vorinostat has been researched along with Adenocarcinoma 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).
Adenocarcinoma: A malignant epithelial tumor with a glandular organization.
| Excerpt | Relevance | Reference |
|---|---|---|
| "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) |
| " We have reported previously that treatment with HDACIs, including trichostatin A and suberoylanilide hydroxamic acid (SAHA) or progesterone in combination with estrogen, can induce cytodifferentiation of endometrial adenocarcinoma Ishikawa cells through up-regulation of glycodelin, a progesterone-induced endometrial glycoprotein." | 3.74 | Histone deacetylase inhibitors stimulate cell migration in human endometrial adenocarcinoma cells through up-regulation of glycodelin. ( Arase, T; Asada, H; Kajitani, T; Maruyama, T; Masuda, H; Nagashima, T; Ohta, K; Ono, M; Uchida, H; Yoshimura, Y, 2007) |
| " In this study, we show that TSA and SAHA, belonging to the hydroxamic acid group of HDACIs, can induce the phenotype of a human endometrial adenocarcinoma cell line, Ishikawa (originally derived from the glandular component of the endometrium), to differentiate to closely resemble normal endometrial epithelium in a time- and dose-dependent manner, as determined by morphological changes, synthesis of glycogen, and expression of secretory phase-specific proteins, including glycodelin." | 3.73 | Histone deacetylase inhibitors induce differentiation of human endometrial adenocarcinoma cells through up-regulation of glycodelin. ( Asada, H; Maruyama, T; Nagashima, T; Uchida, H; Yoshimura, Y, 2005) |
| "Vorinostat-XP is a feasible first-line chemotherapy for patients with advanced GC." | 2.82 | Vorinostat in combination with capecitabine plus cisplatin as a first-line chemotherapy for patients with metastatic or unresectable gastric cancer: phase II study and biomarker analysis. ( Kang, YK; Lee, CW; Na, YS; Ryoo, BY; Ryu, MH; Yoo, C, 2016) |
| "Vorinostat has been shown to overcome resistance to gefitinib." | 2.80 | Phase I/II study of gefitinib (Iressa(®)) and vorinostat (IVORI) in previously treated patients with advanced non-small cell lung cancer. ( Han, JY; Hwang, KH; Kim, HT; Kim, JY; Lee, GK; Lee, SH; Lee, YJ; Yun, T, 2015) |
| "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) |
| "Pretreatment with vorinostat led to radiosensitisation of the intrinsically radioresistant DU 145 cells, but not the radiosensitive PC-3 and 22Rv1 cells, and was independent of hypoxia status." | 1.43 | Hypoxia-independent gene expression signature associated with radiosensitisation of prostate cancer cell lines by histone deacetylase inhibition. ( Clancy, T; Flatmark, K; Frikstad, KM; Jonsson, M; Julin, CH; Lyng, H; Matias-Guiu, X; Ragnum, HB; Ree, AH; Seierstad, T; Stokke, T; Yeramian, A, 2016) |
| "Esophageal cancers are highly aggressive tumors with poor prognosis despite some recent advances in surgical and radiochemotherapy treatment options." | 1.42 | Selective inhibition of esophageal cancer cells by combination of HDAC inhibitors and Azacytidine. ( Ahrens, TD; Boerries, M; Busch, H; Follo, M; Hembach, S; Hoeppner, J; Hopt, UT; Lassmann, S; Ostendorp, J; Timme, S; Werner, M, 2015) |
| "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) |
| "This combined therapeutic effect on esophageal cancer epithelial-mesenchymal transition was associated with upregulation of E-cadherin protein expression." | 1.36 | Combined proteasome and histone deacetylase inhibition attenuates epithelial-mesenchymal transition through E-cadherin in esophageal cancer cells. ( Jones, DR; Liu, Y; Nagji, AS; Taylor, MD; Theodosakis, N, 2010) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 0 (0.00) | 18.7374 |
| 1990's | 0 (0.00) | 18.2507 |
| 2000's | 9 (32.14) | 29.6817 |
| 2010's | 18 (64.29) | 24.3611 |
| 2020's | 1 (3.57) | 2.80 |
| Authors | Studies |
|---|---|
| Chen, B | 1 |
| Li, P | 1 |
| Liu, M | 1 |
| Liu, K | 1 |
| Zou, M | 1 |
| Geng, Y | 1 |
| Zhuang, S | 1 |
| Xu, H | 1 |
| Wang, L | 1 |
| Chen, T | 1 |
| Li, Y | 1 |
| Zhao, Z | 1 |
| Qi, L | 1 |
| Gu, Y | 1 |
| Xiong, K | 1 |
| Zhang, H | 1 |
| Du, Y | 1 |
| Tian, J | 1 |
| Ding, S | 1 |
| Booth, L | 1 |
| Roberts, JL | 1 |
| Poklepovic, A | 1 |
| Dent, P | 1 |
| You, BR | 1 |
| Park, WH | 1 |
| Reguart, N | 1 |
| Rosell, R | 1 |
| Cardenal, F | 1 |
| Cardona, AF | 1 |
| Isla, D | 1 |
| Palmero, R | 1 |
| Moran, T | 1 |
| Rolfo, C | 1 |
| Pallarès, MC | 1 |
| Insa, A | 1 |
| Carcereny, E | 1 |
| Majem, M | 1 |
| De Castro, J | 1 |
| Queralt, C | 1 |
| Molina, MA | 1 |
| Taron, M | 1 |
| Rich, A | 1 |
| Sun, J | 1 |
| Aldayel, AS | 1 |
| Yin, CC | 1 |
| Medeiros, LJ | 1 |
| Konoplev, S | 1 |
| Han, JY | 1 |
| Lee, SH | 1 |
| Lee, GK | 1 |
| Yun, T | 1 |
| Lee, YJ | 1 |
| Hwang, KH | 1 |
| Kim, JY | 1 |
| Kim, HT | 1 |
| Kuo, WY | 1 |
| Wu, CY | 1 |
| Hwu, L | 1 |
| Lee, JS | 1 |
| Tsai, CH | 1 |
| Lin, KP | 1 |
| Wang, HE | 1 |
| Chou, TY | 1 |
| Tsai, CM | 1 |
| Gelovani, J | 1 |
| Liu, RS | 1 |
| Ahrens, TD | 1 |
| Timme, S | 1 |
| Hoeppner, J | 1 |
| Ostendorp, J | 1 |
| Hembach, S | 1 |
| Follo, M | 1 |
| Hopt, UT | 1 |
| Werner, M | 1 |
| Busch, H | 1 |
| Boerries, M | 1 |
| Lassmann, S | 1 |
| Yoo, C | 1 |
| Ryu, MH | 1 |
| Na, YS | 1 |
| Ryoo, BY | 1 |
| Lee, CW | 1 |
| Kang, YK | 1 |
| Li, R | 1 |
| Huang, J | 1 |
| Ma, M | 1 |
| Lou, Y | 1 |
| Zhang, Y | 1 |
| Wu, L | 1 |
| Chang, DW | 1 |
| Zhao, P | 1 |
| Dong, Q | 1 |
| Wu, X | 1 |
| Han, B | 1 |
| Jonsson, M | 1 |
| Ragnum, HB | 1 |
| Julin, CH | 1 |
| Yeramian, A | 1 |
| Clancy, T | 1 |
| Frikstad, KM | 1 |
| Seierstad, T | 1 |
| Stokke, T | 1 |
| Matias-Guiu, X | 1 |
| Ree, AH | 1 |
| Flatmark, K | 1 |
| Lyng, H | 1 |
| Portanova, P | 1 |
| Russo, T | 1 |
| Pellerito, O | 1 |
| Calvaruso, G | 1 |
| Giuliano, M | 1 |
| Vento, R | 1 |
| Tesoriere, G | 1 |
| Dedes, KJ | 1 |
| Dedes, I | 1 |
| Imesch, P | 1 |
| von Bueren, AO | 1 |
| Fink, D | 1 |
| Fedier, A | 1 |
| Fakih, MG | 1 |
| Pendyala, L | 1 |
| Fetterly, G | 1 |
| Toth, K | 1 |
| Zwiebel, JA | 1 |
| Espinoza-Delgado, I | 1 |
| Litwin, A | 1 |
| Rustum, YM | 1 |
| Ross, ME | 1 |
| Holleran, JL | 1 |
| Egorin, MJ | 1 |
| Chun, SG | 1 |
| Zhou, W | 1 |
| Yee, NS | 1 |
| Freeman, JW | 1 |
| Wang, Y | 1 |
| Giles, FJ | 1 |
| Billam, M | 1 |
| Sobolewski, MD | 1 |
| Davidson, NE | 1 |
| Owonikoko, TK | 1 |
| Ramalingam, SS | 1 |
| Kanterewicz, B | 1 |
| Balius, TE | 1 |
| Belani, CP | 1 |
| Hershberger, PA | 1 |
| Taylor, MD | 1 |
| Liu, Y | 1 |
| Nagji, AS | 1 |
| Theodosakis, N | 1 |
| Jones, DR | 2 |
| Kurtze, I | 1 |
| Sonnemann, J | 1 |
| Beck, JF | 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 |
| Moskaluk, CA | 1 |
| Gillenwater, HH | 1 |
| Petroni, GR | 1 |
| Burks, SG | 1 |
| Philips, J | 1 |
| Rehm, PK | 1 |
| Olazagasti, J | 1 |
| Kozower, BD | 1 |
| Bao, Y | 1 |
| García-Morales, P | 1 |
| Gómez-Martínez, A | 1 |
| Carrato, A | 1 |
| Martínez-Lacaci, I | 1 |
| Barberá, VM | 1 |
| Soto, JL | 1 |
| Carrasco-García, E | 1 |
| Menéndez-Gutierrez, MP | 1 |
| Castro-Galache, MD | 1 |
| Ferragut, JA | 1 |
| Saceda, M | 1 |
| Uchida, H | 2 |
| Maruyama, T | 2 |
| Nagashima, T | 2 |
| Asada, H | 2 |
| Yoshimura, Y | 2 |
| Ono, M | 1 |
| Ohta, K | 1 |
| Kajitani, T | 1 |
| Masuda, H | 1 |
| Arase, T | 1 |
| Sargeant, AM | 1 |
| Rengel, RC | 1 |
| Kulp, SK | 1 |
| Klein, RD | 1 |
| Clinton, SK | 1 |
| Wang, YC | 1 |
| Chen, CS | 1 |
| Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
|---|---|---|---|---|---|---|---|
| Phase I/II Study of Vorinostat and Gefitinib in Relapsed/ or Refractory Patients With Advanced Non-small Cell Carcinoma (NSCLC)[NCT01027676] | Phase 1/Phase 2 | 50 participants (Anticipated) | Interventional | 2010-06-30 | Active, not recruiting | ||
| [information is prepared from clinicaltrials.gov, extracted Sep-2024] | |||||||
1 review available for vorinostat and Adenocarcinoma
| Article | Year |
|---|---|
Myelomastocytic leukemia with aberrant CD25 expression: case report and review of the literature.
Topics: Adenocarcinoma; Antigens, Neoplasm; Antineoplastic Combined Chemotherapy Protocols; Biomarkers, Tumo | 2014 |
5 trials available for vorinostat and Adenocarcinoma
| Article | Year |
|---|---|
Phase I/II trial of vorinostat (SAHA) and erlotinib for non-small cell lung cancer (NSCLC) patients with epidermal growth factor receptor (EGFR) mutations after erlotinib progression.
Topics: Adenocarcinoma; Adult; Aged; Antineoplastic Combined Chemotherapy Protocols; Carcinoma, Non-Small-Ce | 2014 |
Phase I/II study of gefitinib (Iressa(®)) and vorinostat (IVORI) in previously treated patients with advanced non-small cell lung cancer.
Topics: Adenocarcinoma; Adult; Aged; Antineoplastic Combined Chemotherapy Protocols; Carcinoma, Non-Small-Ce | 2015 |
Vorinostat in combination with capecitabine plus cisplatin as a first-line chemotherapy for patients with metastatic or unresectable gastric cancer: phase II study and biomarker analysis.
Topics: Acetylation; Adenocarcinoma; Adult; Aged; Anorexia; Antineoplastic Combined Chemotherapy Protocols; | 2016 |
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 |
Phase I trial of induction histone deacetylase and proteasome inhibition followed by surgery in non-small-cell lung cancer.
Topics: Adenocarcinoma; Aged; Aged, 80 and over; Antineoplastic Combined Chemotherapy Protocols; Biomarkers, | 2012 |
22 other studies available for vorinostat and Adenocarcinoma
| Article | Year |
|---|---|
A genetic map of the chromatin regulators to drug response in cancer cells.
Topics: Adenocarcinoma; Biomarkers; Chromatin; Colonic Neoplasms; DNA-Binding Proteins; Humans; Vorinostat | 2022 |
Identification of HDAC9 as a viable therapeutic target for the treatment of gastric cancer.
Topics: Adenocarcinoma; Animals; Antineoplastic Agents; Apoptosis; Cell Cycle Checkpoints; Cell Proliferatio | 2019 |
Prior exposure of pancreatic tumors to [sorafenib + vorinostat] enhances the efficacy of an anti-PD-1 antibody.
Topics: Adenocarcinoma; Animals; Antineoplastic Agents, Immunological; Antineoplastic Combined Chemotherapy | 2019 |
Suberoylanilide hydroxamic acid-induced HeLa cell death is closely correlated with oxidative stress and thioredoxin 1 levels.
Topics: Adenocarcinoma; Antineoplastic Agents; Apoptosis; Caspase Inhibitors; Caspases; Cell Cycle; Female; | 2014 |
Enhancement of tumor initiation and expression of KCNMA1, MORF4L2 and ASPM genes in the adenocarcinoma of lung xenograft after vorinostat treatment.
Topics: Adenocarcinoma; Aldehyde Dehydrogenase; Animals; Carcinoma, Non-Small-Cell Lung; Cell Self Renewal; | 2015 |
Selective inhibition of esophageal cancer cells by combination of HDAC inhibitors and Azacytidine.
Topics: Acetylation; Adenocarcinoma; Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Azacitidine; | 2015 |
Two-stage induced differentiation of OCT4+/Nanog+ stem-like cells in lung adenocarcinoma.
Topics: Adenocarcinoma; Animals; Antineoplastic Agents; Cell Differentiation; Cell Line, Tumor; Cholecalcife | 2016 |
Hypoxia-independent gene expression signature associated with radiosensitisation of prostate cancer cell lines by histone deacetylase inhibition.
Topics: Adenocarcinoma; Antineoplastic Agents; Biomarkers, Tumor; Cell Cycle; Cell Hypoxia; Cell Line, Tumor | 2016 |
The role of oxidative stress in apoptosis induced by the histone deacetylase inhibitor suberoylanilide hydroxamic acid in human colon adenocarcinoma HT-29 cells.
Topics: Adenocarcinoma; Antioxidants; Apoptosis; Blotting, Western; Caspases; Cell Survival; Colonic Neoplas | 2008 |
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 |
Combined targeting of histone deacetylases and hedgehog signaling enhances cytoxicity in pancreatic cancer.
Topics: Adenocarcinoma; Antimetabolites, Antineoplastic; Antineoplastic Agents; Apoptosis; Cell Cycle; Cell | 2009 |
Epigenetic modulation and attacking the hedgehog pathway: potentially synergistic therapeutic targets for pancreatic cancer.
Topics: Adenocarcinoma; Antimetabolites, Antineoplastic; Antineoplastic Agents; Cell Line, Tumor; Deoxycytid | 2009 |
Effects of a novel DNA methyltransferase inhibitor zebularine on human breast cancer cells.
Topics: Adenocarcinoma; Apoptosis Regulatory Proteins; Azacitidine; Breast Neoplasms; Cell Cycle Proteins; C | 2010 |
Vorinostat increases carboplatin and paclitaxel activity in non-small-cell lung cancer cells.
Topics: Acetylation; Adenocarcinoma; Adenocarcinoma, Bronchiolo-Alveolar; Antineoplastic Combined Chemothera | 2010 |
Combined proteasome and histone deacetylase inhibition attenuates epithelial-mesenchymal transition through E-cadherin in esophageal cancer cells.
Topics: Adenocarcinoma; Antigens, CD; Antineoplastic Combined Chemotherapy Protocols; Boronic Acids; Bortezo | 2010 |
KRAS-mutated non-small cell lung cancer cells are responsive to either co-treatment with erlotinib or gefitinib and histone deacetylase inhibitors or single treatment with lapatinib.
Topics: Adenocarcinoma; Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Carcinoma, Non-Small-Cell | 2011 |
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 |
Histone deacetylase inhibitors induced caspase-independent apoptosis in human pancreatic adenocarcinoma cell lines.
Topics: Adenocarcinoma; Antineoplastic Agents; Apoptosis; Apoptosis Inducing Factor; bcl-2-Associated X Prot | 2005 |
Histone deacetylase inhibitors induce differentiation of human endometrial adenocarcinoma cells through up-regulation of glycodelin.
Topics: Adenocarcinoma; Cell Differentiation; Cell Line, Tumor; Cell Proliferation; Endometrial Neoplasms; E | 2005 |
Histone deacetylase inhibitors stimulate cell migration in human endometrial adenocarcinoma cells through up-regulation of glycodelin.
Topics: Adenocarcinoma; Antineoplastic Agents; Cell Line, Tumor; Cell Movement; Endometrial Neoplasms; Enzym | 2007 |
OSU-HDAC42, a histone deacetylase inhibitor, blocks prostate tumor progression in the transgenic adenocarcinoma of the mouse prostate model.
Topics: Adenocarcinoma; Administration, Oral; Animals; Antineoplastic Agents; Cell Line, Tumor; Enzyme Inhib | 2008 |