Compounds > niacinamide
Page last updated: 2024-10-19

niacinamide and Colorectal Neoplasms

niacinamide has been researched along with Colorectal Neoplasms in 59 studies

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

Colorectal Neoplasms: Tumors or cancer of the COLON or the RECTUM or both. Risk factors for colorectal cancer include chronic ULCERATIVE COLITIS; FAMILIAL POLYPOSIS COLI; exposure to ASBESTOS; and irradiation of the CERVIX UTERI.

Research Excerpts

ExcerptRelevanceReference
"Adult patients with histologically documented, measurable, EGFR-expressing, KRAS-mutated metastatic colorectal cancer (mCRC) that had progressed after 5-fluorouracil-based regimens were treated with sorafenib 400 mg orally twice daily and intravenous cetuximab weekly in 28-day cycles."9.20A Phase II Study of Sorafenib Combined With Cetuximab in EGFR-Expressing, KRAS-Mutated Metastatic Colorectal Cancer. ( Cao, L; Choyke, P; Do, K; Doroshow, JH; Eugeni, M; Figg, WD; Holkova, B; Jacobs, P; Kang, Z; Kummar, S; Larkins, E; Lindenberg, ML; Peer, CJ; Raffeld, M; Steinberg, SM; Turkbey, B; Wright, JJ, 2015)
"This trial evaluated the feasibility and efficacy of combined sorafenib and irinotecan (NEXIRI) as second- or later-line treatment of patients with KRAS-mutated metastatic colorectal cancer (mCRC), who had progressed after irinotecan-based chemotherapy."9.19Sorafenib and irinotecan (NEXIRI) as second- or later-line treatment for patients with metastatic colorectal cancer and KRAS-mutated tumours: a multicentre Phase I/II trial. ( Adenis, A; Assenat, E; Bennouna, J; Bibeau, F; Boissière, F; Bouché, O; Conroy, T; Crapez, E; Desseigne, F; Francois, E; Galais, MP; Laurent-Puig, P; Mazard, T; Poujol, S; Samalin, E; Seitz, JF; Taieb, J; Thézenas, S; Ychou, M, 2014)
"This randomized, double-blind, placebo-controlled, phase IIb study evaluated adding sorafenib to first-line modified FOLFOX6 (mFOLFOX6) for metastatic colorectal cancer (mCRC)."9.17Sorafenib 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)
"To examine whether carbogen and nicotinamide increases 5-fluorouracil (5-FU) delivery to colorectal cancer metastases."9.12Carbogen and nicotinamide increase blood flow and 5-fluorouracil delivery but not 5-fluorouracil retention in colorectal cancer metastases in patients. ( Aboagye, EO; Gupta, N; Hoskin, PJ; Jones, T; Kötz, B; Osman, S; Phillips, R; Price, PM; Saleem, A; Vernon, C; Wasan, H, 2006)
" During the exploration of small molecules that inhibit RAF1 kinase, regorafenib (BAY 73-4506) was discovered as a multikinase inhibitor which demonstrated anti-cancer, anti-angiogenic, and apoptotic activities in metastatic colorectal cancer."8.90The preclinical development of regorafenib for the treatment of colorectal cancer. ( Fujiya, T; Hasegawa, Y; Kakugawa, Y; Kinouchi, M; Miura, K; Philchenkov, A; Satoh, M; Yamamoto, K, 2014)
" In the present study, we investigated the feasibility of combined treatment with dabrafenib and sorafenib, type I and type II BRAF inhibitor respectively, on colorectal cancer cells with BRAF V600E mutation."7.85AKT is critically involved in the antagonism of BRAF inhibitor sorafenib against dabrafenib in colorectal cancer cells harboring both wild-type and mutant (V600E) BRAF genes. ( Lou, L; Quan, H; Wang, H, 2017)
"To analyze the efficacy of last line sorafenib treatment in colorectal cancer patients."7.83Last line therapy with sorafenib in colorectal cancer: A retrospective analysis. ( Becker, M; Galle, PR; Martchenko, K; Möhler, M; Schimanski, CC; Schmidtmann, I; Thole, V; Thomaidis, T; Wehler, TC, 2016)
" Vemurafenib and sorafenib treatment did not significantly reduce the total CSE1L levels; however, they inhibited ERK1/2 and CSE1L phosphorylation in A375 melanoma cells and HT-29 colorectal cancer cells."7.81Early decline in serum phospho-CSE1L levels in vemurafenib/sunitinib-treated melanoma and sorafenib/lapatinib-treated colorectal tumor xenografts. ( Chen, YC; Chin, SY; Chou, CL; Jiang, MC; Lee, WR; Liu, KH; Shen, SC; Shih, YH; Tseng, JT, 2015)
"We initiated this preclinical study in order to analyze the impact of sorafenib single treatment versus combination treatment in human colorectal cancer."7.79Single-agent therapy with sorafenib or 5-FU is equally effective in human colorectal cancer xenograft--no benefit of combination therapy. ( Berger, MR; Galle, PR; Gockel, I; Graf, C; Hainz, M; Hamdi, S; Maderer, A; Moehler, M; Schimanski, CC; Schmidtmann, I; Theobald, M; Wehler, TC, 2013)
"HT29 and SW48 colorectal cancer cells were studied in vitro using MTT assays to establish the optimal timing of radiation and sorafenib."7.76Sorafenib 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)
" Pharmacokinetic analyses suggest sorafenib and metabolite exposure correlate with OS and DLTs."6.78Phase I pharmacokinetic and pharmacodynamic study of cetuximab, irinotecan and sorafenib in advanced colorectal cancer. ( Arcaroli, J; Azad, N; Carducci, MA; Dasari, A; Diaz, LA; Donehower, RC; Hidalgo, M; Laheru, DA; McManus, M; Messersmith, WA; Quackenbush, K; Rudek, MA; Taylor, GE; Wright, JJ; Zhao, M, 2013)
" In phase I studies, sorafenib demonstrated single-agent activity in patients with advanced solid tumors and was successfully combined with oxaliplatin in preclinical studies."6.71Results of a phase I trial of sorafenib (BAY 43-9006) in combination with oxaliplatin in patients with refractory solid tumors, including colorectal cancer. ( Brendel, E; Christensen, O; Henning, BF; Hilger, RA; Hofstra, E; Kupsch, P; Passarge, K; Richly, H; Scheulen, ME; Schwartz, B; Seeber, S; Strumberg, D; Voigtmann, R; Wiesemann, K, 2005)
"Regorafenib has a closely related chemical structure as sorafenib and is approved for the pharmacotherapy of mCRC."5.43Regorafenib (Stivarga) pharmacologically targets epithelial-mesenchymal transition in colorectal cancer. ( Chen, KF; Fan, LC; Hung, MH; Jiang, JK; Shiau, CW; Tai, WT; Teng, HW; Yang, SH, 2016)
" The aim of the study was to assess the predictive value of early metabolic response (mR) evaluation after one cycle, and its interlesional heterogeneity to a later metabolic and morphological response assessment performed after three cycles in metastatic colorectal cancer (mCRC) patients treated with combined sorafenib and capecitabine."5.22Monitoring metabolic response using FDG PET-CT during targeted therapy for metastatic colorectal cancer. ( Ameye, L; Delaunoit, T; Deleporte, A; Demolin, G; Flamen, P; Garcia, C; Gauthier, N; Guiot, T; Hendlisz, A; Holbrechts, S; Lhommel, R; Maréchal, R; Van den Eynde, M; Vierasu, I; Woff, E, 2016)
"Adult patients with histologically documented, measurable, EGFR-expressing, KRAS-mutated metastatic colorectal cancer (mCRC) that had progressed after 5-fluorouracil-based regimens were treated with sorafenib 400 mg orally twice daily and intravenous cetuximab weekly in 28-day cycles."5.20A Phase II Study of Sorafenib Combined With Cetuximab in EGFR-Expressing, KRAS-Mutated Metastatic Colorectal Cancer. ( Cao, L; Choyke, P; Do, K; Doroshow, JH; Eugeni, M; Figg, WD; Holkova, B; Jacobs, P; Kang, Z; Kummar, S; Larkins, E; Lindenberg, ML; Peer, CJ; Raffeld, M; Steinberg, SM; Turkbey, B; Wright, JJ, 2015)
"This trial evaluated the feasibility and efficacy of combined sorafenib and irinotecan (NEXIRI) as second- or later-line treatment of patients with KRAS-mutated metastatic colorectal cancer (mCRC), who had progressed after irinotecan-based chemotherapy."5.19Sorafenib and irinotecan (NEXIRI) as second- or later-line treatment for patients with metastatic colorectal cancer and KRAS-mutated tumours: a multicentre Phase I/II trial. ( Adenis, A; Assenat, E; Bennouna, J; Bibeau, F; Boissière, F; Bouché, O; Conroy, T; Crapez, E; Desseigne, F; Francois, E; Galais, MP; Laurent-Puig, P; Mazard, T; Poujol, S; Samalin, E; Seitz, JF; Taieb, J; Thézenas, S; Ychou, M, 2014)
"This randomized, double-blind, placebo-controlled, phase IIb study evaluated adding sorafenib to first-line modified FOLFOX6 (mFOLFOX6) for metastatic colorectal cancer (mCRC)."5.17Sorafenib 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)
"To examine whether carbogen and nicotinamide increases 5-fluorouracil (5-FU) delivery to colorectal cancer metastases."5.12Carbogen and nicotinamide increase blood flow and 5-fluorouracil delivery but not 5-fluorouracil retention in colorectal cancer metastases in patients. ( Aboagye, EO; Gupta, N; Hoskin, PJ; Jones, T; Kötz, B; Osman, S; Phillips, R; Price, PM; Saleem, A; Vernon, C; Wasan, H, 2006)
" During the exploration of small molecules that inhibit RAF1 kinase, regorafenib (BAY 73-4506) was discovered as a multikinase inhibitor which demonstrated anti-cancer, anti-angiogenic, and apoptotic activities in metastatic colorectal cancer."4.90The preclinical development of regorafenib for the treatment of colorectal cancer. ( Fujiya, T; Hasegawa, Y; Kakugawa, Y; Kinouchi, M; Miura, K; Philchenkov, A; Satoh, M; Yamamoto, K, 2014)
" In the present study, we investigated the feasibility of combined treatment with dabrafenib and sorafenib, type I and type II BRAF inhibitor respectively, on colorectal cancer cells with BRAF V600E mutation."3.85AKT is critically involved in the antagonism of BRAF inhibitor sorafenib against dabrafenib in colorectal cancer cells harboring both wild-type and mutant (V600E) BRAF genes. ( Lou, L; Quan, H; Wang, H, 2017)
"To analyze the efficacy of last line sorafenib treatment in colorectal cancer patients."3.83Last line therapy with sorafenib in colorectal cancer: A retrospective analysis. ( Becker, M; Galle, PR; Martchenko, K; Möhler, M; Schimanski, CC; Schmidtmann, I; Thole, V; Thomaidis, T; Wehler, TC, 2016)
" Vemurafenib and sorafenib treatment did not significantly reduce the total CSE1L levels; however, they inhibited ERK1/2 and CSE1L phosphorylation in A375 melanoma cells and HT-29 colorectal cancer cells."3.81Early decline in serum phospho-CSE1L levels in vemurafenib/sunitinib-treated melanoma and sorafenib/lapatinib-treated colorectal tumor xenografts. ( Chen, YC; Chin, SY; Chou, CL; Jiang, MC; Lee, WR; Liu, KH; Shen, SC; Shih, YH; Tseng, JT, 2015)
"We initiated this preclinical study in order to analyze the impact of sorafenib single treatment versus combination treatment in human colorectal cancer."3.79Single-agent therapy with sorafenib or 5-FU is equally effective in human colorectal cancer xenograft--no benefit of combination therapy. ( Berger, MR; Galle, PR; Gockel, I; Graf, C; Hainz, M; Hamdi, S; Maderer, A; Moehler, M; Schimanski, CC; Schmidtmann, I; Theobald, M; Wehler, TC, 2013)
"HT29 and SW48 colorectal cancer cells were studied in vitro using MTT assays to establish the optimal timing of radiation and sorafenib."3.76Sorafenib 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)
"Sorafenib, erlotinib, and cetuximab, alone or in combination, were tested in vitro in a panel of non-small cell lung cancer (NSCLC) and colorectal cancer cell lines and in vivo in H1299 tumor xenografts."3.76Synergistic antitumor activity of sorafenib in combination with epidermal growth factor receptor inhibitors in colorectal and lung cancer cells. ( Berrino, L; Capasso, A; Ciardiello, F; De Vita, F; Eckhardt, SG; Martinelli, E; Morelli, MP; Morgillo, F; Orditura, M; Rodolico, G; Santoro, M; Troiani, T; Tuccillo, C; Vecchione, L; Vitagliano, D, 2010)
"The dose escalation, confirmation, and expansion results support the dosing of merestinib at 120 mg once daily, based on acceptable exposure and safety at this dose."2.90First-in-Human Phase I Study of Merestinib, an Oral Multikinase Inhibitor, in Patients with Advanced Cancer. ( Birnbaum, A; Cohen, RB; Denlinger, CS; Giles, J; He, AR; Hwang, J; Lewis, N; Moser, B; Mynderse, M; Niland, M; Plimack, ER; Sama, A; Sato, T; Walgren, R; Wallin, J; Zhang, W, 2019)
" Pharmacokinetic analyses suggest sorafenib and metabolite exposure correlate with OS and DLTs."2.78Phase I pharmacokinetic and pharmacodynamic study of cetuximab, irinotecan and sorafenib in advanced colorectal cancer. ( Arcaroli, J; Azad, N; Carducci, MA; Dasari, A; Diaz, LA; Donehower, RC; Hidalgo, M; Laheru, DA; McManus, M; Messersmith, WA; Quackenbush, K; Rudek, MA; Taylor, GE; Wright, JJ; Zhao, M, 2013)
" Clinical and pharmacodynamic activity was observed in kidney cancer and melanoma."2.75Safety, efficacy, pharmacokinetics, and pharmacodynamics of the combination of sorafenib and tanespimycin. ( Burger, AM; Egorin, MJ; Heilbrun, LK; Horiba, MN; Ivy, P; Li, J; Lorusso, PM; Pacey, S; Sausville, EA; Vaishampayan, UN, 2010)
" In phase I studies, sorafenib demonstrated single-agent activity in patients with advanced solid tumors and was successfully combined with oxaliplatin in preclinical studies."2.71Results of a phase I trial of sorafenib (BAY 43-9006) in combination with oxaliplatin in patients with refractory solid tumors, including colorectal cancer. ( Brendel, E; Christensen, O; Henning, BF; Hilger, RA; Hofstra, E; Kupsch, P; Passarge, K; Richly, H; Scheulen, ME; Schwartz, B; Seeber, S; Strumberg, D; Voigtmann, R; Wiesemann, K, 2005)
"In the present study, we investigated the effects of motesanib (AMG 706), a multikinase inhibitor alone and in combination with DuP-697, an irreversible selective inhibitor of COX-2, on cell proliferation, angiogenesis, and apoptosis induction in a human colorectal cancer cell line (HT29)."1.43Effects of a Multikinase Inhibitor Motesanib (AMG 706) Alone and Combined with the Selective DuP-697 COX-2 Inhibitor on Colorectal Cancer Cells. ( Altun, A; Ataseven, H; Kaya, TT; Koyluoglu, G; Turgut, NH, 2016)
"Regorafenib has a closely related chemical structure as sorafenib and is approved for the pharmacotherapy of mCRC."1.43Regorafenib (Stivarga) pharmacologically targets epithelial-mesenchymal transition in colorectal cancer. ( Chen, KF; Fan, LC; Hung, MH; Jiang, JK; Shiau, CW; Tai, WT; Teng, HW; Yang, SH, 2016)
"Colorectal cancer is one of the most common malignancies in the world, and is generally treated more effectively by chemoradiotherapy rather than radiotherapy or chemotherapy alone."1.40The mechanisms responsible for the radiosensitizing effects of sorafenib on colon cancer cells. ( Jung, WG; Kim, EH; Kim, MS, 2014)
"Sorafenib is a multi-kinase inhibitor that blocks cell proliferation and angiogenesis."1.39Monitoring anti-angiogenic therapy in colorectal cancer murine model using dynamic contrast-enhanced MRI: comparing pixel-by-pixel with region of interest analysis. ( Fan, X; Haney, CR; Karczmar, GS; Markiewicz, E; Mustafi, D; Stadler, WM, 2013)
"Sorafenib was found to decrease Mcl-1 levels in most cell lines tested, but this decrease did not correlate with apoptotic sensitivity."1.34Cell cycle dependent and schedule-dependent antitumor effects of sorafenib combined with radiation. ( Cerniglia, G; Dicker, DT; Diehl, JA; Dorsey, JF; El-Deiry, WS; Flaherty, KT; Gupta, A; Kim, SH; Liu, YY; McDonough, J; Plastaras, JP; Rajendran, RR; Rustgi, AK; Smith, CD, 2007)

Research

Studies (59)

TimeframeStudies, this research(%)All Research%
pre-19900 (0.00)18.7374
1990's1 (1.69)18.2507
2000's10 (16.95)29.6817
2010's47 (79.66)24.3611
2020's1 (1.69)2.80

Authors

AuthorsStudies
Farooqi, AS1
Hong, JY1
Cao, J1
Lu, X1
Price, IR1
Zhao, Q1
Kosciuk, T1
Yang, M1
Bai, JJ1
Lin, H1
Wu, W1
Bours, MJL1
Koole, A1
Kenkhuis, MF1
Eussen, SJPM1
Breukink, SO1
van Schooten, FJ1
Weijenberg, MP1
Hageman, GJ1
Wang, H1
Quan, H1
Lou, L1
Karasic, TB1
Rosen, MA1
O'Dwyer, PJ2
Hata, AN1
Rowley, S1
Archibald, HL1
Gomez-Caraballo, M1
Siddiqui, FM1
Ji, F1
Jung, J1
Light, M1
Lee, JS1
Debussche, L1
Sidhu, S1
Sadreyev, RI1
Watters, J1
Engelman, JA1
Yau, EH1
Kummetha, IR1
Lichinchi, G1
Tang, R1
Zhang, Y1
Rana, TM1
Codony-Servat, J1
Cuatrecasas, M1
Asensio, E1
Montironi, C1
Martínez-Cardús, A1
Marín-Aguilera, M1
Horndler, C1
Martínez-Balibrea, E1
Rubini, M1
Jares, P1
Reig, O1
Victoria, I1
Gaba, L1
Martín-Richard, M1
Alonso, V1
Escudero, P1
Fernández-Martos, C1
Feliu, J1
Méndez, JC1
Méndez, M1
Gallego, J1
Salud, A1
Rojo, F1
Castells, A1
Prat, A1
Rosell, R1
García-Albéniz, X1
Camps, J1
Maurel, J1
He, AR1
Cohen, RB1
Denlinger, CS1
Sama, A1
Birnbaum, A1
Hwang, J1
Sato, T1
Lewis, N1
Mynderse, M1
Niland, M1
Giles, J1
Wallin, J1
Moser, B1
Zhang, W1
Walgren, R1
Plimack, ER1
Tabernero, J2
Garcia-Carbonero, R1
Cassidy, J1
Sobrero, A1
Van Cutsem, E2
Köhne, CH1
Tejpar, S2
Gladkov, O1
Davidenko, I1
Salazar, R2
Vladimirova, L1
Cheporov, S1
Burdaeva, O1
Rivera, F1
Samuel, L1
Bulavina, I1
Potter, V1
Chang, YL1
Lokker, NA1
Al-Marrawi, MY1
Saroya, BS1
Brennan, MC1
Yang, Z1
Dykes, TM1
El-Deiry, WS3
Mazard, T2
Causse, A1
Simony, J1
Leconet, W1
Vezzio-Vie, N1
Torro, A1
Jarlier, M1
Evrard, A1
Del Rio, M1
Assenat, E2
Martineau, P1
Ychou, M2
Robert, B1
Gongora, C2
Samalin, E1
Bouché, O2
Thézenas, S1
Francois, E1
Adenis, A1
Bennouna, J1
Taieb, J1
Desseigne, F1
Seitz, JF1
Conroy, T1
Galais, MP1
Crapez, E1
Poujol, S1
Bibeau, F1
Boissière, F1
Laurent-Puig, P1
Smith, MA1
García-Alfonso, P1
Grande, E1
Polo, E1
Afonso, R1
Reina, JJ1
Jorge, M1
Campos, JM1
Martínez, V1
Angeles, C1
Montagut, C1
Miura, K1
Satoh, M1
Kinouchi, M1
Yamamoto, K1
Hasegawa, Y1
Philchenkov, A1
Kakugawa, Y1
Fujiya, T1
Kim, EH1
Kim, MS1
Jung, WG1
Tebbutt, N1
Kotasek, D1
Burris, HA1
Schwartzberg, LS1
Hurwitz, H1
Stephenson, J1
Warner, DJ1
Chen, L1
Hsu, CP1
Goldstein, D1
Do, K1
Cao, L1
Kang, Z1
Turkbey, B1
Lindenberg, ML1
Larkins, E1
Holkova, B1
Steinberg, SM1
Raffeld, M1
Peer, CJ1
Figg, WD1
Eugeni, M1
Jacobs, P1
Choyke, P1
Wright, JJ2
Doroshow, JH1
Kummar, S1
Macarulla, T1
Cervantes, A1
Roselló, S1
Prenen, H1
Martinelli, E2
Troiani, T2
Laffranchi, B1
Jego, V1
von Richter, O1
Ciardiello, F2
Lee, WR1
Shen, SC1
Shih, YH1
Chou, CL1
Tseng, JT1
Chin, SY1
Liu, KH1
Chen, YC1
Jiang, MC1
An, H1
Stoops, SL1
Deane, NG1
Zhu, J1
Zi, J1
Weaver, C1
Waterson, AG1
Zijlstra, A1
Lindsley, CW1
Beauchamp, RD1
Hendlisz, A2
Deleporte, A2
Delaunoit, T2
Maréchal, R2
Peeters, M1
Holbrechts, S2
Van den Eynde, M2
Houbiers, G1
Filleul, B1
Van Laethem, JL1
Ceyssens, S1
Barbuto, AM1
Lhommel, R2
Demolin, G2
Garcia, C2
El Mansy, H1
Ameye, L2
Moreau, M1
Guiot, T2
Paesmans, M1
Piccart, M1
Flamen, P2
Abdel-Rahman, O1
Kaya, TT1
Altun, A1
Turgut, NH1
Ataseven, H1
Koyluoglu, G1
Woff, E1
Vierasu, I1
Gauthier, N1
Martchenko, K1
Schmidtmann, I2
Thomaidis, T1
Thole, V1
Galle, PR2
Becker, M1
Möhler, M1
Wehler, TC2
Schimanski, CC2
Tong, J1
Tan, S1
Zou, F1
Yu, J1
Zhang, L1
Fan, LC1
Teng, HW1
Shiau, CW1
Tai, WT1
Hung, MH1
Yang, SH1
Jiang, JK1
Chen, KF1
Queralt, B1
Cuyàs, E1
Bosch-Barrera, J1
Massaguer, A1
de Llorens, R1
Martin-Castillo, B1
Brunet, J1
Menendez, JA1
Pehserl, AM1
Ress, AL1
Stanzer, S1
Resel, M1
Karbiener, M1
Stadelmeyer, E1
Stiegelbauer, V1
Gerger, A1
Mayr, C1
Scheideler, M1
Hutterer, GC1
Bauernhofer, T1
Kiesslich, T1
Pichler, M1
Shi, L1
Hu, Y1
Lin, A1
Ma, C1
Zhang, C1
Su, Y1
Zhou, L1
Niu, Y1
Zhu, X1
Di Nicolantonio, F1
Martini, M1
Molinari, F1
Sartore-Bianchi, A1
Arena, S1
Saletti, P1
De Dosso, S1
Mazzucchelli, L1
Frattini, M1
Siena, S1
Bardelli, A1
Halimi, JM1
Azizi, M1
Bobrie, G1
Deray, G1
des Guetz, G1
Lecomte, T1
Levy, B1
Mourad, JJ1
Nochy, D1
Oudard, S1
Rieu, P1
Sahali, D1
Shrubsole, MJ1
Yang, G1
Gao, YT1
Chow, WH1
Shu, XO1
Cai, Q1
Rothman, N1
Gao, J1
Wagner, C1
Zheng, W1
Boonstra, JJ1
van Marion, R1
Beer, DG1
Lin, L1
Chaves, P1
Ribeiro, C1
Pereira, AD1
Roque, L1
Darnton, SJ1
Altorki, NK1
Schrump, DS1
Klimstra, DS1
Tang, LH1
Eshleman, JR1
Alvarez, H1
Shimada, Y1
van Dekken, H1
Tilanus, HW1
Dinjens, WN1
Hubbard, J1
Grothey, A1
Vaishampayan, UN1
Burger, AM1
Sausville, EA1
Heilbrun, LK1
Li, J1
Horiba, MN1
Egorin, MJ1
Ivy, P1
Pacey, S1
Lorusso, PM1
Suen, AW1
Galoforo, S1
Marples, B1
McGonagle, M1
Downing, L1
Martinez, AA1
Robertson, JM1
Wilson, GD1
Morgillo, F1
Rodolico, G1
Vitagliano, D1
Morelli, MP1
Tuccillo, C1
Vecchione, L1
Capasso, A1
Orditura, M1
De Vita, F1
Eckhardt, SG1
Santoro, M1
Berrino, L1
Yoon, J1
Koo, KH1
Choi, KY1
Mansi, L1
Viel, E1
Curtit, E1
Medioni, J1
Le Tourneau, C1
Gallant, JN1
Allen, JE1
Smith, CD2
Dicker, DT2
Wang, W1
Dolloff, NG1
Navaraj, A1
Kuo, YC1
Lin, WC1
Chiang, IT1
Chang, YF1
Chen, CW1
Su, SH1
Chen, CL1
Hwang, JJ1
Azad, N1
Dasari, A1
Arcaroli, J1
Taylor, GE1
Laheru, DA1
Carducci, MA1
McManus, M1
Quackenbush, K1
Hidalgo, M1
Diaz, LA1
Donehower, RC1
Zhao, M1
Rudek, MA1
Messersmith, WA1
Gulhati, P1
Zaytseva, YY1
Valentino, JD1
Stevens, PD1
Kim, JT1
Sasazuki, T1
Shirasawa, S1
Lee, EY1
Weiss, HL1
Dong, J1
Gao, T1
Evers, BM1
Haney, CR1
Fan, X1
Markiewicz, E1
Mustafi, D1
Karczmar, GS1
Stadler, WM1
Kim, YB1
Jeung, HC1
Jeong, I1
Lee, K1
Rha, SY1
Chung, HC1
Kim, GE1
Hamdi, S1
Maderer, A1
Graf, C1
Gockel, I1
Hainz, M1
Berger, MR1
Theobald, M1
Moehler, M1
Grossi, V1
Liuzzi, M1
Murzilli, S1
Martelli, N1
Napoli, A1
Ingravallo, G1
Del Rio, A1
Simone, C1
Török, S1
Cserepes T, M1
Rényi-Vámos, F1
Döme, B1
Kupsch, P1
Henning, BF1
Passarge, K1
Richly, H1
Wiesemann, K1
Hilger, RA1
Scheulen, ME1
Christensen, O1
Brendel, E1
Schwartz, B1
Hofstra, E1
Voigtmann, R1
Seeber, S1
Strumberg, D1
Zakarija, A1
Soff, G1
Gupta, N1
Saleem, A1
Kötz, B1
Osman, S1
Aboagye, EO1
Phillips, R1
Vernon, C1
Wasan, H1
Jones, T1
Hoskin, PJ1
Price, PM1
Plastaras, JP1
Kim, SH1
Liu, YY1
Dorsey, JF1
McDonough, J1
Cerniglia, G1
Rajendran, RR1
Gupta, A1
Rustgi, AK1
Diehl, JA1
Flaherty, KT1
Quesada, AR1
Medina, MA1
Alba, E1
Ronen, SM1
DiStefano, F1
McCoy, CL1
Robertson, D1
Smith, TA1
Al-Saffar, NM1
Titley, J1
Cunningham, DC1
Griffiths, JR1
Leach, MO1
Clarke, PA1

Clinical Trials (9)

Trial Overview

TrialPhaseEnrollmentStudy TypeStart DateStatus
A Phase 1 Study of LY2801653 in Patients With Advanced Cancer[NCT01285037]Phase 1190 participants (Actual)Interventional2009-09-09Completed
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 2198 participants (Actual)Interventional2009-03-31Completed
SORAFENIB (NEXAVAR®) in Combination With Irinotecan in the Second Line Treatment or More of Metastatic Colorectal Cancer With K-RAS Mutation : a Multicentre Two-part Phase I/II Study.[NCT00989469]Phase 1/Phase 264 participants (Actual)Interventional2009-02-28Completed
A Randomized Phase III Trial Assessing a Regorafenib-irinotecan Combination (REGIRI) Versus Regorafenib Alone in Metastatic Colorectal Cancer Patients After Failure of Standard Therapies, According to the A/A Genotype of Cyclin D1[NCT03829462]Phase 378 participants (Anticipated)Interventional2019-03-28Recruiting
An Open-Label, Dose-Finding Study to Evaluate the Safety of AMG 706 Plus Panitumumab Plus Chemotherapy in the Treatment of Subjects With Metastatic Colorectal Cancer[NCT00101894]Phase 1119 participants (Actual)Interventional2004-12-31Completed
A Phase II Study of BAY 43-9006 (Sorafenib) in Combination With Cetuximab (Erbitux ) in EGFR Expressing Metastatic Colorectal Cancer (CRC)[NCT00326495]Phase 251 participants (Actual)Interventional2006-05-10Completed
Sorafenib Plus Capecitabine Efficacy Assessment in Patients With Advanced Pre-treated Colorectal Cancer[NCT01290926]Phase 297 participants (Actual)Interventional2011-02-28Completed
Angiogenesis Inhibitors and Hypertension: Clinical Aspects[NCT00511511]80 participants (Anticipated)Observational2007-08-31Completed
Phase I Study of Radiation Therapy With Concurrent Sorafenib for Hepatocellular Carcinoma Not Responding to Transarterial Chemoembolization[NCT01618253]Phase 10 participants (Actual)Interventional2012-06-30Withdrawn (stopped due to Closed due to poor accrual.)
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

Duration of Response

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

Interventionmonths (Number)
Sorafenib (Nexavar, BAY43-9006) + mFOLFOX67.5
Matching Placebo + mFOLFOX66.7

Overall Response

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.

Interventionparticipants (Number)
Sorafenib (Nexavar, BAY43-9006) + mFOLFOX645
Matching Placebo + mFOLFOX661

Overall Survival (OS)

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.

Interventiondays (Median)
Sorafenib (Nexavar, BAY43-9006) + mFOLFOX6535
Matching Placebo + mFOLFOX6552

Progression-Free Survival (PFS)

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.

InterventionMonths (Median)
Sorafenib (Nexavar, BAY43-9006) + mFOLFOX69.1
Matching Placebo + mFOLFOX68.7

Time to Progression (TTP)

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.

InterventionMonths (Median)
Sorafenib (Nexavar, BAY43-9006) + mFOLFOX69.2
Matching Placebo + mFOLFOX69.0

Count of Participants With Adverse Events

Here is the number of participants with adverse events. For a detailed list of adverse events, see the adverse event module. (NCT00326495)
Timeframe: 96 months, 26 days

InterventionParticipants (Count of Participants)
BAY 43-9006 & Cetuximab50

Overall Rate of Response

Rate of response is defined as the percentage of participants with a complete response (CR) + partial response (PR) + stable disease (SD) for 4 months. Response is defined by the Response is determined by the Response Evaluation Criteria in Solid Tumors (RECIST). Partial response is at least a 30% decrease in the sum of the longest diameter (LD) of target lesions, taking as reference the baseline sum LD. Complete response is a disappearance of all target lesions. Stable disease is neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD (progressive disease), taking as reference the smallest sum LD since the treatment started. Progressive disease is at least a 20% increase in the sum of the LD of target lesions, taking as reference the smallest sum LD recorded since the treatment started or the appearance of one or more new lesions. (NCT00326495)
Timeframe: 4 months

Interventionpercentage of participants (Number)
BAY 43-9006 & Cetuximab15

Reviews

10 reviews available for niacinamide and Colorectal Neoplasms

ArticleYear
Antiangiogenic tyrosine kinase inhibitors in colorectal cancer: is there a path to making them more effective?
    Cancer chemotherapy and pharmacology, 2017, Volume: 80, Issue:4

    Topics: Angiogenesis Inhibitors; Animals; Antineoplastic Agents; Colorectal Neoplasms; Humans; Models, Biolo

2017
The role of antiangiogenic agents in the treatment of patients with advanced colorectal cancer according to K-RAS status.
    Angiogenesis, 2014, Volume: 17, Issue:4

    Topics: Angiogenesis Inhibitors; Antibodies, Monoclonal, Humanized; Antineoplastic Combined Chemotherapy Pro

2014
The preclinical development of regorafenib for the treatment of colorectal cancer.
    Expert opinion on drug discovery, 2014, Volume: 9, Issue:9

    Topics: Angiogenesis Inhibitors; Animals; Antineoplastic Agents; Colorectal Neoplasms; Drug Design; Drug Dis

2014
Targeting BRAF aberrations in advanced colorectal carcinoma: from bench to bedside.
    Future oncology (London, England), 2016, Volume: 12, Issue:1

    Topics: Antineoplastic Combined Chemotherapy Protocols; Colorectal Neoplasms; Drug Resistance, Neoplasm; Erb

2016
Antiangiogenesis agents in colorectal cancer.
    Current opinion in oncology, 2010, Volume: 22, Issue:4

    Topics: Angiogenesis Inhibitors; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Antineoplastic C

2010
[Targeting the RAS signalling pathway in cancer].
    Bulletin du cancer, 2011, Volume: 98, Issue:9

    Topics: Antineoplastic Agents; Benzenesulfonates; Colorectal Neoplasms; ErbB Receptors; Extracellular Signal

2011
[Nintedanib (BIBF 1120) in the treatment of solid cancers: an overview of biological and clinical aspects].
    Magyar onkologia, 2012, Volume: 56, Issue:3

    Topics: Animals; Antineoplastic Agents; Axitinib; Benzenesulfonates; Carcinoma, Hepatocellular; Clinical Tri

2012
Activity of the Raf kinase inhibitor BAY 43-9006 in patients with advanced solid tumors.
    Clinical colorectal cancer, 2003, Volume: 3, Issue:1

    Topics: Benzenesulfonates; Clinical Trials, Phase I as Topic; Colorectal Neoplasms; Dose-Response Relationsh

2003
Update on angiogenesis inhibitors.
    Current opinion in oncology, 2005, Volume: 17, Issue:6

    Topics: Angiogenesis Inhibitors; Animals; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Benzene

2005
Playing only one instrument may be not enough: limitations and future of the antiangiogenic treatment of cancer.
    BioEssays : news and reviews in molecular, cellular and developmental biology, 2007, Volume: 29, Issue:11

    Topics: Angiogenesis Inhibitors; Antibodies, Monoclonal; Antineoplastic Agents; Benzenesulfonates; Carcinoma

2007

Trials

12 trials available for niacinamide and Colorectal Neoplasms

ArticleYear
First-in-Human Phase I Study of Merestinib, an Oral Multikinase Inhibitor, in Patients with Advanced Cancer.
    The oncologist, 2019, Volume: 24, Issue:9

    Topics: Adult; Aged; Angiogenesis Inhibitors; Antibodies, Monoclonal, Humanized; Antineoplastic Agents; Cell

2019
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
Sorafenib and irinotecan (NEXIRI) as second- or later-line treatment for patients with metastatic colorectal cancer and KRAS-mutated tumours: a multicentre Phase I/II trial.
    British journal of cancer, 2014, Mar-04, Volume: 110, Issue:5

    Topics: Adult; Aged; Aged, 80 and over; Antineoplastic Combined Chemotherapy Protocols; Camptothecin; Colore

2014
Sorafenib and irinotecan (NEXIRI) as second- or later-line treatment for patients with metastatic colorectal cancer and KRAS-mutated tumours: a multicentre Phase I/II trial.
    British journal of cancer, 2014, Mar-04, Volume: 110, Issue:5

    Topics: Adult; Aged; Aged, 80 and over; Antineoplastic Combined Chemotherapy Protocols; Camptothecin; Colore

2014
Sorafenib and irinotecan (NEXIRI) as second- or later-line treatment for patients with metastatic colorectal cancer and KRAS-mutated tumours: a multicentre Phase I/II trial.
    British journal of cancer, 2014, Mar-04, Volume: 110, Issue:5

    Topics: Adult; Aged; Aged, 80 and over; Antineoplastic Combined Chemotherapy Protocols; Camptothecin; Colore

2014
Sorafenib and irinotecan (NEXIRI) as second- or later-line treatment for patients with metastatic colorectal cancer and KRAS-mutated tumours: a multicentre Phase I/II trial.
    British journal of cancer, 2014, Mar-04, Volume: 110, Issue:5

    Topics: Adult; Aged; Aged, 80 and over; Antineoplastic Combined Chemotherapy Protocols; Camptothecin; Colore

2014
Motesanib with or without panitumumab plus FOLFIRI or FOLFOX for the treatment of metastatic colorectal cancer.
    Cancer chemotherapy and pharmacology, 2015, Volume: 75, Issue:5

    Topics: Adult; Aged; Aged, 80 and over; Antibodies, Monoclonal; Antineoplastic Combined Chemotherapy Protoco

2015
A Phase II Study of Sorafenib Combined With Cetuximab in EGFR-Expressing, KRAS-Mutated Metastatic Colorectal Cancer.
    Clinical colorectal cancer, 2015, Volume: 14, Issue:3

    Topics: Adult; Aged; Aged, 80 and over; Antineoplastic Combined Chemotherapy Protocols; Cetuximab; Colorecta

2015
Phase I study of FOLFIRI plus pimasertib as second-line treatment for KRAS-mutated metastatic colorectal cancer.
    British journal of cancer, 2015, Jun-09, Volume: 112, Issue:12

    Topics: Aged; Aged, 80 and over; Antineoplastic Combined Chemotherapy Protocols; Camptothecin; Colorectal Ne

2015
The Prognostic Significance of Metabolic Response Heterogeneity in Metastatic Colorectal Cancer.
    PloS one, 2015, Volume: 10, Issue:9

    Topics: Adult; Aged; Aged, 80 and over; Antineoplastic Combined Chemotherapy Protocols; Capecitabine; Colore

2015
Monitoring metabolic response using FDG PET-CT during targeted therapy for metastatic colorectal cancer.
    European journal of nuclear medicine and molecular imaging, 2016, Volume: 43, Issue:10

    Topics: Adult; Aged; Antineoplastic Combined Chemotherapy Protocols; Capecitabine; Colorectal Neoplasms; Dru

2016
Safety, efficacy, pharmacokinetics, and pharmacodynamics of the combination of sorafenib and tanespimycin.
    Clinical cancer research : an official journal of the American Association for Cancer Research, 2010, Jul-15, Volume: 16, Issue:14

    Topics: Adult; Aged; Antineoplastic Combined Chemotherapy Protocols; Benzenesulfonates; Benzoquinones; Clini

2010
Phase I pharmacokinetic and pharmacodynamic study of cetuximab, irinotecan and sorafenib in advanced colorectal cancer.
    Investigational new drugs, 2013, Volume: 31, Issue:2

    Topics: Adult; Aged; Antibodies, Monoclonal, Humanized; Antineoplastic Combined Chemotherapy Protocols; Camp

2013
Results of a phase I trial of sorafenib (BAY 43-9006) in combination with oxaliplatin in patients with refractory solid tumors, including colorectal cancer.
    Clinical colorectal cancer, 2005, Volume: 5, Issue:3

    Topics: Administration, Oral; Adult; Aged; Aged, 80 and over; Antineoplastic Combined Chemotherapy Protocols

2005
Carbogen and nicotinamide increase blood flow and 5-fluorouracil delivery but not 5-fluorouracil retention in colorectal cancer metastases in patients.
    Clinical cancer research : an official journal of the American Association for Cancer Research, 2006, May-15, Volume: 12, Issue:10

    Topics: Administration, Inhalation; Administration, Oral; Aged; Antimetabolites, Antineoplastic; Carbon Diox

2006

Other Studies

37 other studies available for niacinamide and Colorectal Neoplasms

ArticleYear
Novel Lysine-Based Thioureas as Mechanism-Based Inhibitors of Sirtuin 2 (SIRT2) with Anticancer Activity in a Colorectal Cancer Murine Model.
    Journal of medicinal chemistry, 2019, 04-25, Volume: 62, Issue:8

    Topics: Animals; Antineoplastic Agents; Binding Sites; Cell Line, Tumor; Cell Proliferation; Colorectal Neop

2019
Cross-Sectional Associations between Dietary Daily Nicotinamide Intake and Patient-Reported Outcomes in Colorectal Cancer Survivors, 2 to 10 Years Post-Diagnosis.
    Nutrients, 2021, Oct-21, Volume: 13, Issue:11

    Topics: Aged; Anxiety; Cancer Survivors; Cognition; Colorectal Neoplasms; Cross-Sectional Studies; Depressio

2021
AKT is critically involved in the antagonism of BRAF inhibitor sorafenib against dabrafenib in colorectal cancer cells harboring both wild-type and mutant (V600E) BRAF genes.
    Biochemical and biophysical research communications, 2017, 07-15, Volume: 489, Issue:1

    Topics: Antineoplastic Agents; Cell Proliferation; Colorectal Neoplasms; Dose-Response Relationship, Drug; D

2017
Synergistic activity and heterogeneous acquired resistance of combined MDM2 and MEK inhibition in KRAS mutant cancers.
    Oncogene, 2017, 11-23, Volume: 36, Issue:47

    Topics: A549 Cells; Animals; Apoptosis; Apoptosis Regulatory Proteins; Bcl-2-Like Protein 11; Carcinoma, Non

2017
Genome-Wide CRISPR Screen for Essential Cell Growth Mediators in Mutant KRAS Colorectal Cancers.
    Cancer research, 2017, 11-15, Volume: 77, Issue:22

    Topics: ATPases Associated with Diverse Cellular Activities; Cell Line, Tumor; Cell Proliferation; Colorecta

2017
Nuclear IGF-1R predicts chemotherapy and targeted therapy resistance in metastatic colorectal cancer.
    British journal of cancer, 2017, Dec-05, Volume: 117, Issue:12

    Topics: Aged; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Antineoplastic Agents; Antineoplast

2017
Off-label use of cetuximab plus sorafenib and panitumumab plus regorafenib to personalize therapy for a patient with V600E BRAF-mutant metastatic colon cancer.
    Cancer biology & therapy, 2013, Volume: 14, Issue:8

    Topics: Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Antineoplastic Combined Chemotherapy Prot

2013
Sorafenib overcomes irinotecan resistance in colorectal cancer by inhibiting the ABCG2 drug-efflux pump.
    Molecular cancer therapeutics, 2013, Volume: 12, Issue:10

    Topics: Animals; ATP Binding Cassette Transporter, Subfamily G, Member 2; ATP-Binding Cassette Transporters;

2013
Sorafenib inhibits ABCG2 and overcomes irinotecan resistance--letter.
    Molecular cancer therapeutics, 2014, Volume: 13, Issue:3

    Topics: Animals; ATP-Binding Cassette Transporters; Camptothecin; Colorectal Neoplasms; Humans; Neoplasm Pro

2014
Sorafenib inhibits ABCG2 and overcomes irinotecan resistance--response.
    Molecular cancer therapeutics, 2014, Volume: 13, Issue:3

    Topics: Animals; ATP-Binding Cassette Transporters; Camptothecin; Colorectal Neoplasms; Humans; Neoplasm Pro

2014
The mechanisms responsible for the radiosensitizing effects of sorafenib on colon cancer cells.
    Oncology reports, 2014, Volume: 32, Issue:6

    Topics: Cell Cycle; Cell Line, Tumor; Cell Movement; Cell Proliferation; Colorectal Neoplasms; DNA Damage; H

2014
Early decline in serum phospho-CSE1L levels in vemurafenib/sunitinib-treated melanoma and sorafenib/lapatinib-treated colorectal tumor xenografts.
    Journal of translational medicine, 2015, Jun-13, Volume: 13

    Topics: Animals; Antibodies, Neoplasm; Cell Line, Tumor; Cell Proliferation; Cellular Apoptosis Susceptibili

2015
Small molecule/ML327 mediated transcriptional de-repression of E-cadherin and inhibition of epithelial-to-mesenchymal transition.
    Oncotarget, 2015, Sep-08, Volume: 6, Issue:26

    Topics: Animals; Cadherins; Cell Line, Tumor; Chick Embryo; Colorectal Neoplasms; Epithelial-Mesenchymal Tra

2015
Effects of a Multikinase Inhibitor Motesanib (AMG 706) Alone and Combined with the Selective DuP-697 COX-2 Inhibitor on Colorectal Cancer Cells.
    Asian Pacific journal of cancer prevention : APJCP, 2016, Volume: 17, Issue:3

    Topics: Angiogenesis Inhibitors; Animals; Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Cell Li

2016
Last line therapy with sorafenib in colorectal cancer: A retrospective analysis.
    World journal of gastroenterology, 2016, Jun-21, Volume: 22, Issue:23

    Topics: Aged; Antineoplastic Agents; Antineoplastic Combined Chemotherapy Protocols; Colorectal Neoplasms; D

2016
FBW7 mutations mediate resistance of colorectal cancer to targeted therapies by blocking Mcl-1 degradation.
    Oncogene, 2017, 02-09, Volume: 36, Issue:6

    Topics: Animals; Cell Cycle Proteins; Cell Line, Tumor; Colorectal Neoplasms; Drug Resistance, Neoplasm; F-B

2017
Regorafenib (Stivarga) pharmacologically targets epithelial-mesenchymal transition in colorectal cancer.
    Oncotarget, 2016, Sep-27, Volume: 7, Issue:39

    Topics: Animals; Antigens, CD; Antineoplastic Agents; Cadherins; Cell Movement; Colorectal Neoplasms; Dose-R

2016
Synthetic lethal interaction of cetuximab with MEK1/2 inhibition in NRAS-mutant metastatic colorectal cancer.
    Oncotarget, 2016, Dec-13, Volume: 7, Issue:50

    Topics: Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Benzimidazoles; Cell Line, Tumor; Cell Pr

2016
Comprehensive Analysis of miRNome Alterations in Response to Sorafenib Treatment in Colorectal Cancer Cells.
    International journal of molecular sciences, 2016, Dec-01, Volume: 17, Issue:12

    Topics: Animals; Caco-2 Cells; Cell Cycle Checkpoints; Colorectal Neoplasms; Drug Resistance, Neoplasm; Gene

2016
Matrix Metalloproteinase Responsive Nanoparticles for Synergistic Treatment of Colorectal Cancer via Simultaneous Anti-Angiogenesis and Chemotherapy.
    Bioconjugate chemistry, 2016, Dec-21, Volume: 27, Issue:12

    Topics: Angiogenesis Inhibitors; Animals; Antineoplastic Combined Chemotherapy Protocols; Camptothecin; Colo

2016
Wild-type BRAF is required for response to panitumumab or cetuximab in metastatic colorectal cancer.
    Journal of clinical oncology : official journal of the American Society of Clinical Oncology, 2008, Dec-10, Volume: 26, Issue:35

    Topics: Adult; Aged; Aged, 80 and over; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Antineopl

2008
[Vascular and renal effects of anti-angiogenic therapy].
    Nephrologie & therapeutique, 2008, Volume: 4, Issue:7

    Topics: Angiogenesis Inhibitors; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Antineoplastic A

2008
Dietary B vitamin and methionine intakes and plasma folate are not associated with colorectal cancer risk in Chinese women.
    Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology, 2009, Volume: 18, Issue:3

    Topics: Adult; Aged; Case-Control Studies; China; Colorectal Neoplasms; Diet; Female; Folic Acid; Humans; Lo

2009
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 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
Synergistic antitumor activity of sorafenib in combination with epidermal growth factor receptor inhibitors in colorectal and lung cancer cells.
    Clinical cancer research : an official journal of the American Association for Cancer Research, 2010, Oct-15, Volume: 16, Issue:20

    Topics: Animals; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Antineoplastic Combined Chemothe

2010
MEK1/2 inhibitors AS703026 and AZD6244 may be potential therapies for KRAS mutated colorectal cancer that is resistant to EGFR monoclonal antibody therapy.
    Cancer research, 2011, Jan-15, Volume: 71, Issue:2

    Topics: Animals; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Benzimidazoles; Cell Growth Proc

2011
Quinacrine synergizes with 5-fluorouracil and other therapies in colorectal cancer.
    Cancer biology & therapy, 2011, Aug-01, Volume: 12, Issue:3

    Topics: Animals; Antineoplastic Agents; Antineoplastic Combined Chemotherapy Protocols; Benzenesulfonates; C

2011
Sorafenib sensitizes human colorectal carcinoma to radiation via suppression of NF-κB expression in vitro and in vivo.
    Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie, 2012, Volume: 66, Issue:1

    Topics: Animals; Antineoplastic Agents; Apoptosis; Benzenesulfonates; Blotting, Western; Cell Cycle; Cell Li

2012
Sorafenib enhances the therapeutic efficacy of rapamycin in colorectal cancers harboring oncogenic KRAS and PIK3CA.
    Carcinogenesis, 2012, Volume: 33, Issue:9

    Topics: Animals; Antineoplastic Agents; Apoptosis; Benzenesulfonates; Cell Cycle; Cell Line, Tumor; Class I

2012
Monitoring anti-angiogenic therapy in colorectal cancer murine model using dynamic contrast-enhanced MRI: comparing pixel-by-pixel with region of interest analysis.
    Technology in cancer research & treatment, 2013, Volume: 12, Issue:1

    Topics: Angiogenesis Inhibitors; Animals; Colorectal Neoplasms; Contrast Media; Disease Models, Animal; Huma

2013
Mechanism of enhancement of radiation-induced cytotoxicity by sorafenib in colorectal cancer.
    Journal of radiation research, 2013, Volume: 54, Issue:1

    Topics: Animals; Antineoplastic Agents; Cell Survival; Chemoradiotherapy; Colorectal Neoplasms; Dose-Respons

2013
Single-agent therapy with sorafenib or 5-FU is equally effective in human colorectal cancer xenograft--no benefit of combination therapy.
    International journal of colorectal disease, 2013, Volume: 28, Issue:3

    Topics: Animals; Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Blotting, Western; Caspases; Cel

2013
Sorafenib inhibits p38α activity in colorectal cancer cells and synergizes with the DFG-in inhibitor SB202190 to increase apoptotic response.
    Cancer biology & therapy, 2012, Volume: 13, Issue:14

    Topics: Animals; Apoptosis; Caspase 3; Cell Line, Tumor; Colorectal Neoplasms; Drug Synergism; Female; Human

2012
ASCO 2007: plenary top 5.
    Oncology (Williston Park, N.Y.), 2007, Volume: 21, Issue:7

    Topics: Antineoplastic Agents; Benzenesulfonates; Carcinoma, Hepatocellular; Carcinoma, Renal Cell; Carcinom

2007
Cell cycle dependent and schedule-dependent antitumor effects of sorafenib combined with radiation.
    Cancer research, 2007, Oct-01, Volume: 67, Issue:19

    Topics: Animals; Antineoplastic Agents; Benzenesulfonates; Cell Division; Cell Growth Processes; Colorectal

2007
Magnetic resonance detects metabolic changes associated with chemotherapy-induced apoptosis.
    British journal of cancer, 1999, Volume: 80, Issue:7

    Topics: Animals; Antineoplastic Agents; Apoptosis; Benzamides; Caspases; Cell Survival; Colorectal Neoplasms

1999