vorinostat has been researched along with Astrocytoma, Grade IV in 36 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 |
|---|---|---|
| "Vorinostat combined with standard chemoradiation had acceptable tolerability in newly diagnosed glioblastoma." | 9.27 | Phase I/II trial of vorinostat combined with temozolomide and radiation therapy for newly diagnosed glioblastoma: results of Alliance N0874/ABTC 02. ( Ahluwalia, MS; Anderson, SK; Ballman, KV; Buckner, JC; Cerhan, J; Galanis, E; Gerstner, ER; Giannini, C; Grossman, SA; Jaeckle, K; Lee, EQ; Lesser, GJ; Ligon, KL; Loboda, A; Miller, CR; Moore, DF; Nebozhyn, M; Prados, M; Sarkaria, JN; Schiff, D; Wen, PY, 2018) |
| "A phase I study was conducted to determine the dose-limiting toxicities (DLT) and maximum tolerated dose (MTD) for the combination of vorinostat with bevacizumab and CPT-11 in recurrent glioblastoma." | 9.16 | Phase I trial of vorinostat combined with bevacizumab and CPT-11 in recurrent glioblastoma. ( Brem, S; Chinnaiyan, P; Chowdhary, S; Kahali, S; Murtagh, R; Pan, E; Potthast, L; Prabhu, A; Rojiani, A; Sarcar, B; Tsai, YY; Yu, HM, 2012) |
| "Vorinostat, a histone deacetylase (HDAC) inhibitor, has shown evidence of single-agent activity in glioblastoma (GBM), and in preclinical studies, we have demonstrated significant synergistic cytotoxicity between HDAC inhibitors and proteasome inhibitors in GBM cell lines." | 9.16 | Phase II trial of vorinostat in combination with bortezomib in recurrent glioblastoma: a north central cancer treatment group study. ( Anderson, SK; Buckner, J; Friday, BB; Galanis, E; Geoffroy, F; Giannini, C; Gross, H; Jaeckle, K; Mazurczak, M; Pajon, E; Schwerkoske, J; Yu, C, 2012) |
| "Vorinostat, a histone deacetylase inhibitor, represents a rational therapeutic target in glioblastoma multiforme (GBM)." | 9.14 | Phase II trial of vorinostat in recurrent glioblastoma multiforme: a north central cancer treatment group study. ( Ames, MM; Buckner, JC; Fantin, VR; Flynn, PJ; Galanis, E; Giannini, C; Hardwick, JS; Jaeckle, KA; Loboda, A; Maurer, MJ; Moore, DF; Nebozhyn, M; Reid, JM; Reilly, JF; Richon, VM; Scheithauer, B; Zwiebel, J, 2009) |
| "Arginine auxotrophy constitutes a weak point of several tumors, among them glioblastoma multiforme (GBM)." | 7.81 | Arginine deprivation by arginine deiminase of Streptococcus pyogenes controls primary glioblastoma growth in vitro and in vivo. ( Classen, CF; Fiedler, T; Hering, S; Kreikemeyer, B; Linnebacher, M; Maletzki, C; Redanz, U; Rosche, Y; Strauss, M; William, D, 2015) |
| " Histone deacetylase inhibitors (HDACIs) represent a class of agents that can modulate gene expression to reduce tumor growth, and we and others have noted some antiglioma activity from HDACIs, such as vorinostat, although insufficient to warrant use as monotherapy." | 7.79 | Bortezomib-induced sensitization of malignant human glioma cells to vorinostat-induced apoptosis depends on reactive oxygen species production, mitochondrial dysfunction, Noxa upregulation, Mcl-1 cleavage, and DNA damage. ( Agostino, NR; DiDomenico, JD; Jane, EP; Pollack, IF; Premkumar, DR, 2013) |
| "The therapeutic benefit of temozolomide in glioblastoma multiforme (GBM) is limited by resistance." | 7.78 | Inhibition of histone deacetylation potentiates the evolution of acquired temozolomide resistance linked to MGMT upregulation in glioblastoma xenografts. ( Carlson, BL; Cen, L; Decker, PA; Gupta, SK; Kitange, GJ; Lomberk, GA; Mladek, AC; Pokorny, JL; Sarkaria, JN; Schroeder, MA; Urrutia, RA; Wu, W, 2012) |
| "Effects of combinations of the US Food and Drug Administation (FDA) approved proteasome inhibitor bortezomib and the histone deacetylase (HDAC) inhibitors vorinostat, valproic acid and sodium phenylbutyrate were studied on primary glioblastoma stem cell lines and conventional glioblastoma cell lines." | 7.78 | Synergistic killing of glioblastoma stem-like cells by bortezomib and HDAC inhibitors. ( Asklund, T; Bergenheim, T; Hedman, H; Henriksson, R; Holmlund, C; Kvarnbrink, S; Wibom, C, 2012) |
| "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) |
| "Rhein has antitumor and SGK1 suppression effects, although its biological activity is limited by poor bioavailability." | 5.56 | Discovery of a novel rhein-SAHA hybrid as a multi-targeted anti-glioblastoma drug. ( Chen, J; Luo, B; Pi, R; Wen, S, 2020) |
| " There are several potential mechanisms by which histone deacetylase inhibition may alter dapsone metabolism including changes in hepatic acetylation or N-glucuronidation leading to an increase in the bioavailability of dapsone's hematotoxic metabolites." | 5.42 | Hemolytic anemia in two patients with glioblastoma multiforme: A possible interaction between vorinostat and dapsone. ( Harmon, M; Lesser, GJ; Lewis, JA; Owen, J; Peacock, JE; Petty, WJ; Pirmohamed, M; Valente, K, 2015) |
| "Vorinostat combined with standard chemoradiation had acceptable tolerability in newly diagnosed glioblastoma." | 5.27 | Phase I/II trial of vorinostat combined with temozolomide and radiation therapy for newly diagnosed glioblastoma: results of Alliance N0874/ABTC 02. ( Ahluwalia, MS; Anderson, SK; Ballman, KV; Buckner, JC; Cerhan, J; Galanis, E; Gerstner, ER; Giannini, C; Grossman, SA; Jaeckle, K; Lee, EQ; Lesser, GJ; Ligon, KL; Loboda, A; Miller, CR; Moore, DF; Nebozhyn, M; Prados, M; Sarkaria, JN; Schiff, D; Wen, PY, 2018) |
| "A phase I study was conducted to determine the dose-limiting toxicities (DLT) and maximum tolerated dose (MTD) for the combination of vorinostat with bevacizumab and CPT-11 in recurrent glioblastoma." | 5.16 | Phase I trial of vorinostat combined with bevacizumab and CPT-11 in recurrent glioblastoma. ( Brem, S; Chinnaiyan, P; Chowdhary, S; Kahali, S; Murtagh, R; Pan, E; Potthast, L; Prabhu, A; Rojiani, A; Sarcar, B; Tsai, YY; Yu, HM, 2012) |
| "Vorinostat, a histone deacetylase (HDAC) inhibitor, has shown evidence of single-agent activity in glioblastoma (GBM), and in preclinical studies, we have demonstrated significant synergistic cytotoxicity between HDAC inhibitors and proteasome inhibitors in GBM cell lines." | 5.16 | Phase II trial of vorinostat in combination with bortezomib in recurrent glioblastoma: a north central cancer treatment group study. ( Anderson, SK; Buckner, J; Friday, BB; Galanis, E; Geoffroy, F; Giannini, C; Gross, H; Jaeckle, K; Mazurczak, M; Pajon, E; Schwerkoske, J; Yu, C, 2012) |
| "Vorinostat, a histone deacetylase inhibitor, represents a rational therapeutic target in glioblastoma multiforme (GBM)." | 5.14 | Phase II trial of vorinostat in recurrent glioblastoma multiforme: a north central cancer treatment group study. ( Ames, MM; Buckner, JC; Fantin, VR; Flynn, PJ; Galanis, E; Giannini, C; Hardwick, JS; Jaeckle, KA; Loboda, A; Maurer, MJ; Moore, DF; Nebozhyn, M; Reid, JM; Reilly, JF; Richon, VM; Scheithauer, B; Zwiebel, J, 2009) |
| "We examined the apoptotic response of two glioblastoma cells, p53 wild type U87 and p53 mutated T98G, to doxorubicin, bortezomib, and vorinostat, which respectively target DNA, 26S proteasome and histone deacetylase, to clarify p53's function in apoptosis." | 4.12 | Compound cellular stress maximizes apoptosis independently of p53 in glioblastoma. ( Chen, CH; Chen, HW; Ho, CJ; Hong, YR; Hu, CJ; Huang, TS; Lee, YL; Loh, JK; Pao, YH; Tsai, CY; Wang, C; Zhu, WH, 2022) |
| "Arginine auxotrophy constitutes a weak point of several tumors, among them glioblastoma multiforme (GBM)." | 3.81 | Arginine deprivation by arginine deiminase of Streptococcus pyogenes controls primary glioblastoma growth in vitro and in vivo. ( Classen, CF; Fiedler, T; Hering, S; Kreikemeyer, B; Linnebacher, M; Maletzki, C; Redanz, U; Rosche, Y; Strauss, M; William, D, 2015) |
| " Histone deacetylase inhibitors (HDACIs) represent a class of agents that can modulate gene expression to reduce tumor growth, and we and others have noted some antiglioma activity from HDACIs, such as vorinostat, although insufficient to warrant use as monotherapy." | 3.79 | Bortezomib-induced sensitization of malignant human glioma cells to vorinostat-induced apoptosis depends on reactive oxygen species production, mitochondrial dysfunction, Noxa upregulation, Mcl-1 cleavage, and DNA damage. ( Agostino, NR; DiDomenico, JD; Jane, EP; Pollack, IF; Premkumar, DR, 2013) |
| "The therapeutic benefit of temozolomide in glioblastoma multiforme (GBM) is limited by resistance." | 3.78 | Inhibition of histone deacetylation potentiates the evolution of acquired temozolomide resistance linked to MGMT upregulation in glioblastoma xenografts. ( Carlson, BL; Cen, L; Decker, PA; Gupta, SK; Kitange, GJ; Lomberk, GA; Mladek, AC; Pokorny, JL; Sarkaria, JN; Schroeder, MA; Urrutia, RA; Wu, W, 2012) |
| "Effects of combinations of the US Food and Drug Administation (FDA) approved proteasome inhibitor bortezomib and the histone deacetylase (HDAC) inhibitors vorinostat, valproic acid and sodium phenylbutyrate were studied on primary glioblastoma stem cell lines and conventional glioblastoma cell lines." | 3.78 | Synergistic killing of glioblastoma stem-like cells by bortezomib and HDAC inhibitors. ( Asklund, T; Bergenheim, T; Hedman, H; Henriksson, R; Holmlund, C; Kvarnbrink, S; Wibom, C, 2012) |
| "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) |
| "Rhein has antitumor and SGK1 suppression effects, although its biological activity is limited by poor bioavailability." | 1.56 | Discovery of a novel rhein-SAHA hybrid as a multi-targeted anti-glioblastoma drug. ( Chen, J; Luo, B; Pi, R; Wen, S, 2020) |
| "One of the major challenges in treatment of glioblastoma is drug resistance." | 1.56 | Synergism of 4HPR and SAHA increases anti-tumor actions in glioblastoma cells. ( Khathayer, F; Ray, SK; Taylor, MA, 2020) |
| " There are several potential mechanisms by which histone deacetylase inhibition may alter dapsone metabolism including changes in hepatic acetylation or N-glucuronidation leading to an increase in the bioavailability of dapsone's hematotoxic metabolites." | 1.42 | Hemolytic anemia in two patients with glioblastoma multiforme: A possible interaction between vorinostat and dapsone. ( Harmon, M; Lesser, GJ; Lewis, JA; Owen, J; Peacock, JE; Petty, WJ; Pirmohamed, M; Valente, K, 2015) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 0 (0.00) | 18.7374 |
| 1990's | 0 (0.00) | 18.2507 |
| 2000's | 2 (5.56) | 29.6817 |
| 2010's | 25 (69.44) | 24.3611 |
| 2020's | 9 (25.00) | 2.80 |
| Authors | Studies |
|---|---|
| Nepali, K | 1 |
| Hsu, TI | 2 |
| Hsieh, CM | 1 |
| Lo, WL | 1 |
| Lai, MJ | 1 |
| Hsu, KC | 1 |
| Lin, TE | 1 |
| Chuang, JY | 2 |
| Liou, JP | 2 |
| Zhou, Y | 1 |
| Liu, H | 1 |
| Zheng, W | 1 |
| Chen, Q | 1 |
| Hu, S | 1 |
| Pan, Y | 1 |
| Bai, Y | 1 |
| Zhang, J | 2 |
| Shao, C | 1 |
| Kaur, J | 1 |
| Jakhmola, S | 1 |
| Singh, RR | 1 |
| Joshi, B | 1 |
| Jha, HC | 1 |
| Joshi, A | 1 |
| Mekala, JR | 1 |
| Ramalingam, PS | 1 |
| Mathavan, S | 1 |
| Yamajala, RBRD | 1 |
| Moparthi, NR | 1 |
| Kurappalli, RK | 1 |
| Manyam, RR | 1 |
| Ho, CJ | 1 |
| Tsai, CY | 1 |
| Zhu, WH | 1 |
| Pao, YH | 1 |
| Chen, HW | 1 |
| Hu, CJ | 1 |
| Lee, YL | 1 |
| Huang, TS | 1 |
| Chen, CH | 1 |
| Loh, JK | 1 |
| Hong, YR | 1 |
| Wang, C | 1 |
| Chen, J | 1 |
| Luo, B | 1 |
| Wen, S | 1 |
| Pi, R | 1 |
| Khathayer, F | 1 |
| Taylor, MA | 1 |
| Ray, SK | 1 |
| Puduvalli, VK | 1 |
| Wu, J | 2 |
| Yuan, Y | 1 |
| Armstrong, TS | 1 |
| Vera, E | 1 |
| Xu, J | 1 |
| Giglio, P | 1 |
| Colman, H | 2 |
| Walbert, T | 1 |
| Raizer, J | 1 |
| Groves, MD | 1 |
| Tran, D | 1 |
| Iwamoto, F | 1 |
| Avgeropoulos, N | 1 |
| Paleologos, N | 1 |
| Fink, K | 1 |
| Peereboom, D | 1 |
| Chamberlain, M | 1 |
| Merrell, R | 1 |
| Penas Prado, M | 1 |
| Yung, WKA | 1 |
| Gilbert, MR | 1 |
| Kang, DW | 1 |
| Hwang, WC | 1 |
| Noh, YN | 1 |
| Kang, Y | 1 |
| Jang, Y | 1 |
| Kim, JA | 1 |
| Min, DS | 1 |
| Galanis, E | 4 |
| Anderson, SK | 2 |
| Miller, CR | 1 |
| Sarkaria, JN | 2 |
| Jaeckle, K | 2 |
| Buckner, JC | 2 |
| Ligon, KL | 2 |
| Ballman, KV | 1 |
| Moore, DF | 2 |
| Nebozhyn, M | 2 |
| Loboda, A | 2 |
| Schiff, D | 1 |
| Ahluwalia, MS | 1 |
| Lee, EQ | 1 |
| Gerstner, ER | 2 |
| Lesser, GJ | 2 |
| Prados, M | 2 |
| Grossman, SA | 1 |
| Cerhan, J | 1 |
| Giannini, C | 3 |
| Wen, PY | 2 |
| Tanrikulu, B | 1 |
| Ziyal, I | 1 |
| Bayri, Y | 1 |
| Festuccia, C | 1 |
| Mancini, A | 1 |
| Colapietro, A | 1 |
| Gravina, GL | 1 |
| Vitale, F | 1 |
| Marampon, F | 1 |
| Delle Monache, S | 1 |
| Pompili, S | 1 |
| Cristiano, L | 1 |
| Vetuschi, A | 1 |
| Tombolini, V | 1 |
| Chen, Y | 1 |
| Mehrling, T | 1 |
| Lohitesh, K | 1 |
| Saini, H | 1 |
| Srivastava, A | 1 |
| Mukherjee, S | 1 |
| Roy, A | 1 |
| Chowdhury, R | 1 |
| Ellingson, BM | 1 |
| Abrey, LE | 1 |
| Nelson, SJ | 1 |
| Kaufmann, TJ | 1 |
| Garcia, J | 1 |
| Chinot, O | 1 |
| Saran, F | 1 |
| Nishikawa, R | 1 |
| Henriksson, R | 2 |
| Mason, WP | 1 |
| Wick, W | 1 |
| Butowski, N | 1 |
| de Groot, J | 1 |
| Chang, S | 1 |
| Mellinghoff, I | 1 |
| Young, RJ | 1 |
| Alexander, BM | 1 |
| Colen, R | 1 |
| Taylor, JW | 1 |
| Arrillaga-Romany, I | 1 |
| Mehta, A | 1 |
| Huang, RY | 1 |
| Pope, WB | 1 |
| Reardon, D | 1 |
| Batchelor, T | 1 |
| Cloughesy, TF | 1 |
| Sung, GJ | 1 |
| Kim, SH | 1 |
| Kwak, S | 1 |
| Park, SH | 1 |
| Song, JH | 1 |
| Jung, JH | 1 |
| Kim, H | 1 |
| Choi, KC | 1 |
| Chiu, SP | 1 |
| Batsaikhan, B | 1 |
| Huang, HM | 1 |
| Wang, JY | 2 |
| Chiao, MT | 1 |
| Cheng, WY | 1 |
| Yang, YC | 1 |
| Shen, CC | 1 |
| Ko, JL | 1 |
| Booth, L | 1 |
| Roberts, JL | 1 |
| Conley, A | 1 |
| Cruickshanks, N | 1 |
| Ridder, T | 1 |
| Grant, S | 1 |
| Poklepovic, A | 1 |
| Dent, P | 1 |
| Lewis, JA | 1 |
| Petty, WJ | 1 |
| Harmon, M | 1 |
| Peacock, JE | 1 |
| Valente, K | 1 |
| Owen, J | 1 |
| Pirmohamed, M | 1 |
| Bezecny, P | 1 |
| Barazzuol, L | 1 |
| Jeynes, JC | 1 |
| Merchant, MJ | 1 |
| Wéra, AC | 1 |
| Barry, MA | 1 |
| Kirkby, KJ | 1 |
| Suzuki, M | 1 |
| Pont, LM | 1 |
| Naipal, K | 1 |
| Kloezeman, JJ | 1 |
| Venkatesan, S | 1 |
| van den Bent, M | 1 |
| van Gent, DC | 1 |
| Dirven, CM | 1 |
| Kanaar, R | 1 |
| Lamfers, ML | 1 |
| Leenstra, S | 1 |
| Fiedler, T | 1 |
| Strauss, M | 1 |
| Hering, S | 1 |
| Redanz, U | 1 |
| William, D | 1 |
| Rosche, Y | 1 |
| Classen, CF | 1 |
| Kreikemeyer, B | 1 |
| Linnebacher, M | 1 |
| Maletzki, C | 1 |
| Singh, MM | 2 |
| Johnson, B | 1 |
| Venkatarayan, A | 1 |
| Flores, ER | 1 |
| Su, X | 1 |
| Barton, M | 1 |
| Lang, F | 1 |
| Chandra, J | 2 |
| Choi, SA | 1 |
| Kwak, PA | 1 |
| Park, CK | 1 |
| Wang, KC | 1 |
| Phi, JH | 1 |
| Lee, JY | 1 |
| Lee, CS | 1 |
| Lee, JH | 1 |
| Kim, SK | 1 |
| Hsu, CC | 1 |
| Chang, WC | 1 |
| Liu, JJ | 1 |
| Yeh, SH | 1 |
| Ko, CY | 1 |
| Chang, KY | 1 |
| Jaeckle, KA | 1 |
| Maurer, MJ | 1 |
| Reid, JM | 1 |
| Ames, MM | 1 |
| Hardwick, JS | 1 |
| Reilly, JF | 1 |
| Fantin, VR | 1 |
| Richon, VM | 1 |
| Scheithauer, B | 1 |
| Flynn, PJ | 1 |
| Zwiebel, J | 1 |
| Sarcar, B | 2 |
| Kahali, S | 2 |
| Chinnaiyan, P | 2 |
| Manton, CA | 1 |
| Bhat, KP | 1 |
| Tsai, WW | 1 |
| Aldape, K | 1 |
| Barton, MC | 1 |
| Kim, C | 1 |
| Shah, BP | 1 |
| Subramaniam, P | 1 |
| Lee, KB | 1 |
| Chowdhary, S | 1 |
| Potthast, L | 1 |
| Prabhu, A | 1 |
| Tsai, YY | 1 |
| Brem, S | 1 |
| Yu, HM | 1 |
| Rojiani, A | 1 |
| Murtagh, R | 1 |
| Pan, E | 1 |
| Premkumar, DR | 1 |
| Jane, EP | 1 |
| Agostino, NR | 1 |
| DiDomenico, JD | 1 |
| Pollack, IF | 1 |
| Friday, BB | 1 |
| Buckner, J | 1 |
| Yu, C | 1 |
| Geoffroy, F | 1 |
| Schwerkoske, J | 1 |
| Mazurczak, M | 1 |
| Gross, H | 1 |
| Pajon, E | 1 |
| Kitange, GJ | 1 |
| Mladek, AC | 1 |
| Carlson, BL | 1 |
| Schroeder, MA | 1 |
| Pokorny, JL | 1 |
| Cen, L | 1 |
| Decker, PA | 1 |
| Wu, W | 1 |
| Lomberk, GA | 1 |
| Gupta, SK | 1 |
| Urrutia, RA | 1 |
| Asklund, T | 1 |
| Kvarnbrink, S | 1 |
| Holmlund, C | 1 |
| Wibom, C | 1 |
| Bergenheim, T | 1 |
| Hedman, H | 1 |
| Kim, MS | 1 |
| Blake, M | 1 |
| Baek, JH | 1 |
| Kohlhagen, G | 1 |
| Pommier, Y | 1 |
| Carrier, F | 1 |
| Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
|---|---|---|---|---|---|---|---|
| Valproic Acid for Children With Recurrent and Progressive Brain Tumors[NCT01861990] | Phase 1 | 0 participants (Actual) | Interventional | 2013-05-31 | Withdrawn (stopped due to Feasibility of the trial was proven to be absent.) | ||
| [information is prepared from clinicaltrials.gov, extracted Sep-2024] | |||||||
1 review available for vorinostat and Astrocytoma, Grade IV
| Article | Year |
|---|---|
Histone deacetylase inhibitors in glioblastoma: pre-clinical and clinical experience.
Topics: Animals; Brain Neoplasms; Clinical Trials as Topic; Depsipeptides; Epigenesis, Genetic; Glioblastoma | 2014 |
6 trials available for vorinostat and Astrocytoma, Grade IV
| Article | Year |
|---|---|
A Bayesian adaptive randomized phase II multicenter trial of bevacizumab with or without vorinostat in adults with recurrent glioblastoma.
Topics: Adult; Antineoplastic Combined Chemotherapy Protocols; Bayes Theorem; Bevacizumab; Brain Neoplasms; | 2020 |
Phase I/II trial of vorinostat combined with temozolomide and radiation therapy for newly diagnosed glioblastoma: results of Alliance N0874/ABTC 02.
Topics: Adult; Aged; Aged, 80 and over; Antineoplastic Combined Chemotherapy Protocols; Brain Neoplasms; Che | 2018 |
Validation of postoperative residual contrast-enhancing tumor volume as an independent prognostic factor for overall survival in newly diagnosed glioblastoma.
Topics: Antineoplastic Combined Chemotherapy Protocols; Chemoradiotherapy; Contrast Media; Female; Follow-Up | 2018 |
Phase II trial of vorinostat in recurrent glioblastoma multiforme: a north central cancer treatment group study.
Topics: Acetylation; Adult; Aged; Antineoplastic Agents; Brain Neoplasms; Cyclin-Dependent Kinase Inhibitor | 2009 |
Phase I trial of vorinostat combined with bevacizumab and CPT-11 in recurrent glioblastoma.
Topics: Adult; Aged; Antibodies, Monoclonal, Humanized; Antineoplastic Combined Chemotherapy Protocols; Beva | 2012 |
Phase II trial of vorinostat in combination with bortezomib in recurrent glioblastoma: a north central cancer treatment group study.
Topics: Adult; Aged; Aged, 80 and over; Antineoplastic Combined Chemotherapy Protocols; Boronic Acids; Borte | 2012 |
29 other studies available for vorinostat and Astrocytoma, Grade IV
| Article | Year |
|---|---|
Pragmatic recruitment of memantine as the capping group for the design of HDAC inhibitors: A preliminary attempt to unravel the enigma of glioblastoma.
Topics: Animals; Antineoplastic Agents; Blood-Brain Barrier; Brain Neoplasms; Cell Proliferation; Dose-Respo | 2021 |
MMP14 Contributes to HDAC Inhibition-Induced Radiosensitization of Glioblastoma.
Topics: Cell Line, Tumor; Chemoradiotherapy; Databases, Nucleic Acid; Glioblastoma; Histone Deacetylase Inhi | 2021 |
Ultrasonic Atomizer-Driven Development of Biocompatible and Biodegradable Poly(d,l-lactide-
Topics: Brain Neoplasms; Glioblastoma; Humans; Nebulizers and Vaporizers; Polylactic Acid-Polyglycolic Acid | 2021 |
Synthesis, in vitro and structural aspects of cap substituted Suberoylanilide hydroxamic acid analogs as potential inducers of apoptosis in Glioblastoma cancer cells via HDAC /microRNA regulation.
Topics: Antineoplastic Agents; Apoptosis; Cell Line, Tumor; Cell Proliferation; Glioblastoma; Histone Deacet | 2022 |
Compound cellular stress maximizes apoptosis independently of p53 in glioblastoma.
Topics: Apoptosis; Bortezomib; Cell Line, Tumor; Doxorubicin; Glioblastoma; Humans; Tumor Suppressor Protein | 2022 |
Discovery of a novel rhein-SAHA hybrid as a multi-targeted anti-glioblastoma drug.
Topics: Anthraquinones; Antineoplastic Agents; Biological Availability; Cell Line, Tumor; Cell Movement; Cel | 2020 |
Synergism of 4HPR and SAHA increases anti-tumor actions in glioblastoma cells.
Topics: Angiogenic Proteins; Animals; Antineoplastic Agents; Apoptosis; Cell Differentiation; Cell Line, Tum | 2020 |
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 |
In Vitro Effects of Mesenchymal Stem Cells and Various Agents on Apoptosis of Glioblastoma Cells.
Topics: Adult; Antineoplastic Agents; Apoptosis; Benzoquinones; Cell Line, Tumor; Gene Silencing; Glioblasto | 2019 |
The first-in-class alkylating deacetylase inhibitor molecule tinostamustine shows antitumor effects and is synergistic with radiotherapy in preclinical models of glioblastoma.
Topics: Animals; Antineoplastic Agents, Alkylating; Bendamustine Hydrochloride; Benzimidazoles; Brain Neopla | 2018 |
Autophagy inhibition potentiates SAHA‑mediated apoptosis in glioblastoma cells by accumulation of damaged mitochondria.
Topics: Autophagosomes; Autophagy; Brain Neoplasms; Cell Line, Tumor; Cell Survival; Chloroquine; Drug Syner | 2018 |
Inhibition of TFEB oligomerization by co-treatment of melatonin with vorinostat promotes the therapeutic sensitivity in glioblastoma and glioma stem cells.
Topics: Animals; Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Basic Helix-Loop-Helix Leucine Z | 2019 |
Application of Electric Cell-Substrate Impedance Sensing to Investigate the Cytotoxic Effects of Andrographolide on U-87 MG Glioblastoma Cell Migration and Apoptosis.
Topics: Apoptosis; Biosensing Techniques; Cell Line, Tumor; Cell Movement; Cell Proliferation; Cell Survival | 2019 |
Suberoylanilide hydroxamic acid (SAHA) causes tumor growth slowdown and triggers autophagy in glioblastoma stem cells.
Topics: Apoptosis; Autophagy; Cell Line, Tumor; Glioblastoma; Histone Deacetylase Inhibitors; Humans; Hydrox | 2013 |
HDAC inhibitors enhance the lethality of low dose salinomycin in parental and stem-like GBM cells.
Topics: Antineoplastic Agents; Apoptosis; Autophagy; Breast Neoplasms; Cell Line, Tumor; Drug Synergism; Fem | 2014 |
Hemolytic anemia in two patients with glioblastoma multiforme: A possible interaction between vorinostat and dapsone.
Topics: Anemia, Hemolytic; Dapsone; Female; Glioblastoma; Humans; Hydroxamic Acids; Middle Aged; Vorinostat | 2015 |
Radiosensitization of glioblastoma cells using a histone deacetylase inhibitor (SAHA) comparing carbon ions with X-rays.
Topics: Carbon; Cell Line, Tumor; DNA; DNA Repair; Glioblastoma; Histone Deacetylase Inhibitors; Histones; H | 2015 |
DNA damage response and anti-apoptotic proteins predict radiosensitization efficacy of HDAC inhibitors SAHA and LBH589 in patient-derived glioblastoma cells.
Topics: Acetylation; Adult; Aged; Aged, 80 and over; Apoptosis; Apoptosis Regulatory Proteins; Blotting, Wes | 2015 |
Arginine deprivation by arginine deiminase of Streptococcus pyogenes controls primary glioblastoma growth in vitro and in vivo.
Topics: Animals; Antineoplastic Agents; Antineoplastic Combined Chemotherapy Protocols; Arginine; Argininosu | 2015 |
Preclinical activity of combined HDAC and KDM1A inhibition in glioblastoma.
Topics: Animals; Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Brain Neoplasms; Cell Line, Tumo | 2015 |
A novel histone deacetylase inhibitor, CKD5, has potent anti-cancer effects in glioblastoma.
Topics: Animals; Apoptosis; Brain Neoplasms; Cell Line, Tumor; Cell Proliferation; Dose-Response Relationshi | 2017 |
Suberoylanilide hydroxamic acid represses glioma stem-like cells.
Topics: Animals; Apoptosis; Cell Cycle Checkpoints; Cell Line, Tumor; Cell Proliferation; Drug Resistance, N | 2016 |
Vorinostat enhances the cytotoxic effects of the topoisomerase I inhibitor SN38 in glioblastoma cell lines.
Topics: Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Blotting, Western; Brain Neoplasms; Campt | 2010 |
Inhibition of LSD1 sensitizes glioblastoma cells to histone deacetylase inhibitors.
Topics: Acetylation; Astrocytes; Blotting, Western; Brain Neoplasms; Caspases; Cells, Cultured; DNA Methylat | 2011 |
Synergistic induction of apoptosis in brain cancer cells by targeted codelivery of siRNA and anticancer drugs.
Topics: Adjuvants, Pharmaceutic; Animals; Antineoplastic Agents; Apoptosis; Brain Neoplasms; Cell Line, Tumo | 2011 |
Bortezomib-induced sensitization of malignant human glioma cells to vorinostat-induced apoptosis depends on reactive oxygen species production, mitochondrial dysfunction, Noxa upregulation, Mcl-1 cleavage, and DNA damage.
Topics: Antineoplastic Agents; Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Apoptosis Regulato | 2013 |
Inhibition of histone deacetylation potentiates the evolution of acquired temozolomide resistance linked to MGMT upregulation in glioblastoma xenografts.
Topics: Acetylation; Animals; Antineoplastic Agents, Alkylating; Blotting, Western; Dacarbazine; DNA Methyla | 2012 |
Synergistic killing of glioblastoma stem-like cells by bortezomib and HDAC inhibitors.
Topics: Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Boronic Acids; Bortezomib; Brain Neoplasm | 2012 |
Inhibition of histone deacetylase increases cytotoxicity to anticancer drugs targeting DNA.
Topics: Acetylation; Antineoplastic Agents; Apoptosis; Breast Neoplasms; Cell Line, Tumor; DNA Topoisomerase | 2003 |