vorinostat has been researched along with Angiogenesis, Pathologic in 16 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 |
|---|---|---|
| "Treatment of vorinostat upregulates PLD1 through PKCζ-Sp1 axis." | 5.62 | Phospholipase D1 is upregulated by vorinostat and confers resistance to vorinostat in glioblastoma. ( Hwang, WC; Jang, Y; Kang, DW; Kang, Y; Kim, JA; Min, DS; Noh, YN, 2021) |
| "The recommended phase II dosage was oral pazopanib at 600 mg daily plus oral vorinostat at 300 mg daily." | 2.80 | Phase I study of pazopanib and vorinostat: a therapeutic approach for inhibiting mutant p53-mediated angiogenesis and facilitating mutant p53 degradation. ( Araujo, D; Fu, S; Hess, K; Hong, D; Hou, MM; Hwu, P; Janku, F; Karp, D; Kee, B; Kurzrock, R; Meric-Bernstam, F; Naing, A; Piha-Paul, S; Subbiah, V; Tsimberidou, A; Wheler, J; Wolff, R; Zinner, R, 2015) |
| "Treatment of vorinostat upregulates PLD1 through PKCζ-Sp1 axis." | 1.62 | Phospholipase D1 is upregulated by vorinostat and confers resistance to vorinostat in glioblastoma. ( Hwang, WC; Jang, Y; Kang, DW; Kang, Y; Kim, JA; Min, DS; Noh, YN, 2021) |
| " Consistent additive to synergistic interactions were observed in HCT116 cells when PENT was combined with SAHA at all drug tested concentrations." | 1.46 | Enhanced anticancer efficacy of histone deacetyl inhibitor, suberoylanilide hydroxamic acid, in combination with a phosphodiesterase inhibitor, pentoxifylline, in human cancer cell lines and in-vivo tumor xenografts. ( Chandrasekhar, KB; Karthikeyan, K; Khan, FR; Kulkarni, NM; Narayanan, S; Nidhyanandan, S; Raghul, J; Reddy, ND; Thippeswamy, BS; Vijaykanth, G, 2017) |
| "Seven thyroid cancer cell lines (SNU-790, BCPAP, KTC1, TPC1, TPC1-M, KTC2, and FRO) and four HIF1α inhibitors (echinomycin, LAQ824, temsirolimus, and vorinostat) were used in the present study." | 1.42 | Effect of perioperative treatment with a hypoxia-inducible factor-1-alpha inhibitor in an orthotopic surgical mouse model of thyroid cancer. ( Ahn, SH; Cha, W; Jeon, EH; Jeong, WJ; Kim, DW; Kim, SD, 2015) |
| "PaTu8988 pancreatic cancer cells were treated with different concentrations of suberoylanilide hydroxamic acid (SAHA), cell survival, proliferation, migration and vasculogenic mimicry (VM) were analyzed." | 1.40 | Suberoylanilide hydroxamic acid, an inhibitor of histone deacetylase, suppresses vasculogenic mimicry and proliferation of highly aggressive pancreatic cancer PaTu8988 cells. ( Cao, C; Cao, ZF; Pan, YY; Xu, XD; Yang, B; Yang, L; Zhang, ZQ; Zheng, LY; Zhou, QS, 2014) |
| "Current treatments for malignant gliomas produce only a modest increase in survival time." | 1.34 | Continuous intracranial administration of suberoylanilide hydroxamic acid (SAHA) inhibits tumor growth in an orthotopic glioma model. ( Bello, L; Black, PM; Carroll, RS; Kim, SK; Menon, LG; Ramakrishna, N; Ugur, HC, 2007) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 0 (0.00) | 18.7374 |
| 1990's | 0 (0.00) | 18.2507 |
| 2000's | 2 (12.50) | 29.6817 |
| 2010's | 13 (81.25) | 24.3611 |
| 2020's | 1 (6.25) | 2.80 |
| Authors | Studies |
|---|---|
| Kang, DW | 1 |
| Hwang, WC | 1 |
| Noh, YN | 1 |
| Kang, Y | 1 |
| Jang, Y | 1 |
| Kim, JA | 1 |
| Min, DS | 1 |
| Nidhyanandan, S | 1 |
| Thippeswamy, BS | 1 |
| Chandrasekhar, KB | 1 |
| Reddy, ND | 1 |
| Kulkarni, NM | 1 |
| Karthikeyan, K | 1 |
| Khan, FR | 1 |
| Raghul, J | 1 |
| Vijaykanth, G | 1 |
| Narayanan, S | 1 |
| Iizuka, N | 1 |
| Morita, A | 1 |
| Kawano, C | 1 |
| Mori, A | 1 |
| Sakamoto, K | 1 |
| Kuroyama, M | 1 |
| Ishii, K | 1 |
| Nakahara, T | 1 |
| Ghebremariam, YT | 1 |
| Erlanson, DA | 1 |
| Cooke, JP | 1 |
| Xu, XD | 1 |
| Yang, L | 1 |
| Zheng, LY | 1 |
| Pan, YY | 1 |
| Cao, ZF | 1 |
| Zhang, ZQ | 1 |
| Zhou, QS | 1 |
| Yang, B | 1 |
| Cao, C | 1 |
| Zhou, H | 1 |
| Jiang, S | 1 |
| Chen, J | 1 |
| Su, SB | 1 |
| Hiriyan, J | 1 |
| Shivarudraiah, P | 1 |
| Gavara, G | 1 |
| Annamalai, P | 1 |
| Natesan, S | 1 |
| Sambasivam, G | 1 |
| Sukumaran, SK | 1 |
| Fu, S | 1 |
| Hou, MM | 1 |
| Naing, A | 1 |
| Janku, F | 1 |
| Hess, K | 1 |
| Zinner, R | 1 |
| Subbiah, V | 1 |
| Hong, D | 1 |
| Wheler, J | 1 |
| Piha-Paul, S | 1 |
| Tsimberidou, A | 1 |
| Karp, D | 1 |
| Araujo, D | 1 |
| Kee, B | 1 |
| Hwu, P | 1 |
| Wolff, R | 1 |
| Kurzrock, R | 2 |
| Meric-Bernstam, F | 1 |
| Cha, W | 1 |
| Kim, DW | 1 |
| Kim, SD | 1 |
| Jeon, EH | 1 |
| Jeong, WJ | 1 |
| Ahn, SH | 1 |
| Blattmann, C | 1 |
| Oertel, S | 1 |
| Thiemann, M | 1 |
| Dittmar, A | 1 |
| Roth, E | 1 |
| Kulozik, AE | 1 |
| Ehemann, V | 1 |
| Weichert, W | 1 |
| Huber, PE | 1 |
| Stenzinger, A | 1 |
| Debus, J | 1 |
| Shankar, S | 1 |
| Davis, R | 1 |
| Singh, KP | 1 |
| Ross, DD | 1 |
| Srivastava, RK | 1 |
| Jung, HJ | 1 |
| Kim, JH | 1 |
| Shim, JS | 1 |
| Kwon, HJ | 1 |
| Kim, JY | 1 |
| Shim, G | 1 |
| Choi, HW | 1 |
| Park, J | 1 |
| Chung, SW | 1 |
| Kim, S | 1 |
| Kim, K | 1 |
| Kwon, IC | 1 |
| Kim, CW | 1 |
| Kim, SY | 1 |
| Yang, VC | 1 |
| Oh, YK | 1 |
| Byun, Y | 1 |
| Li, J | 1 |
| Gong, C | 1 |
| Feng, X | 1 |
| Zhou, X | 1 |
| Xu, X | 1 |
| Xie, L | 1 |
| Wang, R | 1 |
| Zhang, D | 1 |
| Wang, H | 1 |
| Deng, P | 1 |
| Zhou, M | 1 |
| Ji, N | 1 |
| Zhou, Y | 1 |
| Wang, Y | 1 |
| Wang, Z | 2 |
| Liao, G | 1 |
| Geng, N | 1 |
| Chu, L | 1 |
| Qian, Z | 1 |
| Chen, Q | 1 |
| Li, X | 1 |
| Zhou, Q | 1 |
| Hanus, J | 1 |
| Anderson, C | 1 |
| Zhang, H | 1 |
| Dellinger, M | 1 |
| Brekken, R | 1 |
| Wang, S | 1 |
| Ugur, HC | 1 |
| Ramakrishna, N | 1 |
| Bello, L | 1 |
| Menon, LG | 1 |
| Kim, SK | 1 |
| Black, PM | 1 |
| Carroll, RS | 1 |
| Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
|---|---|---|---|---|---|---|---|
| A Phase I Study of Pazopanib and Vorinostat in Patients With Advanced Malignancies[NCT01339871] | Phase 1 | 152 participants (Actual) | Interventional | 2011-04-20 | Completed | ||
| [information is prepared from clinicaltrials.gov, extracted Sep-2024] | |||||||
1 trial available for vorinostat and Angiogenesis, Pathologic
| Article | Year |
|---|---|
Phase I study of pazopanib and vorinostat: a therapeutic approach for inhibiting mutant p53-mediated angiogenesis and facilitating mutant p53 degradation.
Topics: Administration, Oral; Adolescent; Adult; Aged; Angiogenesis Inhibitors; Antineoplastic Combined Chem | 2015 |
15 other studies available for vorinostat and Angiogenesis, Pathologic
| Article | Year |
|---|---|
Phospholipase D1 is upregulated by vorinostat and confers resistance to vorinostat in glioblastoma.
Topics: Animals; Antineoplastic Agents; Brain Neoplasms; Cell Line, Tumor; Chromatin; Drug Resistance, Neopl | 2021 |
Enhanced anticancer efficacy of histone deacetyl inhibitor, suberoylanilide hydroxamic acid, in combination with a phosphodiesterase inhibitor, pentoxifylline, in human cancer cell lines and in-vivo tumor xenografts.
Topics: Animals; Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Cell Cycle; Cell Growth Processe | 2017 |
Anti-angiogenic effects of valproic acid in a mouse model of oxygen-induced retinopathy.
Topics: Angiogenesis Inhibitors; Animals; Disease Models, Animal; Mice; Neovascularization, Pathologic; Oxyg | 2018 |
A novel and potent inhibitor of dimethylarginine dimethylaminohydrolase: a modulator of cardiovascular nitric oxide.
Topics: Amidohydrolases; Cells, Cultured; Endothelium, Vascular; Female; Humans; Hydroxamic Acids; Imines; N | 2014 |
Suberoylanilide hydroxamic acid, an inhibitor of histone deacetylase, suppresses vasculogenic mimicry and proliferation of highly aggressive pancreatic cancer PaTu8988 cells.
Topics: Apoptosis; CDC2 Protein Kinase; Cell Line, Tumor; Cell Proliferation; Gene Expression Regulation, Ne | 2014 |
Suberoylanilide hydroxamic acid suppresses inflammation-induced neovascularization.
Topics: ADAM Proteins; ADAMTS1 Protein; Administration, Ophthalmic; Animals; Apoptosis; Basic Helix-Loop-Hel | 2014 |
Discovery of PAT-1102, a novel, potent and orally active histone deacetylase inhibitor with antitumor activity in cancer mouse models.
Topics: Administration, Oral; Animals; Antineoplastic Agents; Apoptosis; HCT116 Cells; HeLa Cells; Histone D | 2015 |
Effect of perioperative treatment with a hypoxia-inducible factor-1-alpha inhibitor in an orthotopic surgical mouse model of thyroid cancer.
Topics: Animals; Apoptosis; Cell Proliferation; Disease Models, Animal; Gene Expression Regulation, Neoplast | 2015 |
Histone deacetylase inhibition sensitizes osteosarcoma to heavy ion radiotherapy.
Topics: Animals; Apoptosis; Bone Neoplasms; Cell Division; Cell Line, Tumor; Cyclin-Dependent Kinase Inhibit | 2015 |
Suberoylanilide hydroxamic acid (Zolinza/vorinostat) sensitizes TRAIL-resistant breast cancer cells orthotopically implanted in BALB/c nude mice.
Topics: Animals; Breast Neoplasms; Cell Proliferation; Drug Resistance, Neoplasm; Enzyme Inhibitors; Gene Ex | 2009 |
A novel Ca2+/calmodulin antagonist HBC inhibits angiogenesis and down-regulates hypoxia-inducible factor.
Topics: Animals; Benzoic Acid; Blotting, Western; Bridged Bicyclo Compounds; Calcium; Calmodulin; Cell Line; | 2010 |
Tumor vasculature targeting following co-delivery of heparin-taurocholate conjugate and suberoylanilide hydroxamic acid using cationic nanolipoplex.
Topics: Animals; Antineoplastic Agents; Cations; Cell Line, Tumor; Cell Proliferation; Drug Delivery Systems | 2012 |
Biodegradable thermosensitive hydrogel for SAHA and DDP delivery: therapeutic effects on oral squamous cell carcinoma xenografts.
Topics: Animals; Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Carcinoma, Squamous Cell; Cell L | 2012 |
Inhibition of multiple pathogenic pathways by histone deacetylase inhibitor SAHA in a corneal alkali-burn injury model.
Topics: Alkalies; Animals; Burns, Chemical; Cornea; Corneal Diseases; Corneal Injuries; Corneal Neovasculari | 2013 |
Continuous intracranial administration of suberoylanilide hydroxamic acid (SAHA) inhibits tumor growth in an orthotopic glioma model.
Topics: Animals; Antineoplastic Agents; Brain Neoplasms; Cell Proliferation; Flow Cytometry; Gene Expression | 2007 |