vorinostat has been researched along with Leukemia, Myeloid in 9 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).
Leukemia, Myeloid: Form of leukemia characterized by an uncontrolled proliferation of the myeloid lineage and their precursors (MYELOID PROGENITOR CELLS) in the bone marrow and other sites.
| Excerpt | Relevance | Reference |
|---|---|---|
| "Children with Down syndrome are at high risk to develop myeloid leukemia (ML-DS)." | 5.43 | Hematologic Response to Vorinostat Treatment in Relapsed Myeloid Leukemia of Down Syndrome. ( Creutzig, U; Klusmann, JH; Kratz, C; Reinhardt, D; Scheer, C; Witt, O, 2016) |
| " A gene expression analysis performed in a phase 1 trial of vorinostat in leukemia indicated that overexpression of genes involved in antioxidant defense was associated with clinical resistance." | 3.76 | Overcoming resistance to histone deacetylase inhibitors in human leukemia with the redox modulating compound β-phenylethyl isothiocyanate. ( Bhalla, K; Chen, G; Fiskus, W; Garcia-Manero, G; Hu, Y; Huang, P; Jia, Y; Keating, M; Lu, W; Wei, Y; Yang, H; Zhang, H; Zhang, W, 2010) |
| "Children with Down syndrome are at high risk to develop myeloid leukemia (ML-DS)." | 1.43 | Hematologic Response to Vorinostat Treatment in Relapsed Myeloid Leukemia of Down Syndrome. ( Creutzig, U; Klusmann, JH; Kratz, C; Reinhardt, D; Scheer, C; Witt, O, 2016) |
| " Etoposide combined with vorinostat was additive to synergistic, and the synergism became more pronounced when etoposide was given after vorinostat." | 1.35 | Preclinical studies of vorinostat (suberoylanilide hydroxamic acid) combined with cytosine arabinoside and etoposide for treatment of acute leukemias. ( Carlton, D; Edelman, MJ; Fang, HB; Gojo, I; Nakanishi, T; Ross, DD; Sausville, EA; Shiozawa, K; Tan, M; Wang, WC, 2009) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 0 (0.00) | 18.7374 |
| 1990's | 0 (0.00) | 18.2507 |
| 2000's | 5 (55.56) | 29.6817 |
| 2010's | 4 (44.44) | 24.3611 |
| 2020's | 0 (0.00) | 2.80 |
| Authors | Studies |
|---|---|
| Mussai, F | 1 |
| Wheat, R | 1 |
| Sarrou, E | 1 |
| Booth, S | 1 |
| Stavrou, V | 1 |
| Fultang, L | 1 |
| Perry, T | 1 |
| Kearns, P | 1 |
| Cheng, P | 1 |
| Keeshan, K | 1 |
| Craddock, C | 2 |
| De Santo, C | 1 |
| Conte, M | 1 |
| Dell'Aversana, C | 1 |
| Benedetti, R | 1 |
| Petraglia, F | 1 |
| Carissimo, A | 1 |
| Petrizzi, VB | 1 |
| D'Arco, AM | 1 |
| Abbondanza, C | 1 |
| Nebbioso, A | 1 |
| Altucci, L | 1 |
| Scheer, C | 1 |
| Kratz, C | 1 |
| Witt, O | 1 |
| Creutzig, U | 1 |
| Reinhardt, D | 1 |
| Klusmann, JH | 1 |
| Shiozawa, K | 1 |
| Nakanishi, T | 1 |
| Tan, M | 1 |
| Fang, HB | 1 |
| Wang, WC | 1 |
| Edelman, MJ | 1 |
| Carlton, D | 1 |
| Gojo, I | 1 |
| Sausville, EA | 1 |
| Ross, DD | 1 |
| Hauswald, S | 1 |
| Duque-Afonso, J | 1 |
| Wagner, MM | 1 |
| Schertl, FM | 1 |
| Lübbert, M | 1 |
| Peschel, C | 1 |
| Keller, U | 1 |
| Licht, T | 1 |
| Hu, Y | 1 |
| Lu, W | 1 |
| Chen, G | 1 |
| Zhang, H | 1 |
| Jia, Y | 1 |
| Wei, Y | 1 |
| Yang, H | 1 |
| Zhang, W | 1 |
| Fiskus, W | 1 |
| Bhalla, K | 1 |
| Keating, M | 1 |
| Huang, P | 1 |
| Garcia-Manero, G | 1 |
| Yu, C | 1 |
| Rahmani, M | 1 |
| Almenara, J | 1 |
| Subler, M | 1 |
| Krystal, G | 1 |
| Conrad, D | 1 |
| Varticovski, L | 1 |
| Dent, P | 1 |
| Grant, S | 1 |
| Bradbury, CA | 1 |
| Khanim, FL | 1 |
| Hayden, R | 1 |
| Bunce, CM | 1 |
| White, DA | 1 |
| Drayson, MT | 1 |
| Turner, BM | 1 |
| Mahlknecht, U | 1 |
| Schönbein, C | 1 |
| Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
|---|---|---|---|---|---|---|---|
| Phase I Study of Cytolytic Viral Activation Therapy (CVAT) for Recurrent/Metastatic Nasopharyngeal Carcinoma[NCT02761291] | Phase 1 | 18 participants (Anticipated) | Interventional | 2016-05-31 | Recruiting | ||
| [information is prepared from clinicaltrials.gov, extracted Sep-2024] | |||||||
1 trial available for vorinostat and Leukemia, Myeloid
| Article | Year |
|---|---|
Targeting the arginine metabolic brake enhances immunotherapy for leukaemia.
Topics: Acute Disease; Antigens, Neoplasm; Antineoplastic Combined Chemotherapy Protocols; Arginase; Arginin | 2019 |
8 other studies available for vorinostat and Leukemia, Myeloid
| Article | Year |
|---|---|
HDAC2 deregulation in tumorigenesis is causally connected to repression of immune modulation and defense escape.
Topics: Acute Disease; Aged; Benzamides; Blotting, Western; Cell Line, Tumor; Cell Proliferation; Female; Ge | 2015 |
Hematologic Response to Vorinostat Treatment in Relapsed Myeloid Leukemia of Down Syndrome.
Topics: Child, Preschool; Cross-Sectional Studies; Down Syndrome; Histone Deacetylase Inhibitors; Humans; Hy | 2016 |
Preclinical studies of vorinostat (suberoylanilide hydroxamic acid) combined with cytosine arabinoside and etoposide for treatment of acute leukemias.
Topics: Acute Disease; Antineoplastic Combined Chemotherapy Protocols; Blast Crisis; Cell Survival; Cytarabi | 2009 |
Histone deacetylase inhibitors induce a very broad, pleiotropic anticancer drug resistance phenotype in acute myeloid leukemia cells by modulation of multiple ABC transporter genes.
Topics: Acute Disease; Antineoplastic Agents; Apoptosis; ATP-Binding Cassette Transporters; Biological Trans | 2009 |
Overcoming resistance to histone deacetylase inhibitors in human leukemia with the redox modulating compound β-phenylethyl isothiocyanate.
Topics: Antioxidants; Base Sequence; Cell Line, Tumor; Cell Survival; DNA Primers; Drug Resistance, Neoplasm | 2010 |
Histone deacetylase inhibitors promote STI571-mediated apoptosis in STI571-sensitive and -resistant Bcr/Abl+ human myeloid leukemia cells.
Topics: Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Benzamides; Drug Synergism; Enzyme Inhibi | 2003 |
Histone deacetylases in acute myeloid leukaemia show a distinctive pattern of expression that changes selectively in response to deacetylase inhibitors.
Topics: Acetylation; Acute Disease; Adult; Antigens, CD34; Butyrates; DNA Methylation; Enzyme Inhibitors; Ge | 2005 |
Histone deacetylase inhibitor treatment downregulates VLA-4 adhesion in hematopoietic stem cells and acute myeloid leukemia blast cells.
Topics: Acute Disease; Bone Marrow Cells; Cell Adhesion; Cell Line, Tumor; Cell Movement; Down-Regulation; D | 2008 |