vorinostat has been researched along with Germinoblastoma in 21 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 |
|---|---|---|
| "Only a minority of patients with high risk lymphoma will be cured with autologous transplant, so maintenance with vorinostat, an oral agent with activity in relapsed lymphoma, was studied starting day + 60 for 21 consecutive days followed by a week off for up to 11 cycles." | 9.20 | A phase 1 study of vorinostat maintenance after autologous transplant in high-risk lymphoma. ( Andritsos, LA; Baiocchi, RA; Benson, DM; Bingman, A; Blum, K; Bowers, MA; Devine, SM; Earl, CT; Flynn, J; Geyer, S; Hade, EM; Hofmeister, CC; Humphries, K; Jaglowski, SM; Lozanski, G; Penza, S; Porcu, P; Vaughn, J; Williams, N, 2015) |
| "Given the poor outcomes of relapsed aggressive lymphomas and preclinical data suggesting that ≥2·5 μmol/l concentrations of vorinostat synergize with both etoposide and platinums, we hypothesized that pulse high-dose vorinostat could safely augment the anti-tumour activity of (R)ICE [(rituximab), ifosphamide, carboplatin, etoposide] chemotherapy." | 9.17 | A phase I study of pulse high-dose vorinostat (V) plus rituximab (R), ifosphamide, carboplatin, and etoposide (ICE) in patients with relapsed lymphoma. ( Boyd, TE; Budde, LE; Chen, TL; Frayo, SL; Gooley, TA; Gopal, AK; Kammerer, BE; Knudsen, NL; Oliveira, GR; Pagel, JM; Press, OW; Roden, JE; Shustov, AR; Warr, TA; Zhang, MM, 2013) |
| " Suberoylanilidehydroxamic acid (SAHA=vorinostat) is the most clinical advanced compound of the class and was approved by the US FDA in October 2006 for the treatment of refractory cutaneous T-cell lymphoma." | 9.16 | Phase I/II intra-patient dose escalation study of vorinostat in children with relapsed solid tumor, lymphoma or leukemia. ( Abel, U; Deubzer, HE; Eisenmenger, A; Karapanagiotou-Schenkel, I; Kulozik, A; Milde, T; Oehme, I; Witt, O; Witt, R, 2012) |
| "A panel of rituximab-chemotherapy-sensitive (RSCL) and rituximab-chemotherapy-resistant cell lines (RRCL) and primary tumor cells isolated from relapsed/refractory B cell lymphoma patients were exposed to escalating doses of vorinostat." | 7.83 | Vorinostat, a histone deacetylase (HDAC) inhibitor, promotes cell cycle arrest and re-sensitizes rituximab- and chemo-resistant lymphoma cells to chemotherapy agents. ( Czuczman, MS; Gu, JJ; Guo, Y; Hernandez-Ilizaliturri, FJ; Mavis, C; Xue, K; Zhang, Q, 2016) |
| "Double epigenetic modulation of Gem/Bu/Mel with azacitidine/vorinostat is feasible and highly active in patients with refractory/poor-risk relapsed lymphomas, warranting further evaluation." | 7.83 | Double epigenetic modulation of high-dose chemotherapy with azacitidine and vorinostat for patients with refractory or poor-risk relapsed lymphoma. ( Ahmed, S; Alousi, A; Anderlini, P; Andersson, BS; Bashir, Q; Champlin, R; Dabaja, B; Fanale, M; Gulbis, A; Hosing, C; Jones, RB; Myers, A; Nieto, Y; Oki, Y; Pinnix, C; Popat, U; Qazilbash, M; Shah, N; Shpall, EJ; Thall, PF; Valdez, BC; Wei, W, 2016) |
| " Growth and survival of multiple lymphoma cell lines were studied with either drug alone or in combination with vorinostat, a histone deacetylase inhibitor (HDACi), using MTS and Annexin V assays, followed by molecular studies." | 7.77 | Combining histone deacetylase inhibitor vorinostat with aurora kinase inhibitors enhances lymphoma cell killing with repression of c-Myc, hTERT, and microRNA levels. ( Dino, PM; Forman, SJ; Jove, R; Kirschbaum, MH; Kowolik, CM; Kretzner, L; Scuto, A; Ventura, P; Wu, J; Yen, Y, 2011) |
| "Enzastaurin is an investigational PKCβ inhibitor that has growth inhibitory and pro-apoptotic effects in both B and T-cell lymphomas." | 7.77 | HDAC inhibitors potentiate the apoptotic effect of enzastaurin in lymphoma cells. ( Almasan, A; Bodo, J; Hsi, ED; Maciejewski, JP; Sedlak, J, 2011) |
| "Only a minority of patients with high risk lymphoma will be cured with autologous transplant, so maintenance with vorinostat, an oral agent with activity in relapsed lymphoma, was studied starting day + 60 for 21 consecutive days followed by a week off for up to 11 cycles." | 5.20 | A phase 1 study of vorinostat maintenance after autologous transplant in high-risk lymphoma. ( Andritsos, LA; Baiocchi, RA; Benson, DM; Bingman, A; Blum, K; Bowers, MA; Devine, SM; Earl, CT; Flynn, J; Geyer, S; Hade, EM; Hofmeister, CC; Humphries, K; Jaglowski, SM; Lozanski, G; Penza, S; Porcu, P; Vaughn, J; Williams, N, 2015) |
| "Given the poor outcomes of relapsed aggressive lymphomas and preclinical data suggesting that ≥2·5 μmol/l concentrations of vorinostat synergize with both etoposide and platinums, we hypothesized that pulse high-dose vorinostat could safely augment the anti-tumour activity of (R)ICE [(rituximab), ifosphamide, carboplatin, etoposide] chemotherapy." | 5.17 | A phase I study of pulse high-dose vorinostat (V) plus rituximab (R), ifosphamide, carboplatin, and etoposide (ICE) in patients with relapsed lymphoma. ( Boyd, TE; Budde, LE; Chen, TL; Frayo, SL; Gooley, TA; Gopal, AK; Kammerer, BE; Knudsen, NL; Oliveira, GR; Pagel, JM; Press, OW; Roden, JE; Shustov, AR; Warr, TA; Zhang, MM, 2013) |
| " Suberoylanilidehydroxamic acid (SAHA=vorinostat) is the most clinical advanced compound of the class and was approved by the US FDA in October 2006 for the treatment of refractory cutaneous T-cell lymphoma." | 5.16 | Phase I/II intra-patient dose escalation study of vorinostat in children with relapsed solid tumor, lymphoma or leukemia. ( Abel, U; Deubzer, HE; Eisenmenger, A; Karapanagiotou-Schenkel, I; Kulozik, A; Milde, T; Oehme, I; Witt, O; Witt, R, 2012) |
| " Gene expression analysis of clinical lymphoma samples suggests that peroxisomes are involved in mediating drug resistance to the histone deacetylase inhibitor (HDACi) Vorinostat (Vor), which promotes ROS-mediated apoptosis." | 3.85 | Peroxisomes protect lymphoma cells from HDAC inhibitor-mediated apoptosis. ( Bolt, AM; Braverman, NE; Dahabieh, MS; Del Rincón, SV; Di Pietro, E; Dupéré-Richer, D; Goncalves, C; Ha, Z; Mann, KK; Miller, WH; Nichol, JN; Pettersson, F, 2017) |
| "A panel of rituximab-chemotherapy-sensitive (RSCL) and rituximab-chemotherapy-resistant cell lines (RRCL) and primary tumor cells isolated from relapsed/refractory B cell lymphoma patients were exposed to escalating doses of vorinostat." | 3.83 | Vorinostat, a histone deacetylase (HDAC) inhibitor, promotes cell cycle arrest and re-sensitizes rituximab- and chemo-resistant lymphoma cells to chemotherapy agents. ( Czuczman, MS; Gu, JJ; Guo, Y; Hernandez-Ilizaliturri, FJ; Mavis, C; Xue, K; Zhang, Q, 2016) |
| "Double epigenetic modulation of Gem/Bu/Mel with azacitidine/vorinostat is feasible and highly active in patients with refractory/poor-risk relapsed lymphomas, warranting further evaluation." | 3.83 | Double epigenetic modulation of high-dose chemotherapy with azacitidine and vorinostat for patients with refractory or poor-risk relapsed lymphoma. ( Ahmed, S; Alousi, A; Anderlini, P; Andersson, BS; Bashir, Q; Champlin, R; Dabaja, B; Fanale, M; Gulbis, A; Hosing, C; Jones, RB; Myers, A; Nieto, Y; Oki, Y; Pinnix, C; Popat, U; Qazilbash, M; Shah, N; Shpall, EJ; Thall, PF; Valdez, BC; Wei, W, 2016) |
| " Growth and survival of multiple lymphoma cell lines were studied with either drug alone or in combination with vorinostat, a histone deacetylase inhibitor (HDACi), using MTS and Annexin V assays, followed by molecular studies." | 3.77 | Combining histone deacetylase inhibitor vorinostat with aurora kinase inhibitors enhances lymphoma cell killing with repression of c-Myc, hTERT, and microRNA levels. ( Dino, PM; Forman, SJ; Jove, R; Kirschbaum, MH; Kowolik, CM; Kretzner, L; Scuto, A; Ventura, P; Wu, J; Yen, Y, 2011) |
| "Enzastaurin is an investigational PKCβ inhibitor that has growth inhibitory and pro-apoptotic effects in both B and T-cell lymphomas." | 3.77 | HDAC inhibitors potentiate the apoptotic effect of enzastaurin in lymphoma cells. ( Almasan, A; Bodo, J; Hsi, ED; Maciejewski, JP; Sedlak, J, 2011) |
| " Herein, we used the small molecule inhibitor ABT-737 to restore sensitivity of Emu-myc lymphomas overexpressing Bcl-2 or Bcl-X(L) to vorinostat and valproic acid (VPA)." | 3.75 | Defining the target specificity of ABT-737 and synergistic antitumor activities in combination with histone deacetylase inhibitors. ( Alsop, AE; Banks, KM; Cluse, LA; Coomans, C; Johnstone, RW; Lindemann, RK; Newbold, A; Peart, MJ; Whitecross, KF; Wiegmans, A, 2009) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 0 (0.00) | 18.7374 |
| 1990's | 0 (0.00) | 18.2507 |
| 2000's | 3 (14.29) | 29.6817 |
| 2010's | 15 (71.43) | 24.3611 |
| 2020's | 3 (14.29) | 2.80 |
| Authors | Studies |
|---|---|
| Ho, TCS | 1 |
| Chan, AHY | 1 |
| Ganesan, A | 1 |
| Pommert, L | 1 |
| Schafer, ES | 1 |
| Malvar, J | 1 |
| Gossai, N | 1 |
| Florendo, E | 1 |
| Pulakanti, K | 1 |
| Heimbruch, K | 1 |
| Stelloh, C | 1 |
| Chi, YY | 1 |
| Sposto, R | 1 |
| Rao, S | 1 |
| Huynh, VT | 1 |
| Brown, P | 1 |
| Chang, BH | 1 |
| Colace, SI | 1 |
| Hermiston, ML | 1 |
| Heym, K | 1 |
| Hutchinson, RJ | 1 |
| Kaplan, JA | 1 |
| Mody, R | 1 |
| O'Brien, TA | 1 |
| Place, AE | 1 |
| Shaw, PH | 1 |
| Ziegler, DS | 1 |
| Wayne, A | 1 |
| Bhojwani, D | 1 |
| Burke, MJ | 1 |
| Witzig, TE | 1 |
| Dahabieh, MS | 1 |
| Ha, Z | 1 |
| Di Pietro, E | 1 |
| Nichol, JN | 1 |
| Bolt, AM | 1 |
| Goncalves, C | 1 |
| Dupéré-Richer, D | 1 |
| Pettersson, F | 1 |
| Mann, KK | 1 |
| Braverman, NE | 1 |
| Del Rincón, SV | 1 |
| Miller, WH | 1 |
| Newbold, A | 2 |
| Matthews, GM | 1 |
| Bots, M | 1 |
| Cluse, LA | 2 |
| Clarke, CJ | 1 |
| Banks, KM | 2 |
| Cullinane, C | 1 |
| Bolden, JE | 1 |
| Christiansen, AJ | 1 |
| Dickins, RA | 1 |
| Miccolo, C | 1 |
| Chiocca, S | 1 |
| Kral, AM | 1 |
| Ozerova, ND | 1 |
| Miller, TA | 1 |
| Methot, JL | 1 |
| Richon, VM | 1 |
| Secrist, JP | 1 |
| Minucci, S | 1 |
| Johnstone, RW | 3 |
| Guo, S | 1 |
| Zhao, H | 1 |
| Zhang, Y | 1 |
| Hofmeister, CC | 1 |
| Williams, N | 1 |
| Geyer, S | 1 |
| Hade, EM | 1 |
| Bowers, MA | 1 |
| Earl, CT | 1 |
| Vaughn, J | 1 |
| Bingman, A | 1 |
| Humphries, K | 1 |
| Lozanski, G | 1 |
| Baiocchi, RA | 1 |
| Jaglowski, SM | 1 |
| Blum, K | 1 |
| Porcu, P | 1 |
| Flynn, J | 1 |
| Penza, S | 1 |
| Benson, DM | 1 |
| Andritsos, LA | 1 |
| Devine, SM | 1 |
| Xue, K | 1 |
| Gu, JJ | 1 |
| Zhang, Q | 1 |
| Mavis, C | 1 |
| Hernandez-Ilizaliturri, FJ | 1 |
| Czuczman, MS | 1 |
| Guo, Y | 1 |
| Ji, J | 1 |
| Valdez, BC | 4 |
| Li, Y | 3 |
| Liu, Y | 2 |
| Teo, EC | 1 |
| Nieto, Y | 4 |
| Champlin, RE | 3 |
| Andersson, BS | 4 |
| Thall, PF | 1 |
| Jones, RB | 1 |
| Wei, W | 1 |
| Myers, A | 1 |
| Hosing, C | 2 |
| Ahmed, S | 1 |
| Popat, U | 1 |
| Shpall, EJ | 1 |
| Qazilbash, M | 1 |
| Gulbis, A | 1 |
| Anderlini, P | 1 |
| Shah, N | 1 |
| Bashir, Q | 1 |
| Alousi, A | 1 |
| Oki, Y | 1 |
| Fanale, M | 1 |
| Dabaja, B | 1 |
| Pinnix, C | 1 |
| Champlin, R | 1 |
| Murray, D | 2 |
| Brammer, JE | 1 |
| Whitecross, KF | 1 |
| Alsop, AE | 1 |
| Wiegmans, A | 1 |
| Coomans, C | 1 |
| Peart, MJ | 1 |
| Lindemann, RK | 1 |
| Kretzner, L | 1 |
| Scuto, A | 1 |
| Dino, PM | 1 |
| Kowolik, CM | 1 |
| Wu, J | 1 |
| Ventura, P | 1 |
| Jove, R | 1 |
| Forman, SJ | 1 |
| Yen, Y | 1 |
| Kirschbaum, MH | 1 |
| Bodo, J | 1 |
| Sedlak, J | 1 |
| Maciejewski, JP | 1 |
| Almasan, A | 1 |
| Hsi, ED | 1 |
| Wang, G | 1 |
| Witt, O | 1 |
| Milde, T | 1 |
| Deubzer, HE | 1 |
| Oehme, I | 1 |
| Witt, R | 1 |
| Kulozik, A | 1 |
| Eisenmenger, A | 1 |
| Abel, U | 1 |
| Karapanagiotou-Schenkel, I | 1 |
| Ogura, M | 1 |
| Karube, K | 1 |
| Tsuzuki, S | 1 |
| Yoshida, N | 1 |
| Arita, K | 1 |
| Kato, H | 1 |
| Katayama, M | 1 |
| Ko, YH | 1 |
| Ohshima, K | 1 |
| Nakamura, S | 1 |
| Kinoshita, T | 1 |
| Seto, M | 1 |
| Budde, LE | 1 |
| Zhang, MM | 1 |
| Shustov, AR | 1 |
| Pagel, JM | 1 |
| Gooley, TA | 1 |
| Oliveira, GR | 1 |
| Chen, TL | 1 |
| Knudsen, NL | 1 |
| Roden, JE | 1 |
| Kammerer, BE | 1 |
| Frayo, SL | 1 |
| Warr, TA | 1 |
| Boyd, TE | 1 |
| Press, OW | 1 |
| Gopal, AK | 1 |
| Sakajiri, S | 1 |
| Kumagai, T | 1 |
| Kawamata, N | 1 |
| Saitoh, T | 1 |
| Said, JW | 1 |
| Koeffler, HP | 1 |
| Rasheed, W | 1 |
| Bishton, M | 1 |
| Prince, HM | 1 |
| Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
|---|---|---|---|---|---|---|---|
| Epigenetic Reprogramming in Relapse AML: A Phase 1 Study of Decitabine and Vorinostat Followed by Fludarabine, Cytarabine and G-CSF (FLAG) in Children and Young Adults With Relapsed/Refractory AML[NCT02412475] | Phase 1 | 3 participants (Actual) | Interventional | 2015-02-21 | Terminated (stopped due to We opened a competing study with the TACL consortium) | ||
| Histone Deacetylase (HDAC) Inhibition Using Vorinostat (SAHA) After Autologous Hematopoietic Stem Cell Transplantation for High Risk Lymphoma[NCT00561418] | Phase 1 | 23 participants (Actual) | Interventional | 2007-11-30 | Completed | ||
| Phase I/II Intra-patient Dose Escalation Study of Vorinostat in Children With Relapsed Solid Tumor, Lymphoma or Leukemia[NCT01422499] | Phase 1/Phase 2 | 50 participants (Actual) | Interventional | 2012-03-31 | Completed | ||
| A Phase I/II Study of Vorinostat Plus Rituximab, Ifosphamide, Carboplatin, and Etoposide for Patients With Relapsed or Refractory Lymphoid Malignancies or Untreated T- or Mantle Cell Lymphoma[NCT00601718] | Phase 1/Phase 2 | 29 participants (Actual) | Interventional | 2007-12-31 | Completed | ||
| A Phase I/II Study of Romidepsin in Combination With Abraxane in Patients With Metastatic Inflammatory Breast Cancer[NCT01938833] | Phase 1/Phase 2 | 9 participants (Actual) | Interventional | 2014-04-30 | Terminated (stopped due to Closed by Sponsor) | ||
| [information is prepared from clinicaltrials.gov, extracted Sep-2024] | |||||||
Median follow up of living patients (NCT00561418)
Timeframe: Up to 5 years
| Intervention | months (Median) |
|---|---|
| Vorinostat (SAHA) | 23.2 |
Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0) for target lesions and assessed by MRI: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Overall Response (OR) = CR + PR. (NCT00561418)
Timeframe: Up to 3 years
| Intervention | patients (Number) | |||
|---|---|---|---|---|
| Complete Response (CR) | Partial Response (PR) | Stable Disease(SD) | Not evaluable | |
| Vorinostat (SAHA) | 13 | 3 | 2 | 5 |
NCI CTCAE version 3.0 was used to assess Adverse Events (AE) Grade 1=Mild AE Grade 2=Moderate AE Grade 3=Severe AE Grade 4=Life-threatening or disabling AE (NCT00561418)
Timeframe: Up to 3 years
| Intervention | patients (Number) | ||||
|---|---|---|---|---|---|
| Fatigue (Grade 1, 2) | Lymphopenia (Grade 1-4) | Thrombocytopenia (Grade 1-3) | Leukopenia (Grade 1-3) | Anemia (Grade 1-3) | |
| Vorinostat (SAHA) | 12 | 11 | 11 | 10 | 10 |
(NCT00601718)
Timeframe: 1-3 weeks post end of treatment
| Intervention | Participants (Count of Participants) |
|---|---|
| Treatment (Enzyme Inhibitor, Monoclonal Antibody, Chemotherapy | 20 |
(NCT00601718)
Timeframe: 3-5 weeks post end of treatment
| Intervention | Participants (Count of Participants) |
|---|---|
| Treatment (Enzyme Inhibitor, Monoclonal Antibody, Chemotherapy | 19 |
(NCT00601718)
Timeframe: 28 days post last dose of study drug
| Intervention | mg twice daily X 5 days (Number) |
|---|---|
| Treatment (Enzyme Inhibitor, Monoclonal Antibody, Chemotherapy | 500 |
Common dose limiting toxicities. (NCT00601718)
Timeframe: 3-5 weeks post end of treatment
| Intervention | Participants (Count of Participants) | |||
|---|---|---|---|---|
| Infection | Hypokalemia | Transaminitis | Grade 3 related gastrointestinal toxicity | |
| Treatment (Enzyme Inhibitor, Monoclonal Antibody, Chemotherapy | 2 | 2 | 2 | 9 |
3 reviews available for vorinostat and Germinoblastoma
| Article | Year |
|---|---|
Thirty Years of HDAC Inhibitors: 2020 Insight and Hindsight.
Topics: Anilides; Biological Products; Clinical Trials as Topic; Histone Deacetylase Inhibitors; Histone Dea | 2020 |
[Phenotypic genetic regulation and treatment of malignant lymphoma].
Topics: Antineoplastic Agents; Enhancer of Zeste Homolog 2 Protein; Epigenesis, Genetic; Histone Deacetylase | 2014 |
Histone deacetylase inhibitors in lymphoma and solid malignancies.
Topics: Animals; Antineoplastic Agents; Antineoplastic Combined Chemotherapy Protocols; Benzamides; Depsipep | 2008 |
5 trials available for vorinostat and Germinoblastoma
| Article | Year |
|---|---|
Decitabine and vorinostat with FLAG chemotherapy in pediatric relapsed/refractory AML: Report from the therapeutic advances in childhood leukemia and lymphoma (TACL) consortium.
Topics: Antineoplastic Combined Chemotherapy Protocols; Child; Cytarabine; Decitabine; Humans; Leukemia, Mye | 2022 |
A phase 1 study of vorinostat maintenance after autologous transplant in high-risk lymphoma.
Topics: Administration, Oral; Adult; Aged; Child; Combined Modality Therapy; Diarrhea; Disease-Free Survival | 2015 |
Phase I/II intra-patient dose escalation study of vorinostat in children with relapsed solid tumor, lymphoma or leukemia.
Topics: Administration, Oral; Adolescent; Antineoplastic Agents; Child; Child, Preschool; Dose-Response Rela | 2012 |
[Current development of new drugs in malignant lymphoma].
Topics: Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Antineoplastic Agents; Bendamustine Hydro | 2012 |
A phase I study of pulse high-dose vorinostat (V) plus rituximab (R), ifosphamide, carboplatin, and etoposide (ICE) in patients with relapsed lymphoma.
Topics: Adult; Aged; Antibodies, Monoclonal, Murine-Derived; Antineoplastic Combined Chemotherapy Protocols; | 2013 |
13 other studies available for vorinostat and Germinoblastoma
| Article | Year |
|---|---|
Myc matters in HIV-associated lymphoma.
Topics: HIV Infections; Humans; Lymphoma; Lymphoma, Non-Hodgkin; Vorinostat | 2020 |
Peroxisomes protect lymphoma cells from HDAC inhibitor-mediated apoptosis.
Topics: Apoptosis; Catalase; Cell Line, Tumor; Cytoprotection; Gene Knockdown Techniques; Gene Silencing; Hi | 2017 |
Molecular and biologic analysis of histone deacetylase inhibitors with diverse specificities.
Topics: Acetylation; Animals; Antineoplastic Agents; Apoptosis; Cell Line, Tumor; Cell Survival; Enzyme Acti | 2013 |
Vorinostat, a histone deacetylase (HDAC) inhibitor, promotes cell cycle arrest and re-sensitizes rituximab- and chemo-resistant lymphoma cells to chemotherapy agents.
Topics: Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Burkitt Lymphoma; Cell Growth Processes; | 2016 |
Cladribine, gemcitabine, busulfan, and SAHA combination as a potential pretransplant conditioning regimen for lymphomas: A preclinical study.
Topics: Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Busulfan; Cell Line, Tumor; Cell Membrane | 2016 |
Double epigenetic modulation of high-dose chemotherapy with azacitidine and vorinostat for patients with refractory or poor-risk relapsed lymphoma.
Topics: Adolescent; Adult; Aged; Antineoplastic Combined Chemotherapy Protocols; Azacitidine; Busulfan; Chil | 2016 |
Differential effects of histone deacetylase inhibitors on cellular drug transporters and their implications for using epigenetic modifiers in combination chemotherapy.
Topics: Antineoplastic Combined Chemotherapy Protocols; Apoptosis; ATP Binding Cassette Transporter, Subfami | 2016 |
Defining the target specificity of ABT-737 and synergistic antitumor activities in combination with histone deacetylase inhibitors.
Topics: Animals; Antineoplastic Combined Chemotherapy Protocols; Biphenyl Compounds; Cell Survival; Drug Del | 2009 |
Combining histone deacetylase inhibitor vorinostat with aurora kinase inhibitors enhances lymphoma cell killing with repression of c-Myc, hTERT, and microRNA levels.
Topics: Antineoplastic Combined Chemotherapy Protocols; Aurora Kinase A; Aurora Kinases; Cell Cycle; Cell Gr | 2011 |
HDAC inhibitors potentiate the apoptotic effect of enzastaurin in lymphoma cells.
Topics: Antineoplastic Agents; Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Blotting, Western; | 2011 |
Synergistic cytotoxicity of the DNA alkylating agent busulfan, nucleoside analogs and suberoylanilide hydroxamic acid in lymphoma cell lines.
Topics: Acetylation; Antineoplastic Agents, Alkylating; Antineoplastic Combined Chemotherapy Protocols; Busu | 2012 |
Comprehensive gene expression profiles of NK cell neoplasms identify vorinostat as an effective drug candidate.
Topics: Antineoplastic Agents; Cell Line, Tumor; Cell Proliferation; Humans; Hydroxamic Acids; Janus Kinase | 2013 |
Histone deacetylase inhibitors profoundly decrease proliferation of human lymphoid cancer cell lines.
Topics: Animals; Antineoplastic Agents; Apoptosis; Cell Cycle Proteins; Cell Line, Tumor; Cell Proliferation | 2005 |