9)	t1/2: Metabolite (dFdU) on Day 1 (n=4,3,3,3,3,11)	t1/2: Metabolite (dFdU) on Day 22(n=2,2,2,2,2,10)
Regimen 1: 120 mg	4.580	4.825	6.242	4.680	10.93	12.17
Regimen 1: 15 mg	4.008	8.660	4.274	7.449	8.956	7.731
Regimen 1: 30 mg	3.807	6.100	2.461	4.553	10.49	8.925
Regimen 1: 45 mg	3.833	3.254	2.421	0.9152	9.836	8.843
Regimen 1: 68 mg	4.232	5.744	5.327	4.493	11.52	11.14
Regimen 1: 90 mg	5.036	3.162	8.940	8.213	8.349	10.21

Plasma decay half-life is the time measured for the plasma concentration to decrease by one half. (NCT01016483)
Timeframe: 0 hour (pre-dose), 0.5, 1, 1.5, 2, 2.5, 4, 8, 12, 24 (post-dose) on Day 1, 22 of Cycle 1

Safety Run-In Part: Time to Reach Maximum Concentration (Tmax) of Pimasertib (MSC1936369B), Gemcitabine (dFdC), and Gemcitabine Inactive Metabolite 2',2'-Difluorodeoxyuridine (dFdU): Regimen 1

Intervention	hours (Median)
	t1/2: MSC1936369B on Day 1 (n=10,11)	t1/2: MSC1936369B on Day 22 (n=8,5)	t1/2: Gemcitabine (dFdC) on Day 1 (n=11,14)	t1/2: Gemcitabine (dFdC) on Day 22 (n=9,4)	t1/2: Metabolite (dFdU) on Day 1 (n=11,13)	t1/2: Metabolite (dFdU) on Day 22 (n=10,5)
Regimen 2: 60 mg	2.757	3.425	5.258	5.522	9.471	10.68
Regimen 2: 75 mg	2.603	3.188	5.376	5.249	10.26	13.58

(NCT01016483)
Timeframe: 0 hour (pre-dose), 0.5, 1, 1.5, 2, 2.5, 4, 8, 12, 24 (post-dose) on Day 1, 22 of Cycle 1

Safety Run-In Part: Time to Reach Maximum Concentration (Tmax) of Pimasertib (MSC1936369B), Gemcitabine (dFdC), and Gemcitabine Inactive Metabolite 2',2'-Difluorodeoxyuridine (dFdU): Regimen 2

Intervention	hours (Median)
	Tmax: MSC1936369B on Day 1 (n= 4,3,3,3,3,11)	Tmax: MSC1936369B on Day 22 (n= 3,3,3 2,3,10)	Tmax: Gemcitabine (dFdC) on Day 1 (n=4,3,3,3,3,11)	Tmax: Gemcitabine (dFdC) on Day 22 (n=2,3,3,2,3,9)	Tmax: Metabolite (dFdU) on Day 1 (n=4,3,3,3,3,11)	Tmax: Metabolite (dFdU) on Day 22 (n=2,3,3,2,3,10
Regimen 1: 120 mg	1.500	2.000	0.27	0.50	0.50	0.75
Regimen 1: 15 mg	1.250	2.017	0.38	0.42	0.64	0.54
Regimen 1: 30 mg	1.000	1.000	0.50	0.50	0.50	0.75
Regimen 1: 45 mg	1.533	1.000	0.25	0.53	0.50	1.00
Regimen 1: 68 mg	2.000	1.750	0.25	1.04	0.75	0.67
Regimen 1: 90 mg	1.083	1.500	0.25	0.25	0.50	0.75

(NCT01016483)
Timeframe: 0 hour (pre-dose), 0.5, 1, 1.5, 2, 2.5, 4, 8, 12, 24 (post-dose) on Day 1, 22 of Cycle 1

Safety Run-In Part: Total Clearance (CL) of Gemcitabine: Regimen 1

Intervention	hours (Median)
	Tmax: MSC1936369B on Day 1 (n=12,13)	Tmax: MSC1936369B on Day 22 (n=10,9)	Tmax: Gemcitabine (dFdC) on Day 1 (n=11,14)	Tmax: Gemcitabine (dFdC) on Day 22 (n=9,4)	Tmax: Metabolite (dFdU) on Day 1 (n=11,13)	Tmax: Metabolite (dFdU) on Day 22 (n=10,5)
Regimen 2: 60 mg	2.000	1.500	0.50	0.25	0.67	0.50
Regimen 2: 75 mg	1.583	2.000	0.38	0.25	0.67	0.50

Clearance of a drug was a measure of the rate at which a drug is metabolized or eliminated by normal biological processes. (NCT01016483)
Timeframe: 0 hour (pre-dose), 0.5, 1, 1.5, 2, 2.5, 4, 8, 12, 24 (post-dose) on Day 1, 22 of Cycle 1

Safety Run-In Part: Total Clearance (CL) of Gemcitabine: Regimen 2

Intervention	liter/hour (Geometric Mean)
	CL: Gemcitabine on Day 1 (n=4,3,3,3,3,11)	CL: Gemcitabine on Day 22 (n=2,2,1,2,2,9)
Regimen 1: 120 mg	151.93	164.6
Regimen 1: 15 mg	60.537	163.37
Regimen 1: 30 mg	133.88	156.93
Regimen 1: 45 mg	190.52	190.69
Regimen 1: 68 mg	95.96	25.123
Regimen 1: 90 mg	210.25	183.97

Duration of Response

Intervention	liter/hour (Geometric Mean)
	CL: Gemcitabine on Day 1 (n=11, 14)	CL: Gemcitabine on Day 22 (n=9, 4)
Regimen 2: 60 mg	145.65	164.68
Regimen 2: 75 mg	221.46	183.85

Duration of Response was defined as the time from date of first response (Complete Response (CR) or Partial Response (PR)) to the date when Progressive Disease (PD) was first documented or to the date of death, whichever occurred first according to Response Evaluation Criteria in Solid Tumors (RECIST). Subjects still having CR or PR and alive at the time of analysis were censored at their last date of tumor evaluation. CR was defined as disappearance of tumor lesions, PR as a decrease of at least 30% and PD as an increase of at least 20% in the sum of tumor lesions sizes. (NCT00865709)
Timeframe: From randomization of the first subject until 23 months later, assessed every 8 weeks

Overall Response

Intervention	months (Number)
Sorafenib (Nexavar, BAY43-9006) + mFOLFOX6	7.5
Matching Placebo + mFOLFOX6	6.7

Overall response of a subject was defined as the best tumor response (Complete Response (CR) or Partial Response (PR)) observed during trial period assessed according to the Response Evaluation Criteria in Solid Tumors (RECIST) criteria. CR was defined as disappearance of tumor lesions, PR was defined as a decrease of at least 30% in the sum of tumor lesion sizes. (NCT00865709)
Timeframe: From randomization of the first subject until 23 months later, assessed every 8 weeks.

Overall Survival (OS)

Intervention	participants (Number)
Sorafenib (Nexavar, BAY43-9006) + mFOLFOX6	45
Matching Placebo + mFOLFOX6	61

Overall Survival (OS) was defined as the time from date of randomization to death due to any cause. Subjects still alive at the time of analysis were censored at their last date of last contact. (NCT00865709)
Timeframe: From randomization of the first subject until 33 months later.

Progression-Free Survival (PFS)

Intervention	days (Median)
Sorafenib (Nexavar, BAY43-9006) + mFOLFOX6	535
Matching Placebo + mFOLFOX6	552

Progression-free Survival (PFS) was defined as the time from date of randomization to disease progression or death due to any cause, whichever occurred first. Subjects without progression or death at the time of analysis were censored at their last date of tumor evaluation. Disease progression was defined as an increase of at least 20% in the sum of tumor lesions sizes. (NCT00865709)
Timeframe: From randomization of the first subject until 23 months later, assessed every 8 weeks.

Time to Progression (TTP)

Intervention	Months (Median)
Sorafenib (Nexavar, BAY43-9006) + mFOLFOX6	9.1
Matching Placebo + mFOLFOX6	8.7

Time to progression (TTP) was defined as the time from date of randomization to disease progression. Subjects without progression at the time of analysis were censored at their last date of tumor evaluation. Disease progression was defined as an increase of at least 20% in the sum of tumor lesions sizes. (NCT00865709)
Timeframe: From randomization of the first subject until 23 months later, assessed every 8 weeks.

Number of Participants With Adverse Events

Percentage of Tumors With High Phosphorylated Extracellular Signal-regulated Kinase Expression

Duration of Response

Intervention	Months (Median)
Sorafenib (Nexavar, BAY43-9006) + mFOLFOX6	9.2
Matching Placebo + mFOLFOX6	9.0

Intervention	Participants (Count of Participants)
Sorafenib	35

Intervention	% of tumors with high pERK expression (Number)
Sorafenib	65

Duration of response (PR or better) is defined as the time from the first documented objective response of PR or CR, whichever is noted earlier, to disease progression or death (if death occurs before progression is documented). (NCT00300885)
Timeframe: Tumor measurements and assessments based on RECIST criteria were performed every 6 weeks for the first 18 weeks of therapy ( week 6, 12, and 18) and every 12 weeks thereafter up to data cutoff (1Oct2007) used for planned formal interim analysis

Overall Survival (OS) in Patients Treated With Carboplatin, Paclitaxel and Sorafenib to OS in Patients Treated With Carboplatin, Paclitaxel and Placebo

Intervention	days (Median)
Sorafenib + C/P	168
Placebo + C/P	134

Overall survival determined as the time (days) from the date of randomization at start of study to the date of death, due to any cause. Outcome measure was assessed regularly, i.e. every 3 weeks during study treatment and every 3 months during post-treatment. (NCT00300885)
Timeframe: Outcome measure was assessed every 3 weeks starting from randomization, during treatment period and every 3 months during follow-up period until death was recorded or up to data cutoff (1Oct2007) used for planned formal interim analysis

Progression Free Survival (PFS)

Intervention	days (Median)
Sorafenib + C/P	324
Placebo + C/P	322

PFS determined as time (days) from the date of randomization at start of study to disease progression (radiological or clinical) or death due to any cause, if death occurs before progression. (NCT00300885)
Timeframe: Tumor measurements and assessments based on RECIST criteria were performed every 6 weeks for the first 18 weeks of therapy ( week 6, 12, and 18) and every 12 weeks thereafter up to data cutoff (1Oct2007) used for planned formal interim analysis

Overall Best Response

Intervention	days (Median)
Sorafenib + C/P	139
Placebo + C/P	163

Best overall tumor response for the ITT population was determined according to Response Evaluation Criteria in Solid Tumors (RECIST). Categories: complete response (CR, tumor disappears), partial response (PR, sum of lesion sizes decreased), stable disease (SD, steady state of disease), progressive disease (PD, sum of lesion sizes increased). (NCT00300885)
Timeframe: Tumor measurements and assessments based on RECIST criteria were performed every 6 weeks for the first 18 weeks of therapy ( week 6, 12, and 18) and every 12 weeks thereafter up to data cutoff (1Oct2007) used for planned formal interim analysis

Patient Reported Outcome as Assessed by FACT-L Score. Change From Baseline in Total FACT-L at Cycles 3,5,7,9 and End of Treatment (EOT)

Intervention	percentage of participants (Number)
	Complete Response (CR)	Partial Response (PR)	Stable Disease (SD)	Progressive Disease (PD)	Not evaluated	Disease control
Placebo + C/P	1.1	22.9	47.8	17.5	10.6	56.3
Sorafenib + C/P	0.0	27.4	45.9	9.9	16.8	49.8

"Functional Assessment of Cancer Therapy - Lung cancer subscore (FACT-L). Patient reported outcome as assessed by FACT-L score. FACT-L questionnaire comprises statements about physical, social / family, emotional and functional well-being as well as additional concerns which have to be rated by the patients (0=not at all to 4=very much). Cycle duration defined as 21 days. Change from baseline in Total FACT-L on day 1 of cycles 3,5,7,9 (weeks 7,13,19 and 25) and end of treatment (EOT); cycle 1, day 1 used as baseline. EOT is determined by patient's last visit after treatment discontinuation." (NCT00300885)
Timeframe: Outcome measure was assessed on Day 1 of Cycle 1 and Day 1 of every other cycle (i.e. Cycle 3, 5, 7 etc.) during treatment and at end of treatment visit or up to data cutoff (10ct2007) used for planned formal interim analysis

Patient Reported Outcome as Assessed by LCS Subscale Score. Change From Baseline in LCS Subscale at Cycles 2 Through 9 and at End of Treatment (EOT)

Intervention	Scores on a scale (Mean)
	Cycle 3, Day 1	Cycle 5, Day 1	Cycle 7, Day 1	Cycle 9, Day 1	End of treatment (EOT)
Placebo + C/P	0.1	-1.3	-0.5	-0.6	-2.7
Sorafenib + C/P	0.0	-1.4	-0.8	-1.2	-3.1

Lung Cancer Symptoms (LCS) subscale ranges from 0 (severe debilitation) to 28 (asymptomatic). Cycle duration defined as 21 days. Change from baseline in LCS Subscale on day 1 of cycles 2 through 9 (weeks 4,7,10,13,16,19,22 and 25) and end of treatment (EOT); cycle 1, day 1 used as baseline. EOT is determined by patient's last visit after treatment discontinuation. (NCT00300885)
Timeframe: Outcome measure was assessed on Day 1 of Cycle 1 and Day 1 of every cycle (i.e. Cycle 2, 3, 4, 5 etc.) during treatment and at end of treatment visit or up to data cutoff (10ct2007) used for planned formal interim analysis

Overall Survival (OS)

Intervention	Scores on a scale (Mean)
	Cycle 2, Day 1	Cycle 3, Day 1	Cycle 4, Day 1	Cycle 5, Day 1	Cycle 6, Day 1	Cycle 7, Day 1	Cycle 8, Day 1	Cycle 9, Day 1	End of treatment (EOT)
Placebo + C/P	-0.1	-0.2	-0.3	-0.5	-0.4	-0.4	-0.2	-0.3	-0.4
Sorafenib + C/P	0.0	-0.4	-0.6	-0.6	-0.8	-0.8	-1.2	-0.9	-0.9

Overall survival was defined as the time from registration to death from any cause. (NCT00253370)
Timeframe: Assessed every 3 months if patient is < 2 years from study entry; then every 6 months if patient is 2-3 years from study entry.

Progression-free Survival (PFS)

Intervention	Months (Median)
BAY 43-9006, Docetaxel, Cisplatin	13.6

"Progression-free survival was defined as the shorter of:~The time from registration to progression. or~The time from registration to death without documentation of progression given that the death occurs within 4 months of the last disease assessment without progression (or registration, whichever is more recent).~Therefore, cases not meeting either of the criteria for a PFS event are censored at the date of last disease assessment without progression (or registration, whichever is more recent).~Progression is defined as at least 20% increase in the sum of the longest diameters of target lesions, taking as reference the smallest sum longest diameter recorded since the baseline measurements, or the appearance of one or more new lesion(s) or unequivocal progression of existing non-target lesions." (NCT00253370)
Timeframe: Assessed every 6 weeks until disease progression or up to 3 years

The Proportion of Patients With Objective Response (Complete Response or Partial Response)

Intervention	Months (Median)
BAY 43-9006, Docetaxel, Cisplatin	5.8

Response was evaluated using RECIST (Response Evaluation Criteria in Solid Tumors) 1.0 criteria. Per RECIST criteria, complete response (CR) = disappearance of all target and non-target lesions. Partial response (PR)= >=30% decrease in the sum of the longest diameters of target lesions from baseline, and persistence of one or more non-target lesion(s) and/or the maintenance of tumor marker level above the normal limits. Objective response = CR + PR. (NCT00253370)
Timeframe: Assessed every 6 weeks until disease progression or up to 3 years

Article	Year
Angiogenesis Inhibitors in NSCLC. International journal of molecular sciences, 2017, Sep-21, Volume: 18, Issue:10 Topics: Adenocarcinoma; Angiogenesis Inhibitors; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized;	2017
Neoadjuvant Therapy in Differentiated Thyroid Cancer. International journal of surgical oncology, 2016, Volume: 2016 Topics: Adenocarcinoma; Antibiotics, Antineoplastic; Antineoplastic Agents; Clinical Trials as Topic; Doxoru	2016
Hepatoid adenocarcinoma - review of the literature illustrated by a rare case originating in the peritoneal cavity. Onkologie, 2010, Volume: 33, Issue:5 Topics: Adenocarcinoma; Antineoplastic Agents; Benzenesulfonates; Biomarkers, Tumor; Biopsy; Diagnosis, Diff	2010
Novel multitargeted anticancer oral therapies: sunitinib and sorafenib as a paradigm. The Israel Medical Association journal : IMAJ, 2010, Volume: 12, Issue:10 Topics: Adenocarcinoma; Antineoplastic Agents; Benzenesulfonates; Humans; Indoles; Niacinamide; Phenylurea C	2010
Targeting angiogenesis in esophagogastric adenocarcinoma. The oncologist, 2011, Volume: 16, Issue:6 Topics: Adenocarcinoma; Angiogenesis Inhibitors; Animals; Antibodies, Monoclonal; Antibodies, Monoclonal, Hu	2011
[Promising new treatment options for metastatic androgen-independent prostate cancer]. Actas urologicas espanolas, 2007, Volume: 31, Issue:6 Topics: Adenocarcinoma; Animals; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Antineoplastic A	2007
A therapeutic benefit from combining normobaric carbogen or oxygen with nicotinamide in fractionated X-ray treatments. Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology, 1991, Volume: 22, Issue:2 Topics: Adenocarcinoma; Animals; Carbon; Disease Models, Animal; Dose-Response Relationship, Radiation; In V	1991

Article	Year
Phase I/II trial of pimasertib plus gemcitabine in patients with metastatic pancreatic cancer. International journal of cancer, 2018, 10-15, Volume: 143, Issue:8 Topics: Adenocarcinoma; Adult; Aged; Aged, 80 and over; Antineoplastic Combined Chemotherapy Protocols; Deox	2018
Sorafenib in combination with oxaliplatin, leucovorin, and fluorouracil (modified FOLFOX6) as first-line treatment of metastatic colorectal cancer: the RESPECT trial. Clinical cancer research : an official journal of the American Association for Cancer Research, 2013, May-01, Volume: 19, Issue:9 Topics: Adenocarcinoma; Adult; Aged; Aged, 80 and over; Antineoplastic Combined Chemotherapy Protocols; Colo	2013
A phase II study of gemcitabine and cisplatin plus sorafenib in patients with advanced biliary adenocarcinomas. British journal of cancer, 2013, Aug-20, Volume: 109, Issue:4 Topics: Adenocarcinoma; Adult; Aged; Aged, 80 and over; Antineoplastic Combined Chemotherapy Protocols; Bile	2013
Multicenter phase II study of oxaliplatin and sorafenib in advanced gastric adenocarcinoma after failure of cisplatin and fluoropyrimidine treatment. A GEMCAD study. Investigational new drugs, 2013, Volume: 31, Issue:6 Topics: Adenocarcinoma; Adult; Aged; Antineoplastic Combined Chemotherapy Protocols; Capecitabine; Cisplatin	2013
Sorafenib does not improve efficacy of chemotherapy in advanced pancreatic cancer: A GISCAD randomized phase II study. Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver, 2014, Volume: 46, Issue:2 Topics: Adenocarcinoma; Aged; Aged, 80 and over; Antineoplastic Combined Chemotherapy Protocols; Cisplatin;	2014
A phase I, dose-finding study of sorafenib in combination with gemcitabine and radiation therapy in patients with unresectable pancreatic adenocarcinoma: a Grupo Español Multidisciplinario en Cáncer Digestivo (GEMCAD) study. PloS one, 2014, Volume: 9, Issue:1 Topics: Adenocarcinoma; Adult; Aged; Antineoplastic Combined Chemotherapy Protocols; Combined Modality Thera	2014
A multicenter phase II study of sorafenib monotherapy in clinically selected patients with advanced lung adenocarcinoma after failure of EGFR-TKI therapy (Chinese Thoracic Oncology Group, CTONG 0805). Lung cancer (Amsterdam, Netherlands), 2014, Volume: 83, Issue:3 Topics: Adenocarcinoma; Adult; Aged; Aged, 80 and over; Antineoplastic Agents; Apoptosis Regulatory Proteins	2014
Phase 1 pharmacogenetic and pharmacodynamic study of sorafenib with concurrent radiation therapy and gemcitabine in locally advanced unresectable pancreatic cancer. International journal of radiation oncology, biology, physics, 2014, Jun-01, Volume: 89, Issue:2 Topics: Adenocarcinoma; Adult; Aged; Aged, 80 and over; Antineoplastic Agents; Antineoplastic Combined Chemo	2014
A phase II study of sorafenib, oxaliplatin, and 2 days of high-dose capecitabine in advanced pancreas cancer. Cancer chemotherapy and pharmacology, 2015, Volume: 76, Issue:2 Topics: Adenocarcinoma; Aged; Aged, 80 and over; Antineoplastic Combined Chemotherapy Protocols; Capecitabin	2015
Phase II Trial of Sorafenib in Patients with Chemotherapy Refractory Metastatic Esophageal and Gastroesophageal (GE) Junction Cancer. PloS one, 2015, Volume: 10, Issue:8 Topics: Adenocarcinoma; Adult; Aged; Antineoplastic Agents; Disease-Free Survival; Drug Resistance, Neoplasm	2015
Phase I study of pre-operative continuous 5-FU and sorafenib with external radiation therapy in locally advanced rectal adenocarcinoma. Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology, 2016, Volume: 118, Issue:2 Topics: Adenocarcinoma; Adult; Aged; Antineoplastic Combined Chemotherapy Protocols; Chemoradiotherapy; Dose	2016
A phase II study of sorafenib in recurrent and/or metastatic salivary gland carcinomas: Translational analyses and clinical impact. European journal of cancer (Oxford, England : 1990), 2016, Volume: 69 Topics: Adenocarcinoma; Adult; Aged; Antineoplastic Agents; Carcinoma, Adenoid Cystic; Carcinoma, Mucoepider	2016
Phase III study of carboplatin and paclitaxel alone or with sorafenib in advanced non-small-cell lung cancer. Journal of clinical oncology : official journal of the American Society of Clinical Oncology, 2010, Apr-10, Volume: 28, Issue:11 Topics: Adenocarcinoma; Adult; Aged; Aged, 80 and over; Antineoplastic Combined Chemotherapy Protocols; Benz	2010
Phase III study of carboplatin and paclitaxel alone or with sorafenib in advanced non-small-cell lung cancer. Journal of clinical oncology : official journal of the American Society of Clinical Oncology, 2010, Apr-10, Volume: 28, Issue:11 Topics: Adenocarcinoma; Adult; Aged; Aged, 80 and over; Antineoplastic Combined Chemotherapy Protocols; Benz	2010
Phase III study of carboplatin and paclitaxel alone or with sorafenib in advanced non-small-cell lung cancer. Journal of clinical oncology : official journal of the American Society of Clinical Oncology, 2010, Apr-10, Volume: 28, Issue:11 Topics: Adenocarcinoma; Adult; Aged; Aged, 80 and over; Antineoplastic Combined Chemotherapy Protocols; Benz	2010
Phase III study of carboplatin and paclitaxel alone or with sorafenib in advanced non-small-cell lung cancer. Journal of clinical oncology : official journal of the American Society of Clinical Oncology, 2010, Apr-10, Volume: 28, Issue:11 Topics: Adenocarcinoma; Adult; Aged; Aged, 80 and over; Antineoplastic Combined Chemotherapy Protocols; Benz	2010
Phase II study of sorafenib in combination with docetaxel and cisplatin in the treatment of metastatic or advanced gastric and gastroesophageal junction adenocarcinoma: ECOG 5203. Journal of clinical oncology : official journal of the American Society of Clinical Oncology, 2010, Jun-20, Volume: 28, Issue:18 Topics: Adenocarcinoma; Adult; Aged; Antineoplastic Combined Chemotherapy Protocols; Benzenesulfonates; Cisp	2010
Phase II study of sorafenib in combination with docetaxel and cisplatin in the treatment of metastatic or advanced gastric and gastroesophageal junction adenocarcinoma: ECOG 5203. Journal of clinical oncology : official journal of the American Society of Clinical Oncology, 2010, Jun-20, Volume: 28, Issue:18 Topics: Adenocarcinoma; Adult; Aged; Antineoplastic Combined Chemotherapy Protocols; Benzenesulfonates; Cisp	2010
Phase II study of sorafenib in combination with docetaxel and cisplatin in the treatment of metastatic or advanced gastric and gastroesophageal junction adenocarcinoma: ECOG 5203. Journal of clinical oncology : official journal of the American Society of Clinical Oncology, 2010, Jun-20, Volume: 28, Issue:18 Topics: Adenocarcinoma; Adult; Aged; Antineoplastic Combined Chemotherapy Protocols; Benzenesulfonates; Cisp	2010
Phase II study of sorafenib in combination with docetaxel and cisplatin in the treatment of metastatic or advanced gastric and gastroesophageal junction adenocarcinoma: ECOG 5203. Journal of clinical oncology : official journal of the American Society of Clinical Oncology, 2010, Jun-20, Volume: 28, Issue:18 Topics: Adenocarcinoma; Adult; Aged; Antineoplastic Combined Chemotherapy Protocols; Benzenesulfonates; Cisp	2010
Gemcitabine plus sorafenib in patients with advanced pancreatic cancer: a phase II trial of the University of Chicago Phase II Consortium. Investigational new drugs, 2012, Volume: 30, Issue:1 Topics: Adenocarcinoma; Aged; Aged, 80 and over; Antineoplastic Combined Chemotherapy Protocols; Benzenesulf	2012
Sorafenib in combination with erlotinib or with gemcitabine in elderly patients with advanced non-small-cell lung cancer: a randomized phase II study. Annals of oncology : official journal of the European Society for Medical Oncology, 2011, Volume: 22, Issue:7 Topics: Adenocarcinoma; Adenocarcinoma, Bronchiolo-Alveolar; Aged; Aged, 80 and over; Antineoplastic Combine	2011
Assessment of objective responses using volumetric evaluation in advanced thymic malignancies and metastatic non-small cell lung cancer. Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer, 2011, Volume: 6, Issue:7 Topics: Adenocarcinoma; Adolescent; Adult; Aged; Antineoplastic Agents; Benzenesulfonates; Carcinoma, Large	2011
Long-term safety and tolerability of sorafenib in patients with advanced non-small-cell lung cancer: a case-based review. Clinical lung cancer, 2011, Volume: 12, Issue:4 Topics: Adenocarcinoma; Adenocarcinoma, Bronchiolo-Alveolar; Adult; Aged; Antineoplastic Agents; Benzenesulf	2011
International, randomized, placebo-controlled, double-blind phase III study of motesanib plus carboplatin/paclitaxel in patients with advanced nonsquamous non-small-cell lung cancer: MONET1. Journal of clinical oncology : official journal of the American Society of Clinical Oncology, 2012, Aug-10, Volume: 30, Issue:23 Topics: Adenocarcinoma; Adult; Aged; Aged, 80 and over; Antineoplastic Combined Chemotherapy Protocols; Carb	2012
A double-blind randomized discontinuation phase-II study of sorafenib (BAY 43-9006) in previously treated non-small-cell lung cancer patients: eastern cooperative oncology group study E2501. Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer, 2012, Volume: 7, Issue:10 Topics: Adenocarcinoma; Adenocarcinoma, Bronchiolo-Alveolar; Adult; Aged; Aged, 80 and over; Antineoplastic	2012
Clinical outcomes and biomarker profiles of elderly pretreated NSCLC patients from the BATTLE trial. Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer, 2012, Volume: 7, Issue:11 Topics: Adenocarcinoma; Adult; Aged; Aged, 80 and over; Antineoplastic Combined Chemotherapy Protocols; Bexa	2012
Phase I study of dovitinib (TKI258), an oral FGFR, VEGFR, and PDGFR inhibitor, in advanced or metastatic renal cell carcinoma. Clinical cancer research : an official journal of the American Association for Cancer Research, 2013, Mar-01, Volume: 19, Issue:5 Topics: Adenocarcinoma; Adult; Aged; Animals; Antineoplastic Combined Chemotherapy Protocols; Benzimidazoles	2013
Evaluation of 6-aminonicotinamide (NSC-21206) in the treatment of metastatic hypernephroma. Cancer chemotherapy reports, 1970, Volume: 54, Issue:3 Topics: Adenocarcinoma; Adult; Aged; Clinical Trials as Topic; Evaluation Studies as Topic; Female; Follow-U	1970

Article	Year
Incidental Finding of Colon Carcinoma Related to High Uptake in 18F-PSMA-1007 PET. Clinical nuclear medicine, 2020, Volume: 45, Issue:7 Topics: Adenocarcinoma; Aged; Biological Transport; Colonic Neoplasms; Humans; Incidental Findings; Male; Ni	2020
Duodenal Adenocarcinoma Mimicking Metastasis of Prostate Cancer on 18F-Prostate-Specific Membrane Antigen-1007 PET/CT. Clinical nuclear medicine, 2021, Volume: 46, Issue:1 Topics: Adenocarcinoma; Aged; Diagnosis, Differential; Duodenal Neoplasms; Humans; Male; Neoplasm Grading; N	2021
Physiologically based pharmacokinetic models for everolimus and sorafenib in mice. Cancer chemotherapy and pharmacology, 2013, Volume: 71, Issue:5 Topics: Adenocarcinoma; Administration, Oral; Animals; Antineoplastic Agents; Antineoplastic Combined Chemot	2013
Novel agents and future prospects in the treatment of pancreatic adenocarcinoma. JOP : Journal of the pancreas, 2013, Jul-10, Volume: 14, Issue:4 Topics: Adenocarcinoma; Anilides; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Antineoplastic	2013
Pancreatic cancer: Sorafenib: no effect on efficacy of chemotherapy in pancreatic cancer. Nature reviews. Gastroenterology & hepatology, 2014, Volume: 11, Issue:1 Topics: Adenocarcinoma; Antineoplastic Agents; Cisplatin; Deoxycytidine; Drug Therapy, Combination; Gemcitab	2014
Characterization of the biological activity of a potent small molecule Hec1 inhibitor TAI-1. Journal of experimental & clinical cancer research : CR, 2014, Jan-09, Volume: 33 Topics: Adenocarcinoma; Administration, Intravenous; Administration, Oral; Animals; Antineoplastic Agents; A	2014
Tyrosine kinase inhibitor treatments in patients with metastatic thyroid carcinomas: a retrospective study of the TUTHYREF network. European journal of endocrinology, 2014, Volume: 170, Issue:4 Topics: Adenocarcinoma; Adenocarcinoma, Follicular; Adenoma, Oxyphilic; Adult; Aged; Antineoplastic Agents;	2014
Oncogenic and sorafenib-sensitive ARAF mutations in lung adenocarcinoma. The Journal of clinical investigation, 2014, Volume: 124, Issue:4 Topics: Adenocarcinoma; Adenocarcinoma of Lung; Aged; Amino Acid Substitution; Antineoplastic Agents; Cell T	2014
Novel combination therapy with imiquimod and sorafenib for renal cell carcinoma. International journal of urology : official journal of the Japanese Urological Association, 2014, Volume: 21, Issue:7 Topics: Adenocarcinoma; Aminoquinolines; Animals; Antineoplastic Agents; Carcinoma, Renal Cell; CD8-Positive	2014
Radiation recall reaction causing cardiotoxicity. Journal of cardiovascular magnetic resonance : official journal of the Society for Cardiovascular Magnetic Resonance, 2014, Apr-22, Volume: 16 Topics: Adenocarcinoma; Adenocarcinoma of Lung; Antineoplastic Agents; Chemoradiotherapy; Coronary Angiograp	2014
Therapeutic effects of sorafenib on the A549/DDP human lung adenocarcinoma cell line in vitro. Molecular medicine reports, 2014, Volume: 10, Issue:1 Topics: Adenocarcinoma; Adenocarcinoma of Lung; Antineoplastic Agents; Apoptosis; Cell Line, Tumor; Cell Mov	2014
Thyroid carcinoma, version 2.2014. Journal of the National Comprehensive Cancer Network : JNCCN, 2014, Volume: 12, Issue:12 Topics: Adenocarcinoma; Anilides; Carcinoma, Neuroendocrine; Guidelines as Topic; Humans; Neoplasm Metastasi	2014
Sorafenib reverses resistance of gastric cancer to treatment by cisplatin through down-regulating MDR1 expression. Medical oncology (Northwood, London, England), 2015, Volume: 32, Issue:2 Topics: Adenocarcinoma; Animals; Antineoplastic Agents; Apoptosis; ATP Binding Cassette Transporter, Subfami	2015
A novel approach using sorafenib in alpha fetoprotein-producing hepatoid adenocarcinoma of the lung. Journal of the National Comprehensive Cancer Network : JNCCN, 2015, Volume: 13, Issue:4 Topics: Adenocarcinoma; alpha-Fetoproteins; Antineoplastic Combined Chemotherapy Protocols; Carboplatin; Fat	2015
A significant response to sorafenib in a woman with advanced lung adenocarcinoma and a BRAF non-V600 mutation. Anti-cancer drugs, 2015, Volume: 26, Issue:9 Topics: Adenocarcinoma; Antineoplastic Agents; Female; Humans; Lung Neoplasms; Middle Aged; Mutation; Niacin	2015
EGF Induced RET Inhibitor Resistance in CCDC6-RET Lung Cancer Cells. Yonsei medical journal, 2017, Volume: 58, Issue:1 Topics: Adenocarcinoma; Cell Line, Tumor; Cetuximab; Drug Resistance, Neoplasm; Epidermal Growth Factor; Erb	2017
Sorafenib triggers antiproliferative and pro-apoptotic signals in human esophageal adenocarcinoma cells. Digestive diseases and sciences, 2008, Volume: 53, Issue:12 Topics: Adenocarcinoma; Antineoplastic Agents; Apoptosis; Benzenesulfonates; Cell Line, Tumor; Cell Prolifer	2008
Sorafenib inhibits MAPK-mediated proliferation in a Barrett's esophageal adenocarcinoma cell line. Diseases of the esophagus : official journal of the International Society for Diseases of the Esophagus, 2008, Volume: 21, Issue:6 Topics: Adenocarcinoma; Analysis of Variance; Barrett Esophagus; Benzenesulfonates; Blotting, Western; Cell	2008
[Toxicity of radiation therapy and antiangiogenics combination: a case report]. Cancer radiotherapie : journal de la Societe francaise de radiotherapie oncologique, 2009, Volume: 13, Issue:3 Topics: Adenocarcinoma; Benzenesulfonates; Humans; Kidney Neoplasms; Magnetic Resonance Imaging; Male; Middl	2009
Preclinical development of the nicotinamide phosphoribosyl transferase inhibitor prodrug GMX1777. Anti-cancer drugs, 2009, Volume: 20, Issue:5 Topics: Adenocarcinoma; Animals; Antineoplastic Agents; Carcinoma, Small Cell; Cell Line, Tumor; Colonic Neo	2009
[Sorafenib-induced multiple eruptive keratoacanthomas]. Annales de dermatologie et de venereologie, 2009, Volume: 136, Issue:12 Topics: Adenocarcinoma; Antineoplastic Agents; Benzenesulfonates; Carcinoma, Renal Cell; Humans; Immunosuppr	2009
[Clinical observation of 21 cases of metastatic renal cell carcinoma treated with sorafenib]. Zhonghua zhong liu za zhi [Chinese journal of oncology], 2009, Volume: 31, Issue:9 Topics: Adenocarcinoma; Adult; Aged; Aged, 80 and over; Antineoplastic Agents; Benzenesulfonates; Carcinoma,	2009
The multikinase inhibitor Sorafenib induces apoptosis and sensitises endometrial cancer cells to TRAIL by different mechanisms. European journal of cancer (Oxford, England : 1990), 2010, Volume: 46, Issue:4 Topics: Adenocarcinoma; Antineoplastic Agents; Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Be	2010
Identification of bona fide esophageal adenocarcinoma cell lines. Journal of the National Cancer Institute, 2010, Feb-24, Volume: 102, Issue:4 Topics: Adenocarcinoma; Antineoplastic Agents; Benzenesulfonates; Cell Line, Tumor; Clinical Trials as Topic	2010
Verification and unmasking of widely used human esophageal adenocarcinoma cell lines. Journal of the National Cancer Institute, 2010, Feb-24, Volume: 102, Issue:4 Topics: Adenocarcinoma; Antineoplastic Agents; Benzenesulfonates; Biomedical Research; Carcinoma; Carcinoma,	2010
Sorafenib in patients with advanced non-small cell lung cancer that harbor K-ras mutations: a brief report. Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer, 2010, Volume: 5, Issue:5 Topics: Adenocarcinoma; Adenocarcinoma, Bronchiolo-Alveolar; Adult; Aged; Antineoplastic Agents; Benzenesulf	2010
Combined anticancer effects of sphingosine kinase inhibitors and sorafenib. Investigational new drugs, 2011, Volume: 29, Issue:6 Topics: Adamantane; Adenocarcinoma; Administration, Oral; Animals; Antineoplastic Combined Chemotherapy Prot	2011
Evolution of an adenocarcinoma in response to selection by targeted kinase inhibitors. Genome biology, 2010, Volume: 11, Issue:8 Topics: Adenocarcinoma; Benzenesulfonates; Gene Dosage; Gene Expression Regulation, Neoplastic; Genes, Neopl	2010
Evolution of an adenocarcinoma in response to selection by targeted kinase inhibitors. Genome biology, 2010, Volume: 11, Issue:8 Topics: Adenocarcinoma; Benzenesulfonates; Gene Dosage; Gene Expression Regulation, Neoplastic; Genes, Neopl	2010
Evolution of an adenocarcinoma in response to selection by targeted kinase inhibitors. Genome biology, 2010, Volume: 11, Issue:8 Topics: Adenocarcinoma; Benzenesulfonates; Gene Dosage; Gene Expression Regulation, Neoplastic; Genes, Neopl	2010
Evolution of an adenocarcinoma in response to selection by targeted kinase inhibitors. Genome biology, 2010, Volume: 11, Issue:8 Topics: Adenocarcinoma; Benzenesulfonates; Gene Dosage; Gene Expression Regulation, Neoplastic; Genes, Neopl	2010
Sorafenib's inhibition of prostate cancer growth in transgenic adenocarcinoma mouse prostate mice and its differential effects on endothelial and pericyte growth during tumor angiogenesis. Analytical and quantitative cytology and histology, 2010, Volume: 32, Issue:3 Topics: Adenocarcinoma; Angiogenesis Inhibitors; Animals; Antineoplastic Agents; Benzenesulfonates; Disease	2010
Sorafenib and radiation: a promising combination in colorectal cancer. International journal of radiation oncology, biology, physics, 2010, Sep-01, Volume: 78, Issue:1 Topics: Adenocarcinoma; Animals; Antineoplastic Agents; Benzenesulfonates; Cell Division; Colorectal Neoplas	2010
Antitumour efficacy of MEK inhibitors in human lung cancer cells and their derivatives with acquired resistance to different tyrosine kinase inhibitors. British journal of cancer, 2011, Jul-26, Volume: 105, Issue:3 Topics: Adenocarcinoma; Adenocarcinoma of Lung; Animals; Benzenesulfonates; Cell Line, Tumor; Cell Prolifera	2011
Long-term expansion of epithelial organoids from human colon, adenoma, adenocarcinoma, and Barrett's epithelium. Gastroenterology, 2011, Volume: 141, Issue:5 Topics: Adenocarcinoma; Adenoma; Adult; Aged; Aged, 80 and over; Animals; Barrett Esophagus; Biopsy; Cell Cu	2011
Long-term expansion of epithelial organoids from human colon, adenoma, adenocarcinoma, and Barrett's epithelium. Gastroenterology, 2011, Volume: 141, Issue:5 Topics: Adenocarcinoma; Adenoma; Adult; Aged; Aged, 80 and over; Animals; Barrett Esophagus; Biopsy; Cell Cu	2011
Long-term expansion of epithelial organoids from human colon, adenoma, adenocarcinoma, and Barrett's epithelium. Gastroenterology, 2011, Volume: 141, Issue:5 Topics: Adenocarcinoma; Adenoma; Adult; Aged; Aged, 80 and over; Animals; Barrett Esophagus; Biopsy; Cell Cu	2011
Long-term expansion of epithelial organoids from human colon, adenoma, adenocarcinoma, and Barrett's epithelium. Gastroenterology, 2011, Volume: 141, Issue:5 Topics: Adenocarcinoma; Adenoma; Adult; Aged; Aged, 80 and over; Animals; Barrett Esophagus; Biopsy; Cell Cu	2011
K-Ras mutation-mediated IGF-1-induced feedback ERK activation contributes to the rapalog resistance in pancreatic ductal adenocarcinomas. Cancer letters, 2012, Sep-01, Volume: 322, Issue:1 Topics: Adenocarcinoma; Animals; Antineoplastic Agents; Benzenesulfonates; Carcinoma, Pancreatic Ductal; Cel	2012
Multitargeted tyrosine kinase inhibitors in unselected patients with advanced non-small-cell lung cancer (NSCLC): impressions from MONET (the motesanib NSCLC efficacy and tolerability study). Journal of clinical oncology : official journal of the American Society of Clinical Oncology, 2012, Aug-10, Volume: 30, Issue:23 Topics: Adenocarcinoma; Antineoplastic Combined Chemotherapy Protocols; Carcinoma, Non-Small-Cell Lung; Fema	2012
Targeting FLIP and Mcl-1 using a combination of aspirin and sorafenib sensitizes colon cancer cells to TRAIL. The Journal of pathology, 2013, Volume: 229, Issue:3 Topics: Adaptor Proteins, Signal Transducing; Adenocarcinoma; Adenoma; Antineoplastic Agents; Apoptosis; Asp	2013
Nicotinamide in adenocarcinoma 755 and in the milk of mice carrying the agent of spontaneous mammary tumor. Experientia, 1957, Dec-15, Volume: 13, Issue:12 Topics: Adenocarcinoma; Animals; Breast Neoplasms; Humans; Mammary Neoplasms, Animal; Mice; Milk; Neoplasms,	1957
AUGMENTATION OF 6-AMINONICOTINAMIDE ANTAGONISM OF TUMOR GROWTH BY COMPOUNDS WITH ESTROGENIC ACTIVITY. Cancer research, 1964, Volume: 24 Topics: 6-Aminonicotinamide; Adenocarcinoma; Animals; Antineoplastic Agents; Breast Neoplasms; Cortisone; Di	1964
Selectivity of effects of redox-active cobalt(III) complexes on tumor tissue. Experimental oncology, 2004, Volume: 26, Issue:2 Topics: Adenocarcinoma; Animals; Carcinoma, Lewis Lung; Cobalt; DNA Damage; Ethylenediamines; Female; Hypoxi	2004
Nicotinamide as a radiosensitizer of a C3H mouse mammary adenocarcinoma. Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology, 1984, Volume: 1, Issue:4 Topics: Adenocarcinoma; Animals; Female; Mammary Neoplasms, Experimental; Mice; Mice, Inbred C3H; NAD; Niaci	1984
The modification of blood flow in tumours and their supplying arteries by nicotinamide. Acta oncologica (Stockholm, Sweden), 1995, Volume: 34, Issue:3 Topics: Adenocarcinoma; Animals; Arteries; Dose-Response Relationship, Drug; Male; Muscle Contraction; Muscl	1995
Pharmacokinetics of varying doses of nicotinamide and tumour radiosensitisation with carbogen and nicotinamide: clinical considerations. British journal of cancer, 1993, Volume: 68, Issue:6 Topics: Adenocarcinoma; Animals; Carbon Dioxide; Cell Hypoxia; Cell Survival; Dose-Response Relationship, Dr	1993
Should carbogen and nicotinamide be given throughout the full course of fractionated radiotherapy regimens? International journal of radiation oncology, biology, physics, 1993, Dec-01, Volume: 27, Issue:5 Topics: Adenocarcinoma; Animals; Carbon Dioxide; Male; Mammary Neoplasms, Experimental; Mice; Mice, Inbred C	1993
Comparison of two techniques for detecting tumour hypoxia: a fluorescent immunochemical method and an in vitro colony assay. Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology, 1996, Volume: 39, Issue:2 Topics: Adenocarcinoma; Animals; Carbon Dioxide; Cell Hypoxia; Cell Survival; Cesium Radioisotopes; DNA Dama	1996
Transient perfusion and radiosensitizing effect after nicotinamide, carbogen, and perflubron emulsion administration. Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology, 1996, Volume: 39, Issue:3 Topics: Adenocarcinoma; Animals; Carbon Dioxide; Emulsions; Female; Fluorocarbons; Humans; Hydrocarbons, Bro	1996
Efficacy of agents counteracting hypoxia in fractionated radiation regimes. Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology, 1996, Volume: 41, Issue:2 Topics: Adenocarcinoma; Animals; Carbon Dioxide; Cell Hypoxia; Emulsions; Female; Fluorocarbons; Humans; Hyd	1996
Nicotinamide reduces tumour interstitial fluid pressure in a dose- and time-dependent manner. The British journal of radiology, 1997, Volume: 70 Topics: Adenocarcinoma; Animals; Dose-Response Relationship, Drug; Extracellular Space; Female; Mice; Mice,	1997
Preclinical evaluation of the novel hypoxic marker 99mTc-HL91 (Prognox) in murine and xenograft systems in vivo. International journal of radiation oncology, biology, physics, 1998, Nov-01, Volume: 42, Issue:4 Topics: Adenocarcinoma; Animals; Carbon Dioxide; Carcinoma; Cell Hypoxia; Colonic Neoplasms; Contrast Media;	1998
Modification of renal tumorigenic effect of streptozotocin by nicotinamide: spontaneous reversibility of streptozotocin diabetes. Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N.Y.), 1976, Volume: 151, Issue:2 Topics: Adenocarcinoma; Adenoma; Adenoma, Islet Cell; Animals; Diabetes Mellitus; Dose-Response Relationship	1976
Specific histidine decarboxylases in the gastric mucosa of man and other mammals. Determination, location and properties. Biochemical pharmacology, 1969, Volume: 18, Issue:10 Topics: Adenocarcinoma; Animals; Benzene; Carboxy-Lyases; Cats; Cattle; Chlorpromazine; Chromatography, Gel;	1969
Inhibition of transfer ribonucleic acid methylase activity from several human tumors by nicotinamide and nicotinamide analogs. Biochemistry, 1972, Feb-01, Volume: 11, Issue:3 Topics: Adenocarcinoma; Aldehydes; Amines; Animals; Carbon Isotopes; Carcinoma; Carcinoma 256, Walker; Cell	1972
[Nicotinic acid and experimental tumor growth]. Ukrains'kyi biokhimichnyi zhurnal, 1966, Volume: 38, Issue:4 Topics: Adenocarcinoma; Animals; Antineoplastic Agents; Cachexia; Depression, Chemical; NAD; NADP; Neoplasms	1966

niacinamide and Adenocarcinoma

Research Excerpts

Research

Studies (81)

Authors

Clinical Trials (15)

Trial Overview

Trial Outcomes

Phase II: Overall Survival (OS) Time

Phase II: Percentage of Subjects With Clinical Benefit

Phase II: Progression-Free Survival (PFS) Time

Phase II: Time to Progression (TTP)

Safety Run-In Part: Number of Subjects With Dose Limiting Toxicities (DLTs)

Phase II: Number of Subjects With Treatment-Emergent Adverse Events (TEAEs), Serious TEAEs, and TEAEs Leading to Permanent Treatment Discontinuation

Phase II: Percentage of Subjects With Best Overall Response (BOR)

Safety Run-In Part: Apparent Oral Clearance (CL/f) of Pimasertib (MSC1936369B): Regimen 1

Safety Run-In Part: Apparent Oral Clearance (CL/f) of Pimasertib (MSC1936369B): Regimen 2

Safety Run-In Part: Apparent Volume of Distribution (V) of Gemcitabine: Regimen 1

Safety Run-In Part: Apparent Volume of Distribution (V) of Gemcitabine: Regimen 2

Safety Run-In Part: Area Under Curve (AUC: 0 to Infinity) of Pimasertib (MSC1936369B), Gemcitabine (dFdC), and Gemcitabine Inactive Metabolite 2',2'-Difluorodeoxyuridine (dFdU): Regimen 1

Safety Run-In Part: Area Under Curve (AUC:0 to Infinity) of Pimasertib (MSC1936369B), Gemcitabine (dFdC), and Gemcitabine Inactive Metabolite 2',2'-Difluorodeoxyuridine (dFdU) Regimen 2

Safety Run-In Part: Levels of Pharmacodynamic (Pd) Markers (Phosphorylated- Extracellular Signal-Regulated Kinase (ERK) in Peripheral Blood Mononuclear Cells [PBMCs]): Regimen 1

Safety Run-In Part: Levels of Pharmacodynamic (Pd) Markers (Phosphorylated- Extracellular Signal-Regulated Kinase (ERK) in Peripheral Blood Mononuclear Cells [PBMCs]): Regimen 2

Safety Run-In Part: Maximum Concentration (Cmax) of Pimasertib (MSC1936369B), Gemcitabine (dFdC), and Gemcitabine Inactive Metabolite 2',2'-Difluorodeoxyuridine (dFdU) for Regimen 1

Safety Run-In Part: Maximum Concentration (Cmax) of Pimasertib (MSC1936369B), Gemcitabine (dFdC), Gemcitabine Inactive Metabolite 2',2'-Difluorodeoxyuridine (dFdU): Regimen 2

Safety Run-In Part: Number of Subjects With Treatment-Emergent Adverse Events (TEAEs), Serious TEAEs, and TEAEs Leading to Permanent Treatment Discontinuation

Safety Run-In Part: Oral Volume of Distribution (V/f) of Pimasertib (MSC1936369B): Regimen 1

Safety Run-In Part: Oral Volume of Distribution (V/f) of Pimasertib (MSC1936369B): Regimen 2

Safety Run-In Part: Time to Reach Apparent Terminal Half-Life (t1/2) of Pimasertib (MSC1936369B), Gemcitabine (dFdC), and Gemcitabine Inactive Metabolite 2',2'-Difluorodeoxyuridine (dFdU): Regimen 1

Safety Run-In Part: Time to Reach Apparent Terminal Half-Life (t1/2) of Pimasertib (MSC1936369B), Gemcitabine (dFdC), and Gemcitabine Inactive Metabolite 2',2'-Difluorodeoxyuridine (dFdU): Regimen 2

Safety Run-In Part: Time to Reach Maximum Concentration (Tmax) of Pimasertib (MSC1936369B), Gemcitabine (dFdC), and Gemcitabine Inactive Metabolite 2',2'-Difluorodeoxyuridine (dFdU): Regimen 1

Safety Run-In Part: Time to Reach Maximum Concentration (Tmax) of Pimasertib (MSC1936369B), Gemcitabine (dFdC), and Gemcitabine Inactive Metabolite 2',2'-Difluorodeoxyuridine (dFdU): Regimen 2

Safety Run-In Part: Total Clearance (CL) of Gemcitabine: Regimen 1

Safety Run-In Part: Total Clearance (CL) of Gemcitabine: Regimen 2

Duration of Response

Overall Response

Overall Survival (OS)

Progression-Free Survival (PFS)

Time to Progression (TTP)

Number of Participants With Adverse Events

Percentage of Tumors With High Phosphorylated Extracellular Signal-regulated Kinase Expression

Duration of Response

Overall Survival (OS) in Patients Treated With Carboplatin, Paclitaxel and Sorafenib to OS in Patients Treated With Carboplatin, Paclitaxel and Placebo

Progression Free Survival (PFS)

Overall Best Response

Patient Reported Outcome as Assessed by FACT-L Score. Change From Baseline in Total FACT-L at Cycles 3,5,7,9 and End of Treatment (EOT)

Patient Reported Outcome as Assessed by LCS Subscale Score. Change From Baseline in LCS Subscale at Cycles 2 Through 9 and at End of Treatment (EOT)

Overall Survival (OS)

Progression-free Survival (PFS)

The Proportion of Patients With Objective Response (Complete Response or Partial Response)

Reviews

Trials

Other Studies