Romidepsin activity in T follicular helper(TFH)-phenotype PTCL versus non TFH treated on the same clinical trials.

Ghione, Paola; Özkaya, Neval; Faruque, Promie; Mehta‐Shah, Neha; Lunning, Matthew A.; Ruan, Jia; Galasso, Natasha; Moskowitz, Alison J.; Doğan, Ahmet; Horwitz, Steven M.

doi:10.1200/jco.2018.36.15_suppl.7509

Cited by 5 publications

(2 citation statements)

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“…A retrospective analysis has demonstrated higher rates of response, more frequent response, and more frequent complete responses to histone-deacetylase inhibition with T-follicular helper subtypes, suggesting that it may be a better therapeutic approach for these diseases. 4 A small study in France demonstrated impressive activity with azacytidine in patients with AITL, with 9 of 12 experiencing response, including complete and durable responses. 5 Conversely, there were almost no responses in the non-AITL, PTCL-NOS subgroup.…”

Section: Subtypes By Therapeutic Vulnerabilitiesmentioning

confidence: 99%

Peripheral T-Cell Lymphomas–Not Otherwise Specified: A Shrinking Entity?

Horwitz¹

2020

Journal of the National Comprehensive Cancer Network

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Peripheral T-cell lymphomas–not otherwise specified (PTCL-NOS) is a broad category of biologically and clinically heterogeneous diseases, which likely does not have a single treatment paradigm. Understanding of subtype-specific approaches is leading to more individualized therapy. There are also therapeutic vulnerabilities to target, such as CD30, JAK/STAT pathway, and epigenetic modifiers, that may cross different histologic subtypes. As new therapies evolve, however, it is important to understand in which situations current standard treatments work, because some of these treatments, such as combination chemotherapy, are potentially curative for a subset of patients. For certain populations, adding to these chemotherapy backbones will produce the best results. For other populations, entirely new approaches may be appropriate. Future treatment advances will, in part, be made by enriching populations based on their likelihood of response to specific therapies and utilizing biomarker-driven or biomarker-informed strategies.

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Section: Subtypes By Therapeutic Vulnerabilitiesmentioning

confidence: 99%

Peripheral T-Cell Lymphomas–Not Otherwise Specified: A Shrinking Entity?

Horwitz¹

2020

Journal of the National Comprehensive Cancer Network

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“…18,19 It has been hypothesized that mutations in chromatin modification including DNA methylation may confer higher sensitivity to HDACi, and the registration trials of belinostat and romidepsin showed that patients with AITL can have sustained remissions with these agents. 15,17,20 Romidepsin-based combination strategies have led to higher response rates in smaller studies including PTCLs. The combination of romidepsin with lenalidomide has shown a response in 6 of 10 patients with PTCLs, including responses in 3 of 3 patients with AITL.…”

Section: Targeting the Epigenome: Histone Deacetylase Inhibitorsmentioning

confidence: 99%

Emerging strategies in peripheral T-cell lymphoma

Mehta‐Shah

2019

Hematology

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Peripheral T-cell lymphomas (PTCLs) are a heterogenous group of aggressive non-Hodgkin lymphomas that are less chemosensitive than their B-cell counterparts. Until recently, standard therapy did not distinguish between subtypes, and deeper understanding of the biology of these diseases was lacking. The availability of targeted therapy and more sophisticated subtype classification has translated into the development of novel treatment options for these rare diseases. This includes the development of a brentuximab vedotin-based upfront chemotherapy regimen that confers an overall survival benefit for a subset of patients. Clinical trials of targeted agents, as well as development of better preclinical models of PTCL, are leading to therapeutic advances in the field, including the development of phosphoinositide-3-kinase inhibitors, histone deacetylase inhibitor-based strategies, CD30-directed strategies, Janus kinase inhibitors, and spleen-associated tyrosine kinase inhibitors. Better understanding of the biology of these diseases based on gene expression profiling, minimal residual disease evaluation, and modeling in patient-derived xenografts should help define mechanisms of response and resistance to therapy. Given the complex biology of these heterogeneous lymphomas, well-tolerated combination strategies targeted toward specific subtypes of PTCL can lead to advances in the field. Similar to the story of brentuximab vedotin, development of effective therapies in the salvage setting will likely lead to improved upfront strategies in PTCLs, and ultimately a more personalized approach.

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