Final Results From a Multicenter, International, Pivotal Study of Romidepsin in Refractory Cutaneous T-Cell Lymphoma

Whittaker, Sean; Demierre, Marie‐France; Kim, Ellen J.; Rook, Alain H.; Lerner, Adam; Duvic, Madeleine; Scarisbrick, Julia; Reddy, Sunil; Robak, Tadeusz; Becker, Jürgen C.; Самцов, А. В.; McCulloch, William; Kim, Youn H.

doi:10.1200/jco.2010.28.9066

Cited by 580 publications

(426 citation statements)

References 25 publications

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“…Romidepsin, administered as a 4-hr intravenous infusion (14 mg/m 2 ) days 1, 8, and 15 every 4 weeks, was evaluated in two phase II studies, the largest of which included 96 patients, most with advanced-stage disease [274,275]. The overall response rate was 38% for patients with advanced-stage disease, with a median duration of response that exceeded 1 year.…”

Section: Hdac Inhibitorsmentioning

confidence: 99%

Cutaneous T‐cell lymphoma: 2011 update on diagnosis, risk‐stratification, and management

Wilcox

2011

American J Hematol

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Disease overview: Cutaneous T‐cell lymphomas are a heterogenous group of T‐cell lymphoproliferative disorders involving the skin, the majority of which may be classified as Mycosis fungoides (MF) or Sézary syndrome (SS).Diagnosis: The diagnosis of MF or SS requires the integration of clinical and histopathologic data.Risk‐adapted therapy: Tumor, node, metastasis, and blood (TNMB) staging remains the most important prognostic factor in MF/SS and forms the basis for a “risk‐adapted,” multidisciplinary approach to treatment. For patients with disease limited to the skin, expectant management or skin‐directed therapies is preferred, as both disease‐specific and overall survival for these patients is favorable. In contrast, patients with advanced‐stage disease with significant nodal, visceral, or blood involvement are generally approached with biologic‐response modifiers, denileukin diftitox, and histone deacetylase inhibitors before escalating therapy to include systemic, single‐agent chemotherapy. Multiagent chemotherapy may be used for those patients with extensive visceral involvement requiring rapid disease control. In highly‐selected patients with disease refractory to standard treatments, allogeneic stem‐cell transplantation may be considered. Am. J. Hematol., 2011. © 2011 Wiley‐Liss, Inc.

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Section: Hdac Inhibitorsmentioning

confidence: 99%

Cutaneous T‐cell lymphoma: 2011 update on diagnosis, risk‐stratification, and management

Wilcox

2011

American J Hematol

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“…Most recently, belinostat was approved as a single agent for relapsed and refractory PTCL. [29][30][31][32] Overall, HDACi appear more active in T-cell malignancies and combination trials with chemotherapy are underway. There are currently two ongoing trials of CHOP plus either romidepsin or belinostat.…”

Section: 28mentioning

confidence: 99%

Advances in the diagnosis and control of lymphomas

Candelaria

2016

Salud Publica Mex

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“…Another class of epigenetic-modifying agents used clinically is histone deacetylase (HDAC) inhibitors [204][205][206][207][208]. In cancer cells, HDAC enzymes, among many other functions, can modulate chromatin configurations and mediate cancer-related gene silencing as components of repressive protein complexes containing DNMTs.…”

Section: Epigenetic Therapeutics In Cancermentioning

confidence: 99%

“…Many HDAC inhibitors have been shown to have potent anti-tumor effects and entered clinical trials. Two such inhibitors, vorinostat (also known as, suberoylanilide hydroxamic acid; SAHA) and romidepsin (also known as depsipeptide or FK228) have been approved by the FDA for treating cutaneous T-cell lymphoma [206][207][208]. In addition to anti-tumor effects, other potential uses of HDAC inhibitors and other epigenetic-modifying agents in clinical oncology are being explored.…”

Section: Epigenetic Therapeutics In Cancermentioning

confidence: 99%

Cancer epigenetics: linking basic biology to clinical medicine

2011

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Cancer evolution at all stages is driven by both epigenetic abnormalities as well as genetic alterations. Dysregulation of epigenetic control events may lead to abnormal patterns of DNA methylation and chromatin configurations, both of which are critical contributors to the pathogenesis of cancer. These epigenetic abnormalities are set and maintained by multiple protein complexes and the interplay between their individual components including DNA methylation machinery, histone modifiers, particularly, polycomb (PcG) proteins, and chromatin remodeling proteins. Recent advances in genome-wide technology have revealed that the involvement of these dysregulated epigenetic components appears to be extensive. Moreover, there is a growing connection between epigenetic abnormalities in cancer and concepts concerning stem-like cell subpopulations as a driving force for cancer. Emerging data suggest that aspects of the epigenetic landscape inherent to normal embryonic and adult stem/ progenitor cells may help foster, under the stress of chronic inflammation or accumulating reactive oxygen species, evolution of malignant subpopulations. Finally, understanding molecular mechanisms involved in initiation and maintenance of epigenetic abnormalities in all types of cancer has great potential for translational purposes. This is already evident for epigenetic biomarker development, and for pharmacological targeting aimed at reversing cancerspecific epigenetic alterations.

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Final Results From a Multicenter, International, Pivotal Study of Romidepsin in Refractory Cutaneous T-Cell Lymphoma

Abstract: Romidepsin has significant and sustainable single-agent activity (including improvement in pruritus) and an acceptable safety profile, making it an important therapeutic option for treatment refractory CTCL.

Cited by 580 publications

References 25 publications

Cutaneous T‐cell lymphoma: 2011 update on diagnosis, risk‐stratification, and management

Cutaneous T‐cell lymphoma: 2011 update on diagnosis, risk‐stratification, and management

Advances in the diagnosis and control of lymphomas

Cancer epigenetics: linking basic biology to clinical medicine

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