vorinostat has been researched along with Triple Negative Breast Neoplasms in 24 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).
Triple Negative Breast Neoplasms: Breast neoplasms that do not express ESTROGEN RECEPTORS; PROGESTERONE RECEPTORS; and do not overexpress the NEU RECEPTOR/HER-2 PROTO-ONCOGENE PROTEIN.
| Excerpt | Relevance | Reference |
|---|---|---|
| "RNAseq studies in triple negative breast cancer cells revealed that gene expression profiles of hybrids were very similar to that of 1,25D, as was that observed with 1,25D and SAHA combined." | 1.72 | Molecular mechanisms of bifunctional vitamin D receptor agonist-histone deacetylase inhibitor hybrid molecules in triple-negative breast cancer. ( Barbier, C; Bouttier, M; Gleason, JL; Ismailova, A; Mansour, A; Sarmadi, F; Scarlata, DA; Wang, C; White, JH; Zeitouni, C, 2022) |
| "Aminoflavone (AF) acts as a ligand of the aryl hydrocarbon receptor (AhR)." | 1.39 | Reactivation of estrogen receptor α by vorinostat sensitizes mesenchymal-like triple-negative breast cancer to aminoflavone, a ligand of the aryl hydrocarbon receptor. ( Burger, A; Li, J; Polin, L; Shelton, P; Stark, K; Wu, J, 2013) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 0 (0.00) | 18.7374 |
| 1990's | 0 (0.00) | 18.2507 |
| 2000's | 0 (0.00) | 29.6817 |
| 2010's | 14 (58.33) | 24.3611 |
| 2020's | 10 (41.67) | 2.80 |
| Authors | Studies |
|---|---|
| Wu, B | 1 |
| Fathi, S | 1 |
| Mortley, S | 1 |
| Mohiuddin, M | 1 |
| Jang, YC | 1 |
| Oyelere, AK | 1 |
| Zhang, K | 1 |
| Liu, Z | 1 |
| Yao, Y | 1 |
| Qiu, Y | 1 |
| Li, F | 1 |
| Chen, D | 1 |
| Hamilton, DJ | 1 |
| Li, Z | 1 |
| Jiang, S | 1 |
| Jiang, XC | 1 |
| Tu, FH | 1 |
| Wei, LY | 1 |
| Wang, BZ | 1 |
| Yuan, H | 1 |
| Yuan, JM | 1 |
| Rao, Y | 1 |
| Huang, SL | 1 |
| Li, QJ | 1 |
| Ou, TM | 1 |
| Wang, HG | 1 |
| Tan, JH | 1 |
| Chen, SB | 1 |
| Huang, ZS | 1 |
| Barbier, C | 1 |
| Mansour, A | 1 |
| Ismailova, A | 1 |
| Sarmadi, F | 1 |
| Scarlata, DA | 1 |
| Bouttier, M | 1 |
| Zeitouni, C | 1 |
| Wang, C | 1 |
| Gleason, JL | 1 |
| White, JH | 1 |
| Gong, Y | 1 |
| Chen, W | 1 |
| Chen, X | 1 |
| He, Y | 1 |
| Jiang, H | 1 |
| Zhang, X | 1 |
| Pan, L | 1 |
| Ni, B | 1 |
| Yang, F | 1 |
| Xu, Y | 1 |
| Zhang, Q | 1 |
| Zhou, L | 1 |
| Cheng, Y | 1 |
| Salahuddin, A | 1 |
| Ghanem, H | 1 |
| Omran, GA | 1 |
| Helmy, MW | 1 |
| Steed, KL | 1 |
| Jordan, HR | 1 |
| Tollefsbol, TO | 1 |
| Ma, W | 1 |
| Sun, J | 1 |
| Xu, J | 1 |
| Luo, Z | 2 |
| Diao, D | 1 |
| Zhang, Z | 1 |
| Oberly, PJ | 1 |
| Minnigh, MB | 1 |
| Xie, W | 1 |
| Poloyac, SM | 1 |
| Huang, Y | 1 |
| Li, S | 1 |
| Nouri Emamzadeh, F | 1 |
| Word, B | 1 |
| Cotton, E | 1 |
| Hawkins, A | 1 |
| Littlejohn, K | 1 |
| Moore, R | 1 |
| Miranda-Carbon, G | 1 |
| Orish, CN | 1 |
| Lyn-Cook, B | 1 |
| Palczewski, MB | 1 |
| Kuschman, HP | 1 |
| Bovee, R | 1 |
| Hickok, JR | 1 |
| Thomas, DD | 1 |
| Kou, X | 1 |
| Yang, Y | 1 |
| Jiang, X | 1 |
| Liu, H | 2 |
| Sun, F | 1 |
| Wang, X | 1 |
| Liu, L | 1 |
| Lin, Z | 1 |
| Jiang, L | 1 |
| Librizzi, M | 2 |
| Caradonna, F | 1 |
| Cruciata, I | 1 |
| Dębski, J | 1 |
| Sansook, S | 1 |
| Dadlez, M | 1 |
| Spencer, J | 2 |
| Luparello, C | 2 |
| Marijon, H | 1 |
| Lee, DH | 1 |
| Ding, L | 1 |
| Sun, H | 1 |
| Gery, S | 1 |
| de Gramont, A | 1 |
| Koeffler, HP | 1 |
| Cázares Marinero, Jde J | 1 |
| Lapierre, M | 1 |
| Cavaillès, V | 1 |
| Saint-Fort, R | 1 |
| Vessières, A | 1 |
| Top, S | 1 |
| Jaouen, G | 1 |
| Stark, K | 1 |
| Burger, A | 1 |
| Wu, J | 1 |
| Shelton, P | 1 |
| Polin, L | 1 |
| Li, J | 1 |
| Ha, K | 1 |
| Fiskus, W | 1 |
| Choi, DS | 1 |
| Bhaskara, S | 1 |
| Cerchietti, L | 1 |
| Devaraj, SG | 1 |
| Shah, B | 1 |
| Sharma, S | 1 |
| Chang, JC | 1 |
| Melnick, AM | 1 |
| Hiebert, S | 1 |
| Bhalla, KN | 1 |
| Sardiu, ME | 1 |
| Smith, KT | 1 |
| Groppe, BD | 1 |
| Gilmore, JM | 1 |
| Saraf, A | 1 |
| Egidy, R | 1 |
| Peak, A | 1 |
| Seidel, CW | 1 |
| Florens, L | 1 |
| Workman, JL | 1 |
| Washburn, MP | 1 |
| de Cremoux, P | 1 |
| Dalvai, M | 1 |
| N'Doye, O | 1 |
| Moutahir, F | 1 |
| Rolland, G | 1 |
| Chouchane-Mlik, O | 1 |
| Assayag, F | 1 |
| Lehmann-Che, J | 1 |
| Kraus-Berthie, L | 1 |
| Nicolas, A | 1 |
| Lockhart, BP | 1 |
| Marangoni, E | 1 |
| de Thé, H | 1 |
| Depil, S | 1 |
| Bystricky, K | 1 |
| Decaudin, D | 1 |
| Vogel, RI | 1 |
| Coughlin, K | 1 |
| Scotti, A | 1 |
| Iizuka, Y | 1 |
| Anchoori, R | 1 |
| Roden, RB | 1 |
| Marastoni, M | 1 |
| Bazzaro, M | 1 |
| Min, A | 1 |
| Im, SA | 1 |
| Kim, DK | 1 |
| Song, SH | 1 |
| Kim, HJ | 1 |
| Lee, KH | 1 |
| Kim, TY | 2 |
| Han, SW | 1 |
| Oh, DY | 1 |
| O'Connor, MJ | 1 |
| Bang, YJ | 1 |
| Wiegmans, AP | 1 |
| Yap, PY | 1 |
| Ward, A | 1 |
| Lim, YC | 1 |
| Khanna, KK | 1 |
| Wu, S | 1 |
| Yu, PJ | 1 |
| Xie, H | 1 |
| He, YW | 1 |
| Wang, ZT | 1 |
| Chen, ZJ | 1 |
| Jiang, GM | 1 |
| Wu, YM | 1 |
| Liu, T | 1 |
| Yi, YM | 1 |
| Zeng, J | 1 |
| Du, J | 1 |
| Wang, HS | 1 |
24 other studies available for vorinostat and Triple Negative Breast Neoplasms
| Article | Year |
|---|---|
Pyrimethamine conjugated histone deacetylase inhibitors: Design, synthesis and evidence for triple negative breast cancer selective cytotoxicity.
Topics: Animals; Antineoplastic Agents; Cell Proliferation; Cells, Cultured; Chlorocebus aethiops; Dose-Resp | 2020 |
Structure-Based Design of a Selective Class I Histone Deacetylase (HDAC) Near-Infrared (NIR) Probe for Epigenetic Regulation Detection in Triple-Negative Breast Cancer (TNBC).
Topics: Animals; Biomarkers, Tumor; Carbocyanines; Cell Line, Tumor; Depsipeptides; Epigenesis, Genetic; Fem | 2021 |
Discovery of a Novel G-Quadruplex and Histone Deacetylase (HDAC) Dual-Targeting Agent for the Treatment of Triple-Negative Breast Cancer.
Topics: Antineoplastic Agents; Apoptosis; Cell Line, Tumor; Cell Proliferation; DNA; Histone Deacetylase Inh | 2022 |
Molecular mechanisms of bifunctional vitamin D receptor agonist-histone deacetylase inhibitor hybrid molecules in triple-negative breast cancer.
Topics: Antineoplastic Agents; Cell Proliferation; Histone Deacetylase Inhibitors; Humans; Receptors, Calcit | 2022 |
An Injectable Epigenetic Autophagic Modulatory Hydrogel for Boosting Umbilical Cord Blood NK Cell Therapy Prevents Postsurgical Relapse of Triple-Negative Breast Cancer.
Topics: Autophagy; Cell- and Tissue-Based Therapy; Epigenesis, Genetic; Fetal Blood; Humans; Hydrogels; Neop | 2022 |
Epigenetic restoration and activation of ERβ: an inspiring approach for treatment of triple-negative breast cancer.
Topics: Caspase 3; Cell Line, Tumor; Cell Proliferation; Cyclin D1; Decitabine; Epigenesis, Genetic; Estroge | 2022 |
SAHA and EGCG Promote Apoptosis in Triple-negative Breast Cancer Cells, Possibly Through the Modulation of cIAP2.
Topics: Apoptosis; Baculoviral IAP Repeat-Containing 3 Protein; Caspase 7; Catechin; Cell Cycle; Cell Line, | 2020 |
Sensitizing Triple Negative Breast Cancer to Tamoxifen Chemotherapy via a Redox-Responsive Vorinostat-containing Polymeric Prodrug Nanocarrier.
Topics: Animals; Antineoplastic Combined Chemotherapy Protocols; Cell Line, Tumor; Drug Carriers; Drug Combi | 2020 |
Modulation of Estrogen α and Progesterone Receptors in Triple Negative Breast Cancer Cell Lines: The Effects of Vorinostat and Indole-3-Carbinol In Vitro.
Topics: Antineoplastic Agents; Cell Line, Tumor; Estrogen Receptor alpha; Female; Gene Expression Regulation | 2020 |
Vorinostat exhibits anticancer effects in triple-negative breast cancer cells by preventing nitric oxide-driven histone deacetylation.
Topics: Acetylation; Antineoplastic Agents; Cell Line, Tumor; Cell Proliferation; Cell Survival; Dose-Respon | 2021 |
Vorinostat and Simvastatin have synergistic effects on triple-negative breast cancer cells via abrogating Rab7 prenylation.
Topics: Animals; Apoptosis; Autophagosomes; Autophagy; Cell Line, Tumor; Cell Proliferation; Female; Histone | 2017 |
Molecular Signatures Associated with Treatment of Triple-Negative MDA-MB231 Breast Cancer Cells with Histone Deacetylase Inhibitors JAHA and SAHA.
Topics: Antineoplastic Agents; Cell Line, Tumor; Computational Biology; Dose-Response Relationship, Drug; Dr | 2017 |
Co-targeting poly(ADP-ribose) polymerase (PARP) and histone deacetylase (HDAC) in triple-negative breast cancer: Higher synergism in BRCA mutated cells.
Topics: Animals; Apoptosis; BRCA1 Protein; Cell Cycle; Cell Line, Tumor; Cell Proliferation; Cell Survival; | 2018 |
Efficient new constructs against triple negative breast cancer cells: synthesis and preliminary biological study of ferrocifen-SAHA hybrids and related species.
Topics: Antineoplastic Agents; Cell Line, Tumor; Cell Proliferation; Cyclin-Dependent Kinase Inhibitor p21; | 2013 |
Reactivation of estrogen receptor α by vorinostat sensitizes mesenchymal-like triple-negative breast cancer to aminoflavone, a ligand of the aryl hydrocarbon receptor.
Topics: Animals; Cell Line, Tumor; Cell Proliferation; Cytoplasm; Drug Synergism; Estrogen Receptor alpha; F | 2013 |
Histone deacetylase inhibitor treatment induces 'BRCAness' and synergistic lethality with PARP inhibitor and cisplatin against human triple negative breast cancer cells.
Topics: Animals; Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Ataxia Telangiectasia Mutated Pr | 2014 |
Suberoylanilide hydroxamic acid (SAHA)-induced dynamics of a human histone deacetylase protein interaction network.
Topics: Cell Line, Tumor; Female; Gene Expression; Gene Expression Regulation; Histone Deacetylase Inhibitor | 2014 |
HDAC inhibition does not induce estrogen receptor in human triple-negative breast cancer cell lines and patient-derived xenografts.
Topics: Benzofurans; Cell Proliferation; Cyclin D1; Estrogen Receptor alpha; Estrogen Receptor beta; Female; | 2015 |
Simultaneous inhibition of deubiquitinating enzymes (DUBs) and autophagy synergistically kills breast cancer cells.
Topics: Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Autophagy; Cell Line, Tumor; Chloroquine; | 2015 |
Histone deacetylase inhibitor, suberoylanilide hydroxamic acid (SAHA), enhances anti-tumor effects of the poly (ADP-ribose) polymerase (PARP) inhibitor olaparib in triple-negative breast cancer cells.
Topics: Animals; Apoptosis; Cell Cycle; Cell Line, Tumor; Cell Proliferation; Dose-Response Relationship, Dr | 2015 |
Differences in Expression of Key DNA Damage Repair Genes after Epigenetic-Induced BRCAness Dictate Synthetic Lethality with PARP1 Inhibition.
Topics: Antineoplastic Agents; Benzimidazoles; BRCA1 Protein; Cell Line, Tumor; Cell Survival; Depsipeptides | 2015 |
Suberoylanilide hydroxamic acid (SAHA) promotes the epithelial mesenchymal transition of triple negative breast cancer cells via HDAC8/FOXA1 signals.
Topics: Epithelial-Mesenchymal Transition; Hepatocyte Nuclear Factor 3-alpha; Histone Deacetylases; Humans; | 2016 |
Histone deacetylase inhibitors suppress mutant p53 transcription via HDAC8/YY1 signals in triple negative breast cancer cells.
Topics: Apoptosis; Butyric Acid; Cell Cycle; Cell Line, Tumor; Cell Proliferation; Down-Regulation; Histone | 2016 |
Biological Effect of a Hybrid Anticancer Agent Based on Kinase and Histone Deacetylase Inhibitors on Triple-Negative (MDA-MB231) Breast Cancer Cells.
Topics: Antineoplastic Agents; Blotting, Western; Cell Cycle; Cell Survival; Female; Flow Cytometry; Histone | 2016 |