vorinostat has been researched along with Granulocytic Leukemia, Chronic in 15 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 |
|---|---|---|
| "We determined the effects of vorinostat (suberoylanalide hydroxamic acid) and/or MK-0457 (VX-680), an Aurora kinase inhibitor on the cultured human (HL-60, OCI-AML3, and K562) and primary acute myelogenous leukemia (AML) and chronic myelogenous leukemia (CML), as well as on the murine pro-B BaF3 cells with ectopic expression of the unmutated and mutant forms of Bcr-Abl." | 3.74 | Cotreatment with vorinostat enhances activity of MK-0457 (VX-680) against acute and chronic myelogenous leukemia cells. ( Balusu, R; Bhalla, K; Buser, CA; Chen, J; Eaton, K; Fiskus, W; Jillella, A; Joshi, R; Kolhe, R; Lee, P; Peiper, S; Rao, R; Ustun, C; Wang, Y; Yang, Y, 2008) |
| "Treatment with ponatinib for 72 h inhibited cell growth and induced apoptosis in K562 cells in a dose-dependent manner." | 1.40 | Combining the ABL1 kinase inhibitor ponatinib and the histone deacetylase inhibitor vorinostat: a potential treatment for BCR-ABL-positive leukemia. ( Kimura, S; Kitahara, T; Maekawa, T; Ohyashiki, K; Okabe, S; Tanaka, Y; Tauchi, T, 2014) |
| "Treatment with dasatinib attenuated the levels of autophosphorylated Bcr-Abl, p-CrkL, phospho-signal transducer and activator of transcription 5 (p-STAT5), p-c-Src, and p-Lyn; inhibited the activity of Lyn and c-Src; and induced apoptosis of the cultured CML cells." | 1.33 | Cotreatment with vorinostat (suberoylanilide hydroxamic acid) enhances activity of dasatinib (BMS-354825) against imatinib mesylate-sensitive or imatinib mesylate-resistant chronic myelogenous leukemia cells. ( Balasis, M; Bali, P; Bhalla, K; Estrella, V; Fiskus, W; Herger, B; Kumaraswamy, S; Lee, F; Pranpat, M; Rao, R; Richon, V; Rocha, K, 2006) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 0 (0.00) | 18.7374 |
| 1990's | 0 (0.00) | 18.2507 |
| 2000's | 11 (73.33) | 29.6817 |
| 2010's | 4 (26.67) | 24.3611 |
| 2020's | 0 (0.00) | 2.80 |
| Authors | Studies |
|---|---|
| Muthyala, R | 1 |
| Shin, WS | 1 |
| Xie, J | 1 |
| Sham, YY | 1 |
| Okabe, S | 1 |
| Tauchi, T | 1 |
| Kimura, S | 1 |
| Maekawa, T | 1 |
| Kitahara, T | 1 |
| Tanaka, Y | 1 |
| Ohyashiki, K | 1 |
| Bu, Q | 1 |
| Cui, L | 1 |
| Li, J | 1 |
| Du, X | 1 |
| Zou, W | 1 |
| Ding, K | 1 |
| Pan, J | 1 |
| Fiskus, W | 2 |
| Wang, Y | 1 |
| Joshi, R | 1 |
| Rao, R | 2 |
| Yang, Y | 1 |
| Chen, J | 1 |
| Kolhe, R | 1 |
| Balusu, R | 1 |
| Eaton, K | 1 |
| Lee, P | 1 |
| Ustun, C | 1 |
| Jillella, A | 1 |
| Buser, CA | 1 |
| Peiper, S | 1 |
| Bhalla, K | 3 |
| Brodská, B | 1 |
| Otevřelová, P | 1 |
| Holoubek, A | 1 |
| Nimmanapalli, R | 1 |
| Fuino, L | 1 |
| Stobaugh, C | 1 |
| Richon, V | 2 |
| Yu, C | 2 |
| Rahmani, M | 1 |
| Conrad, D | 1 |
| Subler, M | 1 |
| Dent, P | 4 |
| Grant, S | 4 |
| Xu, Y | 2 |
| Voelter-Mahlknecht, S | 1 |
| Mahlknecht, U | 1 |
| Dasmahapatra, G | 2 |
| Pranpat, M | 1 |
| Balasis, M | 1 |
| Bali, P | 1 |
| Estrella, V | 1 |
| Kumaraswamy, S | 1 |
| Rocha, K | 1 |
| Herger, B | 1 |
| Lee, F | 1 |
| Carew, JS | 1 |
| Nawrocki, ST | 1 |
| Kahue, CN | 1 |
| Zhang, H | 1 |
| Yang, C | 1 |
| Chung, L | 1 |
| Houghton, JA | 1 |
| Huang, P | 1 |
| Giles, FJ | 1 |
| Cleveland, JL | 1 |
| Tabe, Y | 1 |
| Jin, L | 1 |
| Contractor, R | 1 |
| Gold, D | 1 |
| Ruvolo, P | 1 |
| Radke, S | 1 |
| Tsutusmi-Ishii, Y | 1 |
| Miyake, K | 1 |
| Miyake, N | 1 |
| Kondo, S | 1 |
| Ohsaka, A | 1 |
| Nagaoka, I | 1 |
| Andreeff, M | 1 |
| Konopleva, M | 1 |
| Soverini, S | 1 |
| Iacobucci, I | 1 |
| Baccarani, M | 1 |
| Martinelli, G | 1 |
| Yerram, N | 1 |
| Dai, Y | 2 |
| Chen, S | 1 |
| Venditti, CA | 1 |
| Pei, XY | 1 |
| Nguyen, TK | 1 |
| Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
|---|---|---|---|---|---|---|---|
| Phase II Clinical Evaluation of Vorinostat Combined With Salvage Reinduction Chemotherapy Including Gemtuzumab Ozogamicin, Idarubicin and Cytarabine and Vorinostat Maintenance in Relapse or Refractory Acute Myeloid Leukemia Patients With 50 Years or Older[NCT01039363] | Phase 2 | 27 participants (Anticipated) | Interventional | Not yet recruiting | |||
| An Open-Label Phase I/II Study of Bendamustine, Weekly Bortezomib, Lenalidomide and Dexamethasone for the Treatment of Relapsed or Refractory Multiple Myeloma[NCT01484626] | Phase 1/Phase 2 | 3 participants (Actual) | Interventional | 2011-05-05 | Terminated (stopped due to Celgene would no longer supply lenalidomide for the study) | ||
| [information is prepared from clinicaltrials.gov, extracted Sep-2024] | |||||||
15 other studies available for vorinostat and Granulocytic Leukemia, Chronic
| Article | Year |
|---|---|
Discovery of 1-hydroxypyridine-2-thiones as selective histone deacetylase inhibitors and their potential application for treating leukemia.
Topics: Animals; Cell Line, Tumor; Cell Proliferation; Cell Survival; Crystallography, X-Ray; Dose-Response | 2015 |
Combining the ABL1 kinase inhibitor ponatinib and the histone deacetylase inhibitor vorinostat: a potential treatment for BCR-ABL-positive leukemia.
Topics: Animals; Apoptosis; Cell Proliferation; Fusion Proteins, bcr-abl; Histone Deacetylase Inhibitors; Hu | 2014 |
SAHA and S116836, a novel tyrosine kinase inhibitor, synergistically induce apoptosis in imatinib-resistant chronic myelogenous leukemia cells.
Topics: Antineoplastic Agents; Apoptosis; Benzamides; Cell Line, Tumor; Cell Proliferation; Cell Survival; D | 2014 |
Cotreatment with vorinostat enhances activity of MK-0457 (VX-680) against acute and chronic myelogenous leukemia cells.
Topics: Animals; Antineoplastic Combined Chemotherapy Protocols; Cell Line, Tumor; Drug Synergism; Fusion Pr | 2008 |
Decitabine-induced apoptosis is derived by Puma and Noxa induction in chronic myeloid leukemia cell line as well as in PBL and is potentiated by SAHA.
Topics: Antimetabolites, Antineoplastic; Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Apoptosi | 2011 |
Cotreatment with the histone deacetylase inhibitor suberoylanilide hydroxamic acid (SAHA) enhances imatinib-induced apoptosis of Bcr-Abl-positive human acute leukemia cells.
Topics: Antineoplastic Agents; Apoptosis; Benzamides; Blast Crisis; Cell Cycle Proteins; Computer Systems; C | 2003 |
The proteasome inhibitor bortezomib interacts synergistically with histone deacetylase inhibitors to induce apoptosis in Bcr/Abl+ cells sensitive and resistant to STI571.
Topics: Antineoplastic Agents; Apoptosis; Benzamides; Boronic Acids; Bortezomib; Butyrates; Cell Line, Tumor | 2003 |
The histone deacetylase inhibitor suberoylanilide hydroxamic acid down-regulates expression levels of Bcr-abl, c-Myc and HDAC3 in chronic myeloid leukemia cell lines.
Topics: Apoptosis; Cell Line, Tumor; Down-Regulation; Enzyme Inhibitors; Fusion Proteins, bcr-abl; Gene Expr | 2005 |
Synergistic interactions between MEK1/2 and histone deacetylase inhibitors in BCR/ABL+ human leukemia cells.
Topics: Antigens, CD34; Apoptosis; Benzamides; Bone Marrow Cells; Butadienes; Butyrates; Caspases; Cell Line | 2005 |
Cotreatment with vorinostat (suberoylanilide hydroxamic acid) enhances activity of dasatinib (BMS-354825) against imatinib mesylate-sensitive or imatinib mesylate-resistant chronic myelogenous leukemia cells.
Topics: Animals; Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Benzamides; Dasatinib; Drug Resi | 2006 |
Targeting autophagy augments the anticancer activity of the histone deacetylase inhibitor SAHA to overcome Bcr-Abl-mediated drug resistance.
Topics: Antineoplastic Agents; Autophagy; Cathepsin D; Cell Line, Tumor; Chloroquine; Drug Resistance, Neopl | 2007 |
Novel role of HDAC inhibitors in AML1/ETO AML cells: activation of apoptosis and phagocytosis through induction of annexin A1.
Topics: Acetylation; Annexin A1; Antineoplastic Agents; Apoptosis; Base Sequence; Cell Line, Tumor; Cell Pro | 2007 |
Targeted therapy and the T315I mutation in Philadelphia-positive leukemias.
Topics: Adenosine Triphosphate; Amino Acid Substitution; Antineoplastic Agents; Benzamides; Benzene Derivati | 2007 |
Synergistic interactions between vorinostat and sorafenib in chronic myelogenous leukemia cells involve Mcl-1 and p21CIP1 down-regulation.
Topics: Benzenesulfonates; Cell Line, Tumor; Cell Survival; Cyclin-Dependent Kinase Inhibitor p21; Drug Syne | 2007 |
Vorinostat synergistically potentiates MK-0457 lethality in chronic myelogenous leukemia cells sensitive and resistant to imatinib mesylate.
Topics: Animals; Antineoplastic Combined Chemotherapy Protocols; Apoptosis Regulatory Proteins; Aurora Kinas | 2008 |