vorinostat has been researched along with Colorectal Cancer in 28 studies
Vorinostat: A hydroxamic acid and anilide derivative that acts as a HISTONE DEACETYLASE inhibitor. It is used in the treatment of CUTANEOUS T-CELL LYMPHOMA and SEZARY SYNDROME.
vorinostat : A dicarboxylic acid diamide comprising suberic (octanedioic) acid coupled to aniline and hydroxylamine. A histone deacetylase inhibitor, it is marketed under the name Zolinza for the treatment of cutaneous T cell lymphoma (CTCL).
| Excerpt | Relevance | Reference |
|---|---|---|
| "In metastatic colorectal cancer (mCRC), regorafenib (RGF), a multi-kinase inhibitor with angiogenic inhibition has modest effects on survival." | 9.51 | Modulation of autophagy: a Phase II study of vorinostat plus hydroxychloroquine versus regorafenib in chemotherapy-refractory metastatic colorectal cancer (mCRC). ( Arora, SP; Curiel, T; Liu, Q; Mahalingam, D; Mendez, JA; Michalek, J; Morris, J; Sarantopoulos, J; Tenner, L, 2022) |
| "Patients with refractory metastatic colorectal cancer were randomized in a two-stage design to receive vorinostat at 800 or 1,400 mg/day once a day × 3, every 2 weeks." | 9.16 | A randomized phase II study of two doses of vorinostat in combination with 5-FU/LV in patients with refractory colorectal cancer. ( Fakih, MG; Groman, A; McMahon, J; Muindi, JR; Wilding, G, 2012) |
| "We conducted a phase I/II clinical trial to determine the safety and feasibility of combining vorinostat with 5-fluorouracil (5-FU) in patients with metastatic colorectal cancer (mCRC) and elevated intratumoral thymidylate synthase (TS)." | 9.14 | A phase I/II trial of vorinostat in combination with 5-fluorouracil in patients with metastatic colorectal cancer who previously failed 5-FU-based chemotherapy. ( Cole, S; Danenberg, KD; El-Khoueiry, A; Fazzone, W; Groshen, S; Iqbal, S; Kornacki, M; LaBonte, MJ; Ladner, RD; Lenz, HJ; Wilson, PM; Yang, D, 2010) |
| "Hydroxychloroquine (HCQ) enhances the anti-cancer activity of the histone deacetylase inhibitor, vorinostat (VOR), in pre-clinical models and early phase clinical studies of metastatic colorectal cancer (mCRC)." | 7.83 | Vorinostat and hydroxychloroquine improve immunity and inhibit autophagy in metastatic colorectal cancer. ( Curiel, T; Goros, M; Hurez, V; Mahalingam, D; Michalek, J; Nawrocki, ST; Patel, S; Sarantopoulos, J, 2016) |
| "Radiosensitization by vorinostat under hypoxia was studied in four colorectal carcinoma cell lines and in one colorectal carcinoma xenograft model by analysis of clonogenic survival and tumor growth delay, respectively." | 7.78 | Radiosensitization by the histone deacetylase inhibitor vorinostat under hypoxia and with capecitabine in experimental colorectal carcinoma. ( Flatmark, K; Fleten, KG; Furre, T; Hektoen, HH; Kristian, A; Ree, AH; Saelen, MG, 2012) |
| "Vorinostat was given orally twice daily for 1 week every 2 weeks." | 6.74 | A phase I, pharmacokinetic and pharmacodynamic study on vorinostat in combination with 5-fluorouracil, leucovorin, and oxaliplatin in patients with refractory colorectal cancer. ( Egorin, MJ; Espinoza-Delgado, I; Fakih, MG; Fetterly, G; Holleran, JL; Litwin, A; Pendyala, L; Ross, ME; Rustum, YM; Toth, K; Zwiebel, JA, 2009) |
| "In metastatic colorectal cancer (mCRC), regorafenib (RGF), a multi-kinase inhibitor with angiogenic inhibition has modest effects on survival." | 5.51 | Modulation of autophagy: a Phase II study of vorinostat plus hydroxychloroquine versus regorafenib in chemotherapy-refractory metastatic colorectal cancer (mCRC). ( Arora, SP; Curiel, T; Liu, Q; Mahalingam, D; Mendez, JA; Michalek, J; Morris, J; Sarantopoulos, J; Tenner, L, 2022) |
| "Despite compelling preclinical data in colorectal cancer (CRC), the efficacy of HDACIs has been disappointing in the clinic." | 5.39 | Sustained inhibition of deacetylases is required for the antitumor activity of the histone deactylase inhibitors panobinostat and vorinostat in models of colorectal cancer. ( El-Khoueiry, A; Kuwahara, ST; Labonte, MJ; Ladner, RD; Lenz, HJ; Martin, SC; Wilson, PM, 2013) |
| "Patients with refractory metastatic colorectal cancer were randomized in a two-stage design to receive vorinostat at 800 or 1,400 mg/day once a day × 3, every 2 weeks." | 5.16 | A randomized phase II study of two doses of vorinostat in combination with 5-FU/LV in patients with refractory colorectal cancer. ( Fakih, MG; Groman, A; McMahon, J; Muindi, JR; Wilding, G, 2012) |
| "We conducted a phase I/II clinical trial to determine the safety and feasibility of combining vorinostat with 5-fluorouracil (5-FU) in patients with metastatic colorectal cancer (mCRC) and elevated intratumoral thymidylate synthase (TS)." | 5.14 | A phase I/II trial of vorinostat in combination with 5-fluorouracil in patients with metastatic colorectal cancer who previously failed 5-FU-based chemotherapy. ( Cole, S; Danenberg, KD; El-Khoueiry, A; Fazzone, W; Groshen, S; Iqbal, S; Kornacki, M; LaBonte, MJ; Ladner, RD; Lenz, HJ; Wilson, PM; Yang, D, 2010) |
| "Human intestinal peptide transporter PEPT1 is commonly repressed in human colorectal cancer (CRC), yet its relationship with sensitivity to the common CRC treatment ubenimex has not previously been elucidated." | 4.02 | Epigenetic regulation of intestinal peptide transporter PEPT1 as a potential strategy for colorectal cancer sensitization. ( Hua, Y; Qiu, L; Wang, J; Wang, Y; Wu, S; Yang, L; Yu, L; Zeng, S; Zheng, X, 2021) |
| "Hydroxychloroquine (HCQ) enhances the anti-cancer activity of the histone deacetylase inhibitor, vorinostat (VOR), in pre-clinical models and early phase clinical studies of metastatic colorectal cancer (mCRC)." | 3.83 | Vorinostat and hydroxychloroquine improve immunity and inhibit autophagy in metastatic colorectal cancer. ( Curiel, T; Goros, M; Hurez, V; Mahalingam, D; Michalek, J; Nawrocki, ST; Patel, S; Sarantopoulos, J, 2016) |
| " Here we demonstrate that histone deacetylase (HDAC) inhibitors (Trichostatin A, SAHA and sodium butyrate) promote TTP expression in colorectal cancer cells (HCA-7, HCT-116, Moser and SW480 cells) and cervix carcinoma cells (HeLa)." | 3.81 | Histone Deacetylase Inhibitors Activate Tristetraprolin Expression through Induction of Early Growth Response Protein 1 (EGR1) in Colorectal Cancer Cells. ( Blanco, FF; Dixon, DA; Hu, L; Sanduja, S; Sobolewski, C, 2015) |
| "Radiosensitization by vorinostat under hypoxia was studied in four colorectal carcinoma cell lines and in one colorectal carcinoma xenograft model by analysis of clonogenic survival and tumor growth delay, respectively." | 3.78 | Radiosensitization by the histone deacetylase inhibitor vorinostat under hypoxia and with capecitabine in experimental colorectal carcinoma. ( Flatmark, K; Fleten, KG; Furre, T; Hektoen, HH; Kristian, A; Ree, AH; Saelen, MG, 2012) |
| "Vorinostat doses were escalated in a standard 3 x 3 phase I design." | 2.75 | A phase I, pharmacokinetic, and pharmacodynamic study of two schedules of vorinostat in combination with 5-fluorouracil and leucovorin in patients with refractory solid tumors. ( Diasio, RB; Egorin, MJ; Espinoza-Delgado, I; Fakih, MG; Fetterly, G; Holleran, JL; Litwin, A; Muindi, JR; Wang, K; Zwiebel, JA, 2010) |
| "Vorinostat was given orally twice daily for 1 week every 2 weeks." | 2.74 | A phase I, pharmacokinetic and pharmacodynamic study on vorinostat in combination with 5-fluorouracil, leucovorin, and oxaliplatin in patients with refractory colorectal cancer. ( Egorin, MJ; Espinoza-Delgado, I; Fakih, MG; Fetterly, G; Holleran, JL; Litwin, A; Pendyala, L; Ross, ME; Rustum, YM; Toth, K; Zwiebel, JA, 2009) |
| "Vorinostat (Zolinza) is a histone deacetylase inhibitor that has demonstrated activity in patients with advanced solid tumors in phase I trials." | 2.73 | Early phase II trial of oral vorinostat in relapsed or refractory breast, colorectal, or non-small cell lung cancer. ( Chen, C; Dumez, H; Randolph, SS; Ricker, JL; Schöffski, P; Van Cutsem, E; Vansteenkiste, J, 2008) |
| "Vorinostat was the first drug of this group used in clinical trial in combination with conventional chemotherapy and managed to stabilize advanced colorectal cancer." | 2.50 | Histone deacetylase inhibitors and colorectal cancer: what is new? ( Kouraklis, G; Nebiker, CA; Tampaki, EC; Tampakis, A, 2014) |
| "Despite compelling preclinical data in colorectal cancer (CRC), the efficacy of HDACIs has been disappointing in the clinic." | 1.39 | Sustained inhibition of deacetylases is required for the antitumor activity of the histone deactylase inhibitors panobinostat and vorinostat in models of colorectal cancer. ( El-Khoueiry, A; Kuwahara, ST; Labonte, MJ; Ladner, RD; Lenz, HJ; Martin, SC; Wilson, PM, 2013) |
| "The expression of HDACs in colorectal cancer specimens and the effects of SAHA on colon cancer cells and tumors of nude mice were assessed." | 1.38 | SAHA inhibits the growth of colon tumors by decreasing histone deacetylase and the expression of cyclin D1 and survivin. ( Jin, JS; Sun, PC; Tsao, TY; Tzao, C; Yu, CP, 2012) |
| " It has very favorable pharmacokinetic properties after oral dosing in mice, with >4-fold increased bioavailability and 3." | 1.36 | SB939, a novel potent and orally active histone deacetylase inhibitor with high tumor exposure and efficacy in mouse models of colorectal cancer. ( Bonday, Z; Ethirajulu, K; Goh, KC; Greicius, G; Hart, S; Hentze, H; Hu, CY; Liang, AL; Loh, YK; Novotny-Diermayr, V; Pettersson, S; Sangthongpitag, K; Sausgruber, N; Wang, H; Wood, JM; Wu, X; Yeo, P, 2010) |
| " Moreover, in combination with 5-fluorouracil modulated by folinic acid (5FU-FA) or with Raltitrexed (RTX), both commonly used in the treatment of this disease, it showed a clear schedule-dependent synergistic antiproliferative interaction as demonstrated by calculating combination indexes." | 1.35 | Modulation of thymidilate synthase and p53 expression by HDAC inhibitor vorinostat resulted in synergistic antitumor effect in combination with 5FU or raltitrexed. ( Avallone, A; Bruzzese, F; Budillon, A; Delrio, P; Di Gennaro, E; Leone, A; Pepe, S; Subbarayan, PR, 2009) |
| "MMR-deficient colorectal cancers are classically characterized by right-sided location, multifocality, mucinous histology, and lymphocytic infiltration." | 1.35 | Epigenetic repression of DNA mismatch repair by inflammation and hypoxia in inflammatory bowel disease-associated colorectal cancer. ( Afrasiabi, K; Birnbaumer, L; Edwards, RA; Lipkin, SM; Pham, T; Wang, K; Witherspoon, M, 2009) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 0 (0.00) | 18.7374 |
| 1990's | 0 (0.00) | 18.2507 |
| 2000's | 7 (25.00) | 29.6817 |
| 2010's | 17 (60.71) | 24.3611 |
| 2020's | 4 (14.29) | 2.80 |
| Authors | Studies |
|---|---|
| Ling, Y | 1 |
| Xu, C | 1 |
| Luo, L | 1 |
| Cao, J | 1 |
| Feng, J | 1 |
| Xue, Y | 1 |
| Zhu, Q | 1 |
| Ju, C | 1 |
| Li, F | 1 |
| Zhang, Y | 3 |
| Ling, X | 1 |
| Li, X | 2 |
| Jiang, Y | 1 |
| Wu, J | 1 |
| Inks, ES | 1 |
| Chou, CJ | 1 |
| Gao, S | 1 |
| Hou, J | 1 |
| Ding, Q | 1 |
| Li, J | 1 |
| Wang, X | 1 |
| Huang, Y | 1 |
| Xu, W | 1 |
| Pan, Z | 1 |
| Wang, Y | 2 |
| Jiang, Q | 1 |
| Jiang, L | 1 |
| Zhang, M | 1 |
| Zhang, N | 1 |
| Wu, F | 1 |
| Liu, B | 1 |
| He, G | 1 |
| Tanaka, S | 1 |
| Hosokawa, M | 1 |
| Tatsumi, A | 1 |
| Asaumi, S | 1 |
| Imai, R | 1 |
| Ogawara, KI | 1 |
| Arora, SP | 1 |
| Tenner, L | 1 |
| Sarantopoulos, J | 2 |
| Morris, J | 1 |
| Liu, Q | 1 |
| Mendez, JA | 1 |
| Curiel, T | 2 |
| Michalek, J | 2 |
| Mahalingam, D | 2 |
| Wang, J | 1 |
| Yang, L | 1 |
| Qiu, L | 1 |
| Hua, Y | 1 |
| Wu, S | 1 |
| Zeng, S | 1 |
| Yu, L | 1 |
| Zheng, X | 1 |
| Li, Q | 1 |
| Ding, C | 1 |
| Meng, T | 1 |
| Lu, W | 1 |
| Liu, W | 1 |
| Hao, H | 1 |
| Cao, L | 1 |
| Fatemi, M | 1 |
| Paul, TA | 1 |
| Brodeur, GM | 1 |
| Shokrani, B | 1 |
| Brim, H | 1 |
| Ashktorab, H | 1 |
| Tampakis, A | 1 |
| Tampaki, EC | 1 |
| Nebiker, CA | 1 |
| Kouraklis, G | 1 |
| Sobolewski, C | 1 |
| Sanduja, S | 1 |
| Blanco, FF | 1 |
| Hu, L | 1 |
| Dixon, DA | 1 |
| Alzoubi, S | 1 |
| Brody, L | 1 |
| Rahman, S | 1 |
| Mahul-Mellier, AL | 1 |
| Mercado, N | 1 |
| Ito, K | 1 |
| El-Bahrawy, M | 1 |
| Silver, A | 1 |
| Boobis, A | 1 |
| Bell, JD | 1 |
| Hajji, N | 1 |
| Patel, S | 1 |
| Hurez, V | 1 |
| Nawrocki, ST | 1 |
| Goros, M | 1 |
| Di Gennaro, E | 1 |
| Bruzzese, F | 1 |
| Pepe, S | 1 |
| Leone, A | 1 |
| Delrio, P | 1 |
| Subbarayan, PR | 1 |
| Avallone, A | 1 |
| Budillon, A | 1 |
| Dedes, KJ | 1 |
| Dedes, I | 1 |
| Imesch, P | 1 |
| von Bueren, AO | 1 |
| Fink, D | 1 |
| Fedier, A | 1 |
| Fakih, MG | 3 |
| Pendyala, L | 1 |
| Fetterly, G | 2 |
| Toth, K | 1 |
| Zwiebel, JA | 2 |
| Espinoza-Delgado, I | 2 |
| Litwin, A | 2 |
| Rustum, YM | 1 |
| Ross, ME | 1 |
| Holleran, JL | 2 |
| Egorin, MJ | 2 |
| Folkvord, S | 1 |
| Ree, AH | 2 |
| Furre, T | 2 |
| Halvorsen, T | 1 |
| Flatmark, K | 2 |
| Edwards, RA | 1 |
| Witherspoon, M | 1 |
| Wang, K | 2 |
| Afrasiabi, K | 1 |
| Pham, T | 1 |
| Birnbaumer, L | 1 |
| Lipkin, SM | 1 |
| Wilson, PM | 2 |
| El-Khoueiry, A | 2 |
| Iqbal, S | 1 |
| Fazzone, W | 1 |
| LaBonte, MJ | 2 |
| Groshen, S | 1 |
| Yang, D | 1 |
| Danenberg, KD | 1 |
| Cole, S | 1 |
| Kornacki, M | 1 |
| Ladner, RD | 2 |
| Lenz, HJ | 2 |
| Novotny-Diermayr, V | 1 |
| Sangthongpitag, K | 1 |
| Hu, CY | 1 |
| Wu, X | 1 |
| Sausgruber, N | 1 |
| Yeo, P | 1 |
| Greicius, G | 1 |
| Pettersson, S | 1 |
| Liang, AL | 1 |
| Loh, YK | 1 |
| Bonday, Z | 1 |
| Goh, KC | 1 |
| Hentze, H | 1 |
| Hart, S | 1 |
| Wang, H | 1 |
| Ethirajulu, K | 1 |
| Wood, JM | 1 |
| Muindi, JR | 2 |
| Diasio, RB | 1 |
| Groman, A | 1 |
| McMahon, J | 1 |
| Wilding, G | 1 |
| Morelli, MP | 1 |
| Tentler, JJ | 1 |
| Kulikowski, GN | 1 |
| Tan, AC | 1 |
| Bradshaw-Pierce, EL | 1 |
| Pitts, TM | 1 |
| Brown, AM | 1 |
| Nallapareddy, S | 1 |
| Arcaroli, JJ | 1 |
| Serkova, NJ | 1 |
| Hidalgo, M | 1 |
| Ciardiello, F | 1 |
| Eckhardt, SG | 1 |
| Jin, JS | 1 |
| Tsao, TY | 1 |
| Sun, PC | 1 |
| Yu, CP | 1 |
| Tzao, C | 1 |
| Humphreys, KJ | 1 |
| Cobiac, L | 1 |
| Le Leu, RK | 1 |
| Van der Hoek, MB | 1 |
| Michael, MZ | 1 |
| Saelen, MG | 1 |
| Kristian, A | 1 |
| Fleten, KG | 1 |
| Hektoen, HH | 1 |
| Martin, SC | 1 |
| Kuwahara, ST | 1 |
| Hsi, LC | 1 |
| Xi, X | 1 |
| Lotan, R | 1 |
| Shureiqi, I | 1 |
| Lippman, SM | 1 |
| Vansteenkiste, J | 1 |
| Van Cutsem, E | 1 |
| Dumez, H | 1 |
| Chen, C | 1 |
| Ricker, JL | 1 |
| Randolph, SS | 1 |
| Schöffski, P | 1 |
| Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
|---|---|---|---|---|---|---|---|
| Modulation of Autophagy: A Clinical Study of Vorinostat Plus Hydroxychloroquine Versus Regorafenib in Refractory Metastatic Colorectal Cancer (mCRC) Patients (CTMS# 14-2015)[NCT02316340] | Phase 2 | 44 participants (Actual) | Interventional | 2015-02-11 | Completed | ||
| A Phase II Clinical Study of Oral Suberoylanilide Hydroxamic Acid in Patients With Relapsed or Refractory Breast, Colorectal, and Non-small Cell Lung Cancer.[NCT00126451] | Phase 2 | 16 participants (Actual) | Interventional | 2004-12-01 | Terminated | ||
| [information is prepared from clinicaltrials.gov, extracted Sep-2024] | |||||||
1 review available for vorinostat and Colorectal Cancer
| Article | Year |
|---|---|
Histone deacetylase inhibitors and colorectal cancer: what is new?
Topics: Antineoplastic Agents; Azacitidine; Colorectal Neoplasms; Combined Modality Therapy; Decitabine; His | 2014 |
6 trials available for vorinostat and Colorectal Cancer
| Article | Year |
|---|---|
Modulation of autophagy: a Phase II study of vorinostat plus hydroxychloroquine versus regorafenib in chemotherapy-refractory metastatic colorectal cancer (mCRC).
Topics: Antineoplastic Combined Chemotherapy Protocols; Autophagy; Colorectal Neoplasms; Humans; Hydroxychlo | 2022 |
A phase I, pharmacokinetic and pharmacodynamic study on vorinostat in combination with 5-fluorouracil, leucovorin, and oxaliplatin in patients with refractory colorectal cancer.
Topics: Adenocarcinoma; Adult; Aged; Antineoplastic Combined Chemotherapy Protocols; Cohort Studies; Colorec | 2009 |
A phase I/II trial of vorinostat in combination with 5-fluorouracil in patients with metastatic colorectal cancer who previously failed 5-FU-based chemotherapy.
Topics: Adult; Aged; Antineoplastic Combined Chemotherapy Protocols; Colorectal Neoplasms; Dose-Response Rel | 2010 |
A phase I, pharmacokinetic, and pharmacodynamic study of two schedules of vorinostat in combination with 5-fluorouracil and leucovorin in patients with refractory solid tumors.
Topics: Administration, Oral; Adult; Aged; Antineoplastic Combined Chemotherapy Protocols; Colorectal Neopla | 2010 |
A randomized phase II study of two doses of vorinostat in combination with 5-FU/LV in patients with refractory colorectal cancer.
Topics: Administration, Oral; Adult; Aged; Aged, 80 and over; Antineoplastic Combined Chemotherapy Protocols | 2012 |
Early phase II trial of oral vorinostat in relapsed or refractory breast, colorectal, or non-small cell lung cancer.
Topics: Administration, Oral; Adult; Aged; Breast Neoplasms; Carcinoma, Non-Small-Cell Lung; Colorectal Neop | 2008 |
21 other studies available for vorinostat and Colorectal Cancer
| Article | Year |
|---|---|
Novel β-Carboline/Hydroxamic Acid Hybrids Targeting Both Histone Deacetylase and DNA Display High Anticancer Activity via Regulation of the p53 Signaling Pathway.
Topics: Acetylation; Animals; Antineoplastic Agents; Apoptosis; Carbolines; Cell Proliferation; Colon; Color | 2015 |
Selective HDAC inhibitors with potent oral activity against leukemia and colorectal cancer: Design, structure-activity relationship and anti-tumor activity study.
Topics: Animals; Antineoplastic Agents; Benzamides; Cell Proliferation; Colon; Colorectal Neoplasms; HCT116 | 2017 |
Discovery of Thieno[2,3-
Topics: Animals; Antineoplastic Agents; Apoptosis; Autophagy; Cell Cycle Proteins; Cell Line, Tumor; Cell Pr | 2020 |
Improvement of resistance to oxaliplatin by vorinostat in human colorectal cancer cells through inhibition of Nrf2 nuclear translocation.
Topics: Antineoplastic Agents; Cell Line, Tumor; Colorectal Neoplasms; Drug Resistance, Neoplasm; Humans; Ke | 2022 |
Epigenetic regulation of intestinal peptide transporter PEPT1 as a potential strategy for colorectal cancer sensitization.
Topics: Animals; Antineoplastic Combined Chemotherapy Protocols; Cell Line, Tumor; Colorectal Neoplasms; DNA | 2021 |
Butyrate suppresses motility of colorectal cancer cells via deactivating Akt/ERK signaling in histone deacetylase dependent manner.
Topics: Butyrates; Cell Line, Tumor; Cell Movement; Colorectal Neoplasms; Histone Deacetylase Inhibitors; Hi | 2017 |
Epigenetic silencing of CHD5, a novel tumor-suppressor gene, occurs in early colorectal cancer stages.
Topics: Adenoma; Azacitidine; Black or African American; Cell Line, Tumor; Cell Movement; Cell Proliferation | 2014 |
Histone Deacetylase Inhibitors Activate Tristetraprolin Expression through Induction of Early Growth Response Protein 1 (EGR1) in Colorectal Cancer Cells.
Topics: Butyric Acid; Cell Line, Tumor; Colorectal Neoplasms; Cyclooxygenase 2; Early Growth Response Protei | 2015 |
Synergy between histone deacetylase inhibitors and DNA-damaging agents is mediated by histone deacetylase 2 in colorectal cancer.
Topics: Acetylation; Animals; Antineoplastic Agents; Cell Line, Tumor; Colorectal Neoplasms; Drug Synergism; | 2016 |
Vorinostat and hydroxychloroquine improve immunity and inhibit autophagy in metastatic colorectal cancer.
Topics: Adult; Aged; Antineoplastic Agents; Antineoplastic Combined Chemotherapy Protocols; Autophagy; Color | 2016 |
Modulation of thymidilate synthase and p53 expression by HDAC inhibitor vorinostat resulted in synergistic antitumor effect in combination with 5FU or raltitrexed.
Topics: Antineoplastic Combined Chemotherapy Protocols; Cell Growth Processes; Cell Line, Tumor; Colorectal | 2009 |
Acquired vorinostat resistance shows partial cross-resistance to 'second-generation' HDAC inhibitors and correlates with loss of histone acetylation and apoptosis but not with altered HDAC and HAT activities.
Topics: Acetylation; Adenocarcinoma; Antineoplastic Agents; Apoptosis; Benzamides; Cell Line, Tumor; Colorec | 2009 |
Radiosensitization by SAHA in experimental colorectal carcinoma models-in vivo effects and relevance of histone acetylation status.
Topics: Acetylation; Animals; Colorectal Neoplasms; Enzyme Inhibitors; Female; HCT116 Cells; Histone Deacety | 2009 |
Epigenetic repression of DNA mismatch repair by inflammation and hypoxia in inflammatory bowel disease-associated colorectal cancer.
Topics: Adaptor Proteins, Signal Transducing; Adenoma; Adenosine Triphosphatases; Animals; Cell Hypoxia; Col | 2009 |
SB939, a novel potent and orally active histone deacetylase inhibitor with high tumor exposure and efficacy in mouse models of colorectal cancer.
Topics: Administration, Oral; Animals; Antineoplastic Agents; Biological Availability; Colorectal Neoplasms; | 2010 |
Preclinical activity of the rational combination of selumetinib (AZD6244) in combination with vorinostat in KRAS-mutant colorectal cancer models.
Topics: Animals; Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Benzimidazoles; Cell Cycle; Cell | 2012 |
SAHA inhibits the growth of colon tumors by decreasing histone deacetylase and the expression of cyclin D1 and survivin.
Topics: Adenocarcinoma; Animals; Blotting, Western; Colorectal Neoplasms; Cyclin D1; Female; Histone Deacety | 2012 |
Histone deacetylase inhibition in colorectal cancer cells reveals competing roles for members of the oncogenic miR-17-92 cluster.
Topics: Adaptor Proteins, Signal Transducing; Adenocarcinoma; Apoptosis Regulatory Proteins; Bcl-2-Like Prot | 2013 |
Radiosensitization by the histone deacetylase inhibitor vorinostat under hypoxia and with capecitabine in experimental colorectal carcinoma.
Topics: Animals; Antineoplastic Combined Chemotherapy Protocols; Capecitabine; Colorectal Neoplasms; Deoxycy | 2012 |
Sustained inhibition of deacetylases is required for the antitumor activity of the histone deactylase inhibitors panobinostat and vorinostat in models of colorectal cancer.
Topics: Acetylation; Animals; Antineoplastic Agents; Blotting, Western; Cell Line, Tumor; Cell Proliferation | 2013 |
The histone deacetylase inhibitor suberoylanilide hydroxamic acid induces apoptosis via induction of 15-lipoxygenase-1 in colorectal cancer cells.
Topics: Antineoplastic Agents; Apoptosis; Arachidonate 15-Lipoxygenase; Cell Growth Processes; Cell Line, Tu | 2004 |