vorinostat has been researched along with Carcinoma, Anaplastic in 17 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 |
|---|---|---|
| "Marked synergy of marizomib and vorinostat was seen in tumor cell lines derived from patients with NSCLC, melanoma and pancreatic carcinoma." | 9.16 | Phase 1 clinical trial of the novel proteasome inhibitor marizomib with the histone deacetylase inhibitor vorinostat in patients with melanoma, pancreatic and lung cancer based on in vitro assessments of the combination. ( Drabkin, HA; Gemmill, RM; Lay, A; Lee, L; Lloyd, GK; Longenecker, A; McConkey, DJ; Millward, M; Neuteboom, ST; Palladino, MA; Price, T; Sharma, G; Spear, MA; Spencer, A; Sukumaran, S; Sweeney, C; Townsend, A, 2012) |
| "This multi-institutional phase II trial assessed the activity and toxicity of a new histone deacetylase inhibitor, vorinostat (suberoylanilide hydroxamic acid--SAHA) in patients with recurrent or persistent epithelial ovarian or primary peritoneal carcinoma." | 9.13 | A phase II study of vorinostat in the treatment of persistent or recurrent epithelial ovarian or primary peritoneal carcinoma: a Gynecologic Oncology Group study. ( Bender, DP; Hoffman, JS; Modesitt, SC; Sill, M, 2008) |
| "A novel drug combination of a proteasome inhibitor, bortezomib, and a histone deacetylase inhibitor, suberoylanilide hydroxamic acid (SAHA), was tested in nasopharyngeal carcinoma (NPC), both in vitro and in vivo." | 7.79 | Bortezomib and SAHA synergistically induce ROS-driven caspase-dependent apoptosis of nasopharyngeal carcinoma and block replication of Epstein-Barr virus. ( Chiang, AK; Ho, DN; Hui, KF; Lam, BH; Tsao, SW, 2013) |
| "Marked synergy of marizomib and vorinostat was seen in tumor cell lines derived from patients with NSCLC, melanoma and pancreatic carcinoma." | 5.16 | Phase 1 clinical trial of the novel proteasome inhibitor marizomib with the histone deacetylase inhibitor vorinostat in patients with melanoma, pancreatic and lung cancer based on in vitro assessments of the combination. ( Drabkin, HA; Gemmill, RM; Lay, A; Lee, L; Lloyd, GK; Longenecker, A; McConkey, DJ; Millward, M; Neuteboom, ST; Palladino, MA; Price, T; Sharma, G; Spear, MA; Spencer, A; Sukumaran, S; Sweeney, C; Townsend, A, 2012) |
| "This multi-institutional phase II trial assessed the activity and toxicity of a new histone deacetylase inhibitor, vorinostat (suberoylanilide hydroxamic acid--SAHA) in patients with recurrent or persistent epithelial ovarian or primary peritoneal carcinoma." | 5.13 | A phase II study of vorinostat in the treatment of persistent or recurrent epithelial ovarian or primary peritoneal carcinoma: a Gynecologic Oncology Group study. ( Bender, DP; Hoffman, JS; Modesitt, SC; Sill, M, 2008) |
| "A novel drug combination of a proteasome inhibitor, bortezomib, and a histone deacetylase inhibitor, suberoylanilide hydroxamic acid (SAHA), was tested in nasopharyngeal carcinoma (NPC), both in vitro and in vivo." | 3.79 | Bortezomib and SAHA synergistically induce ROS-driven caspase-dependent apoptosis of nasopharyngeal carcinoma and block replication of Epstein-Barr virus. ( Chiang, AK; Ho, DN; Hui, KF; Lam, BH; Tsao, SW, 2013) |
| " We found that 4 histone deacetylase inhibitors, trichostatin A (TSA), sodium butyrate (SB), valproic acid (VPA) and suberoylanilide hydroxamic acid (SAHA), all significantly induced EBV lytic cycle in EBV-positive gastric carcinoma cells (AGS/BX1, latency II) but only weakly induced in Burkitt lymphoma cells (AK2003, latency I) and did not induce in lymphoblastoid cells (LCLs, latency III)." | 3.76 | Suberoylanilide hydroxamic acid induces viral lytic cycle in Epstein-Barr virus-positive epithelial malignancies and mediates enhanced cell death. ( Chiang, AK; Hui, KF, 2010) |
| "Treatment with vorinostat, a histone deacetylase inhibitor (HDACi) resulted in an objective response, yet she died in less than one year from initial diagnosis." | 1.42 | Histone deacetylase inhibitor for NUT midline carcinoma. ( Bell, D; Christensen, AM; Maher, OM; Tarek, N; Yedururi, S, 2015) |
| "In an in vivo tumor carcinomatosis model, the growth of transplanted SKOV-3 cells was inhibited by 71% after treatment with MHY218 (10 mg/kg), whereas SAHA (25 mg/kg) suppressed growth by 48%." | 1.36 | Anticancer effects of the MHY218 novel hydroxamic acid-derived histone deacetylase inhibitor in human ovarian cancer cells. ( Ahn, MY; Chun, P; Jeon, HS; Jung, JH; Kim, HS; Kim, J; Kim, TH; Kim, WH; Moon, HR; Park, JH, 2010) |
| "In most patients with ovarian cancer, diagnosis occurs after the tumour has disseminated beyond the ovaries." | 1.33 | Comparative evaluation of the treatment efficacy of suberoylanilide hydroxamic acid (SAHA) and paclitaxel in ovarian cancer cell lines and primary ovarian cancer cells from patients. ( Beck, JF; Belau, A; Gänge, J; Lorenz, G; Ohlinger, R; Pilz, S; Sonnemann, J; Stötzer, C, 2006) |
| "Murine erythroleukemia cells developed for resistance to SAHA are cross-resistant to trichostatin A, a known deacetylase inhibitor and differentiation inducer, but are not cross-resistant to HMBA." | 1.30 | A class of hybrid polar inducers of transformed cell differentiation inhibits histone deacetylases. ( Breslow, R; Emiliani, S; Marks, PA; Richon, VM; Rifkind, RA; Verdin, E; Webb, Y, 1998) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 0 (0.00) | 18.7374 |
| 1990's | 1 (5.88) | 18.2507 |
| 2000's | 6 (35.29) | 29.6817 |
| 2010's | 10 (58.82) | 24.3611 |
| 2020's | 0 (0.00) | 2.80 |
| Authors | Studies |
|---|---|
| Jiao, J | 1 |
| Fang, H | 1 |
| Wang, X | 1 |
| Guan, P | 1 |
| Yuan, Y | 1 |
| Xu, W | 1 |
| Hui, KF | 3 |
| Lam, BH | 1 |
| Ho, DN | 2 |
| Tsao, SW | 1 |
| Chiang, AK | 3 |
| Maher, OM | 1 |
| Christensen, AM | 1 |
| Yedururi, S | 1 |
| Bell, D | 1 |
| Tarek, N | 1 |
| Carew, JS | 1 |
| Medina, EC | 1 |
| Esquivel, JA | 1 |
| Mahalingam, D | 1 |
| Swords, R | 1 |
| Kelly, K | 1 |
| Zhang, H | 1 |
| Huang, P | 1 |
| Mita, AC | 1 |
| Mita, MM | 1 |
| Giles, FJ | 1 |
| Nawrocki, ST | 1 |
| Palmieri, D | 1 |
| Lockman, PR | 1 |
| Thomas, FC | 1 |
| Hua, E | 1 |
| Herring, J | 1 |
| Hargrave, E | 1 |
| Johnson, M | 1 |
| Flores, N | 1 |
| Qian, Y | 1 |
| Vega-Valle, E | 1 |
| Taskar, KS | 1 |
| Rudraraju, V | 1 |
| Mittapalli, RK | 1 |
| Gaasch, JA | 1 |
| Bohn, KA | 1 |
| Thorsheim, HR | 1 |
| Liewehr, DJ | 1 |
| Davis, S | 1 |
| Reilly, JF | 1 |
| Walker, R | 1 |
| Bronder, JL | 1 |
| Feigenbaum, L | 1 |
| Steinberg, SM | 1 |
| Camphausen, K | 1 |
| Meltzer, PS | 1 |
| Richon, VM | 3 |
| Smith, QR | 1 |
| Steeg, PS | 1 |
| Borbone, E | 1 |
| Berlingieri, MT | 1 |
| De Bellis, F | 1 |
| Nebbioso, A | 1 |
| Chiappetta, G | 1 |
| Mai, A | 1 |
| Altucci, L | 1 |
| Fusco, A | 1 |
| Jeon, HS | 1 |
| Ahn, MY | 1 |
| Park, JH | 1 |
| Kim, TH | 1 |
| Chun, P | 1 |
| Kim, WH | 1 |
| Kim, J | 1 |
| Moon, HR | 1 |
| Jung, JH | 1 |
| Kim, HS | 1 |
| Li, X | 1 |
| Kaplun, A | 1 |
| Lonardo, F | 1 |
| Heath, E | 1 |
| Sarkar, FH | 1 |
| Irish, J | 1 |
| Sakr, W | 1 |
| Sheng, S | 1 |
| Millward, M | 1 |
| Price, T | 1 |
| Townsend, A | 1 |
| Sweeney, C | 1 |
| Spencer, A | 1 |
| Sukumaran, S | 1 |
| Longenecker, A | 1 |
| Lee, L | 1 |
| Lay, A | 1 |
| Sharma, G | 1 |
| Gemmill, RM | 1 |
| Drabkin, HA | 1 |
| Lloyd, GK | 1 |
| Neuteboom, ST | 1 |
| McConkey, DJ | 1 |
| Palladino, MA | 1 |
| Spear, MA | 1 |
| Tsang, CM | 1 |
| Middeldorp, JM | 1 |
| Tsao, GS | 1 |
| Dom, G | 1 |
| Galdo, VC | 1 |
| Tarabichi, M | 1 |
| Tomás, G | 1 |
| Hébrant, A | 1 |
| Andry, G | 1 |
| De Martelar, V | 1 |
| Libert, F | 1 |
| Leteurtre, E | 1 |
| Dumont, JE | 1 |
| Maenhaut, C | 1 |
| van Staveren, WC | 1 |
| Mitsiades, CS | 1 |
| Poulaki, V | 1 |
| McMullan, C | 1 |
| Negri, J | 1 |
| Fanourakis, G | 1 |
| Goudopoulou, A | 1 |
| Marks, PA | 2 |
| Mitsiades, N | 1 |
| Sonnemann, J | 1 |
| Gänge, J | 1 |
| Pilz, S | 1 |
| Stötzer, C | 1 |
| Ohlinger, R | 1 |
| Belau, A | 1 |
| Lorenz, G | 1 |
| Beck, JF | 1 |
| Luong, QT | 1 |
| O'Kelly, J | 1 |
| Braunstein, GD | 1 |
| Hershman, JM | 1 |
| Koeffler, HP | 1 |
| Modesitt, SC | 1 |
| Sill, M | 1 |
| Hoffman, JS | 1 |
| Bender, DP | 1 |
| Emiliani, S | 1 |
| Verdin, E | 1 |
| Webb, Y | 1 |
| Breslow, R | 1 |
| Rifkind, RA | 1 |
| Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
|---|---|---|---|---|---|---|---|
| A Phase I/II Study of Romidepsin in Combination With Abraxane in Patients With Metastatic Inflammatory Breast Cancer[NCT01938833] | Phase 1/Phase 2 | 9 participants (Actual) | Interventional | 2014-04-30 | Terminated (stopped due to Closed by Sponsor) | ||
| IGHID 11424 - A Pilot Trial of the Effect of Vorinostat and AGS-004 on Persistent HIV-1 Infection (The VOR VAX Study)[NCT02707900] | Phase 1 | 6 participants (Actual) | Interventional | 2016-03-31 | Terminated (stopped due to Manufacturing of the AGS-004 HIV vaccine by Argos could no longer be provided.) | ||
| [information is prepared from clinicaltrials.gov, extracted Sep-2024] | |||||||
2 trials available for vorinostat and Carcinoma, Anaplastic
| Article | Year |
|---|---|
Phase 1 clinical trial of the novel proteasome inhibitor marizomib with the histone deacetylase inhibitor vorinostat in patients with melanoma, pancreatic and lung cancer based on in vitro assessments of the combination.
Topics: Adult; Aged; Antineoplastic Agents; Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Carci | 2012 |
A phase II study of vorinostat in the treatment of persistent or recurrent epithelial ovarian or primary peritoneal carcinoma: a Gynecologic Oncology Group study.
Topics: Adult; Aged; Aged, 80 and over; Antineoplastic Agents; Carcinoma; Disease-Free Survival; Female; Gas | 2008 |
15 other studies available for vorinostat and Carcinoma, Anaplastic
| Article | Year |
|---|---|
Design, synthesis and preliminary biological evaluation of N-hydroxy-4-(3-phenylpropanamido)benzamide (HPPB) derivatives as novel histone deacetylase inhibitors.
Topics: Antineoplastic Agents; Benzamides; Carcinoma; Cell Cycle; Cell Line, Tumor; Cell Proliferation; Colo | 2009 |
Bortezomib and SAHA synergistically induce ROS-driven caspase-dependent apoptosis of nasopharyngeal carcinoma and block replication of Epstein-Barr virus.
Topics: Animals; Antineoplastic Agents; Apoptosis; Boronic Acids; Bortezomib; Carcinoma; Caspases; Cell Line | 2013 |
Histone deacetylase inhibitor for NUT midline carcinoma.
Topics: Adolescent; Carcinoma; Female; Histone Deacetylase Inhibitors; Humans; Hydroxamic Acids; Mandibular | 2015 |
Autophagy inhibition enhances vorinostat-induced apoptosis via ubiquitinated protein accumulation.
Topics: Animals; Antineoplastic Agents; Apoptosis; Autophagy; Boronic Acids; Bortezomib; Carcinoma; Cell Lin | 2010 |
Vorinostat inhibits brain metastatic colonization in a model of triple-negative breast cancer and induces DNA double-strand breaks.
Topics: Animals; Antineoplastic Agents; Biomarkers, Tumor; Blood-Brain Barrier; Brain Neoplasms; Breast Neop | 2009 |
Histone deacetylase inhibitors induce thyroid cancer-specific apoptosis through proteasome-dependent inhibition of TRAIL degradation.
Topics: Animals; Apoptosis; Benzamides; Blotting, Western; Carcinoma; Cell Line; Cell Line, Tumor; Cell Prol | 2010 |
Suberoylanilide hydroxamic acid induces viral lytic cycle in Epstein-Barr virus-positive epithelial malignancies and mediates enhanced cell death.
Topics: Antineoplastic Agents; Apoptosis; Blotting, Western; Burkitt Lymphoma; Butyrates; Carcinoma; Cell Cy | 2010 |
Anticancer effects of the MHY218 novel hydroxamic acid-derived histone deacetylase inhibitor in human ovarian cancer cells.
Topics: Antineoplastic Agents; Apoptosis; Carcinoma; Cell Proliferation; Cell Survival; Dose-Response Relati | 2010 |
HDAC1 inhibition by maspin abrogates epigenetic silencing of glutathione S-transferase pi in prostate carcinoma cells.
Topics: Carcinoma; Cell Line, Tumor; Cell Survival; Gene Silencing; Glutathione S-Transferase pi; Histone De | 2011 |
Activation of lytic cycle of Epstein-Barr virus by suberoylanilide hydroxamic acid leads to apoptosis and tumor growth suppression of nasopharyngeal carcinoma.
Topics: Animals; Antineoplastic Agents; Apoptosis; Blotting, Western; Carcinoma; Cell Proliferation; Epstein | 2012 |
5-aza-2'-deoxycytidine has minor effects on differentiation in human thyroid cancer cell lines, but modulates genes that are involved in adaptation in vitro.
Topics: Antimetabolites, Antineoplastic; Apoptosis; Azacitidine; Carcinoma; Cell Differentiation; Cell Line, | 2013 |
Novel histone deacetylase inhibitors in the treatment of thyroid cancer.
Topics: Antineoplastic Agents; Apoptosis; Carcinoma; Cell Death; Cinnamates; Down-Regulation; Gene Expressio | 2005 |
Comparative evaluation of the treatment efficacy of suberoylanilide hydroxamic acid (SAHA) and paclitaxel in ovarian cancer cell lines and primary ovarian cancer cells from patients.
Topics: Acetylation; Antineoplastic Agents; Antineoplastic Agents, Phytogenic; Carcinoma; Caspase 3; Caspase | 2006 |
Antitumor activity of suberoylanilide hydroxamic acid against thyroid cancer cell lines in vitro and in vivo.
Topics: Animals; Antineoplastic Agents; Apoptosis Regulatory Proteins; Carboplatin; Carcinoma; Cell Cycle Pr | 2006 |
A class of hybrid polar inducers of transformed cell differentiation inhibits histone deacetylases.
Topics: Acetamides; Animals; Carcinoma; Cell Differentiation; Cell Line, Transformed; Cell Transformation, N | 1998 |