vorinostat has been researched along with B-Cell Lymphoma in 13 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 |
|---|---|---|
| "A phase 1 study with carfilzomib and vorinostat was conducted in 20 B-cell lymphoma patients." | 9.22 | Phase 1 trial of carfilzomib (PR-171) in combination with vorinostat (SAHA) in patients with relapsed or refractory B-cell lymphomas. ( Barr, PM; Bose, P; Cebula, EM; Feng, C; Fisher, RI; Friedberg, JW; Grant, S; Herr, M; Hogan, KT; Holkova, B; Kmieciak, M; Peterson, DR; Pierce, E; Rollins, AD; Sankala, H; Shrader, E; Tombes, MB; Wan, W; Weir-Wiggins, C; Yazbeck, VY, 2016) |
| "Vorinostat is a histone deacetylase inhibitor that induces differentiation, growth arrest, and/or apoptosis of malignant cells both in vitro and in vivo and has shown clinical responses in approximately 30% of patients with advanced mycosis fungoides and Sézary syndrome cutaneous T-cell lymphoma (CTCL)." | 7.74 | Constitutive activation of signal transducers and activators of transcription predicts vorinostat resistance in cutaneous T-cell lymphoma. ( Fantin, VR; Frankel, SR; Gooden, F; Harrington, EA; Hendrickson, RC; Hou, XS; Kadin, ME; Korenchuk, S; Li, L; Loboda, A; Paweletz, CP; Pierce, JW; Randolph, S; Reilly, JF; Richon, VM; Roth, JA; Ware, CM, 2008) |
| "A phase 1 study with carfilzomib and vorinostat was conducted in 20 B-cell lymphoma patients." | 5.22 | Phase 1 trial of carfilzomib (PR-171) in combination with vorinostat (SAHA) in patients with relapsed or refractory B-cell lymphomas. ( Barr, PM; Bose, P; Cebula, EM; Feng, C; Fisher, RI; Friedberg, JW; Grant, S; Herr, M; Hogan, KT; Holkova, B; Kmieciak, M; Peterson, DR; Pierce, E; Rollins, AD; Sankala, H; Shrader, E; Tombes, MB; Wan, W; Weir-Wiggins, C; Yazbeck, VY, 2016) |
| " In this protocol, we describe how to monitor the response of murine B-cell lymphomas to an inducer of apoptosis, the anticancer drug vorinostat (a histone deacetylase inhibitor)." | 3.80 | Fluorodeoxyglucose-based positron emission tomography imaging to monitor drug responses in hematological tumors. ( Bots, M; Cullinane, C; Martin, BP; Newbold, A, 2014) |
| " In this protocol, B-cell lymphoma cells are injected into recipient mice and, on tumor formation, the mice are treated with the apoptosis inducer vorinostat (a histone deacetylase inhibitor)." | 3.80 | Detection of apoptotic cells using immunohistochemistry. ( Bots, M; Cullinane, C; Martin, BP; Newbold, A, 2014) |
| " In this protocol, we describe a propidium iodide (PI) flow cytometry assay to evaluate B-cell lymphomas that have undergone apoptosis in vivo." | 3.80 | Detection of apoptotic cells using propidium iodide staining. ( Bots, M; Cullinane, C; Martin, BP; Newbold, A, 2014) |
| "Vorinostat is a histone deacetylase inhibitor that induces differentiation, growth arrest, and/or apoptosis of malignant cells both in vitro and in vivo and has shown clinical responses in approximately 30% of patients with advanced mycosis fungoides and Sézary syndrome cutaneous T-cell lymphoma (CTCL)." | 3.74 | Constitutive activation of signal transducers and activators of transcription predicts vorinostat resistance in cutaneous T-cell lymphoma. ( Fantin, VR; Frankel, SR; Gooden, F; Harrington, EA; Hendrickson, RC; Hou, XS; Kadin, ME; Korenchuk, S; Li, L; Loboda, A; Paweletz, CP; Pierce, JW; Randolph, S; Reilly, JF; Richon, VM; Roth, JA; Ware, CM, 2008) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 0 (0.00) | 18.7374 |
| 1990's | 0 (0.00) | 18.2507 |
| 2000's | 2 (15.38) | 29.6817 |
| 2010's | 10 (76.92) | 24.3611 |
| 2020's | 1 (7.69) | 2.80 |
| Authors | Studies |
|---|---|
| Li, S | 1 |
| He, X | 1 |
| Gan, Y | 1 |
| Zhang, J | 1 |
| Gao, F | 1 |
| Lin, L | 1 |
| Qiu, X | 1 |
| Yu, T | 1 |
| Zhang, X | 1 |
| Chen, P | 1 |
| Tong, J | 1 |
| Qian, W | 1 |
| Xu, Y | 1 |
| Newbold, A | 5 |
| Salmon, JM | 1 |
| Martin, BP | 4 |
| Stanley, K | 1 |
| Johnstone, RW | 2 |
| Ogura, M | 2 |
| Ando, K | 1 |
| Suzuki, T | 1 |
| Ishizawa, K | 1 |
| Oh, SY | 1 |
| Itoh, K | 1 |
| Yamamoto, K | 2 |
| Au, WY | 1 |
| Tien, HF | 1 |
| Matsuno, Y | 1 |
| Terauchi, T | 1 |
| Mori, M | 1 |
| Tanaka, Y | 1 |
| Shimamoto, T | 1 |
| Tobinai, K | 1 |
| Kim, WS | 1 |
| Cullinane, C | 3 |
| Bots, M | 3 |
| Yang, B | 1 |
| Yu, D | 1 |
| Liu, J | 1 |
| Yang, K | 1 |
| Wu, G | 1 |
| Liu, H | 1 |
| Holkova, B | 1 |
| Kmieciak, M | 1 |
| Bose, P | 1 |
| Yazbeck, VY | 1 |
| Barr, PM | 1 |
| Tombes, MB | 1 |
| Shrader, E | 1 |
| Weir-Wiggins, C | 1 |
| Rollins, AD | 1 |
| Cebula, EM | 1 |
| Pierce, E | 1 |
| Herr, M | 1 |
| Sankala, H | 1 |
| Hogan, KT | 1 |
| Wan, W | 1 |
| Feng, C | 1 |
| Peterson, DR | 1 |
| Fisher, RI | 1 |
| Grant, S | 1 |
| Friedberg, JW | 1 |
| Joosten, M | 1 |
| Ginzel, S | 1 |
| Blex, C | 1 |
| Schmidt, D | 1 |
| Gombert, M | 1 |
| Chen, C | 1 |
| Linka, RM | 1 |
| Gräbner, O | 1 |
| Hain, A | 1 |
| Hirsch, B | 1 |
| Sommerfeld, A | 1 |
| Seegebarth, A | 1 |
| Gruber, U | 1 |
| Maneck, C | 1 |
| Zhang, L | 1 |
| Stenin, K | 1 |
| Dieks, H | 1 |
| Sefkow, M | 1 |
| Münk, C | 1 |
| Baldus, CD | 1 |
| Thiele, R | 1 |
| Borkhardt, A | 1 |
| Hummel, M | 1 |
| Köster, H | 1 |
| Fischer, U | 1 |
| Dreger, M | 1 |
| Seitz, V | 1 |
| Ohmachi, K | 1 |
| Lindemann, RK | 1 |
| Whitecross, KF | 1 |
| Cluse, LA | 1 |
| Frew, AJ | 1 |
| Ellis, L | 1 |
| Williams, S | 1 |
| Wiegmans, AP | 1 |
| Dear, AE | 1 |
| Scott, CL | 1 |
| Pellegrini, M | 1 |
| Wei, A | 1 |
| Richon, VM | 2 |
| Marks, PA | 1 |
| Lowe, SW | 1 |
| Smyth, MJ | 1 |
| Fantin, VR | 1 |
| Loboda, A | 1 |
| Paweletz, CP | 1 |
| Hendrickson, RC | 1 |
| Pierce, JW | 1 |
| Roth, JA | 1 |
| Li, L | 1 |
| Gooden, F | 1 |
| Korenchuk, S | 1 |
| Hou, XS | 1 |
| Harrington, EA | 1 |
| Randolph, S | 1 |
| Reilly, JF | 1 |
| Ware, CM | 1 |
| Kadin, ME | 1 |
| Frankel, SR | 1 |
| Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
|---|---|---|---|---|---|---|---|
| A Phase II Study of MK-0683 in Patients With Relapsed / Refractory Follicular Lymphoma (FL), Other Indolent B-cell Non-Hodgkin's Lymphoma (B-NHL) or Mantle Cell Lymphoma (MCL)[NCT00875056] | Phase 2 | 56 participants (Actual) | Interventional | 2009-04-15 | Completed | ||
| Phase IIb Multicenter Clinical Trial of Oral Suberoylanilide Hydroxamic Acid (SAHA) in Advanced Cutaneous T-cell Lymphoma[NCT00091559] | Phase 2 | 74 participants (Actual) | Interventional | 2005-02-03 | Completed | ||
| [information is prepared from clinicaltrials.gov, extracted Sep-2024] | |||||||
An adverse event (AE) was defined as any untoward medical occurrence in a participant administered study treatment and which did not necessarily have to have a causal relationship with this treatment. The number of participants who discontinued from study drug due to an adverse event was reported. (NCT00875056)
Timeframe: Up to 536 days
| Intervention | Participants (Count of Participants) |
|---|---|
| Follicular Lymphoma (FL) | 6 |
| Indolent Non-FL B-NHL or MCL | 1 |
| Other Disease | 2 |
An AE was defined as any untoward medical occurrence in a participant administered study treatment and which did not necessarily have to have a causal relationship with this treatment. The number of participants who experienced an AE was presented. (NCT00875056)
Timeframe: Up to approximately 29 months
| Intervention | Participants (Count of Participants) |
|---|---|
| Follicular Lymphoma (FL) | 39 |
| Indolent Non-FL B-NHL or MCL | 11 |
| Other Disease | 6 |
ORR was defined as the percentage of participants who had a Complete Response (CR: Normal liver/spleen physical exam, all lymph nodes and nodal masses are normal, and there is no bone marrow involvement), a Complete Response/unconfirmed (CRu: Normal liver/spleen physical exam, plus at least a 75% decrease in the sum of the products of the greatest diameters of nodal masses if any are greater than 1.5 cm in their greatest diameter, normal or indeterminate bone marrow involvement), or a Partial Response (PR: Either normal physical exam, lymph nodes, and lymph node masses plus positive bone marrow involvement; OR normal physical exam or decrease in liver/spleen size plus at least a 50% decrease in the diameters of lymph nodes and nodal masses) as assessed using the international working group Non-Hodgkin's lymphoma standardized response criteria described by Cheson, BD in 1999. The percentage of participants who experienced a CR, CRu, or PR is presented. (NCT00875056)
Timeframe: Up to 650 days
| Intervention | Percentage of participants (Number) |
|---|---|
| Follicular Lymphoma (FL) | 48.7 |
| Indolent Non-FL B-NHL or MCL | 27.3 |
Time to Response is defined as the time from allocation until the time of an initial response. Data was censored on the efficacy data cutoff date of 25 February, 2011. (NCT00875056)
Timeframe: Up to 650 days
| Intervention | Days (Median) |
|---|---|
| Follicular Lymphoma (FL) | NA |
Time to Treatment Failure is defined as the time from allocation until the date of any treatment failure, including documented disease progression, or discontinuation of the study medication for any reason. Data was censored on the efficacy data cutoff date of 25 February, 2011. (NCT00875056)
Timeframe: Up to 650 days
| Intervention | Days (Median) |
|---|---|
| Follicular Lymphoma (FL) | 323 |
1 review available for vorinostat and B-Cell Lymphoma
| Article | Year |
|---|---|
[Present status and perspective of targeted therapy for B-cell lymphoma].
Topics: Agammaglobulinaemia Tyrosine Kinase; Antibodies, Monoclonal; Antibodies, Monoclonal, Murine-Derived; | 2011 |
3 trials available for vorinostat and B-Cell Lymphoma
| Article | Year |
|---|---|
A multicentre phase II study of vorinostat in patients with relapsed or refractory indolent B-cell non-Hodgkin lymphoma and mantle cell lymphoma.
Topics: Adult; Aged; Antineoplastic Agents; Combined Modality Therapy; CREB-Binding Protein; DNA Mutational | 2014 |
Phase 1 trial of carfilzomib (PR-171) in combination with vorinostat (SAHA) in patients with relapsed or refractory B-cell lymphomas.
Topics: Adult; Aged; Antineoplastic Combined Chemotherapy Protocols; Biomarkers; Combined Modality Therapy; | 2016 |
[Current development of new drugs in malignant lymphoma].
Topics: Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Antineoplastic Agents; Bendamustine Hydro | 2012 |
9 other studies available for vorinostat and B-Cell Lymphoma
| Article | Year |
|---|---|
Targeting miR-21 with NL101 blocks c-Myc/Mxd1 loop and inhibits the growth of B cell lymphoma.
Topics: Animals; Antineoplastic Agents, Alkylating; Apoptosis; Basic Helix-Loop-Helix Leucine Zipper Transcr | 2021 |
The role of p21(waf1/cip1) and p27(Kip1) in HDACi-mediated tumor cell death and cell cycle arrest in the Eμ-myc model of B-cell lymphoma.
Topics: Animals; Apoptosis; Cell Cycle Checkpoints; Cell Death; Cyclin-Dependent Kinase Inhibitor p21; Cycli | 2014 |
Fluorodeoxyglucose-based positron emission tomography imaging to monitor drug responses in hematological tumors.
Topics: Animals; Antineoplastic Agents; Cell Line, Tumor; Fluorodeoxyglucose F18; Humans; Hydroxamic Acids; | 2014 |
Detection of apoptotic cells using immunohistochemistry.
Topics: Animals; Apoptosis; DNA; DNA Fragmentation; Histone Deacetylase Inhibitors; Hydroxamic Acids; Immuno | 2014 |
Detection of apoptotic cells using propidium iodide staining.
Topics: Animals; Apoptosis; DNA; Flow Cytometry; Histone Deacetylase Inhibitors; Hydroxamic Acids; Lymphoma, | 2014 |
Antitumor activity of SAHA, a novel histone deacetylase inhibitor, against murine B cell lymphoma A20 cells in vitro and in vivo.
Topics: Animals; Antineoplastic Agents; Apoptosis; Cell Cycle; Cell Division; Cell Line, Tumor; Cell Prolife | 2015 |
A novel approach to detect resistance mechanisms reveals FGR as a factor mediating HDAC inhibitor SAHA resistance in B-cell lymphoma.
Topics: Cell Line, Tumor; Drug Resistance, Neoplasm; Gene Knockout Techniques; Gene Regulatory Networks; His | 2016 |
Analysis of the apoptotic and therapeutic activities of histone deacetylase inhibitors by using a mouse model of B cell lymphoma.
Topics: Animals; Apoptosis; Apoptosis Regulatory Proteins; Bcl-2-Like Protein 11; bcl-X Protein; BH3 Interac | 2007 |
Constitutive activation of signal transducers and activators of transcription predicts vorinostat resistance in cutaneous T-cell lymphoma.
Topics: Antineoplastic Agents; Biomarkers, Tumor; Cell Line, Tumor; Cell Proliferation; Drug Resistance, Neo | 2008 |