Recently, histone deacetylase inhibitors (HDACi) have emerged as promising therapies with favorable adverse effect profiles, compared with traditional chemotherapies. In this article, we review the published literature to evaluate the role of HDACi in the treatment of CTCL.

Romidepsin is the second histone deacytelase inhibitor (HDACi) approved for the treatment of advanced stages of cutaneous T cell lymphoma (CTCL). Recent in vitro data suggests that HDACi suppress immune function although these findings have not been confirmed in patients.

The HDACi, vorinostat, and romidepsin are FDA approved for the treatment of CTCL, while belinostat and panobinostat are approved for the treatment of PTCL and multiple myeloma, respectively. At present, the most prominent treatment option for cancers is …

In HDACi monotherapy trials the majority of objective responses have been reported in CTCL and, to a lesser extent, other hematological malignancies. Only occasional objective responses have been reported in solid tumor monotherapy trials.

Jan 1, 2017 · We found that pan- HDACIs (vorinostat and panobinostat) inhibited the migration of CTCL cells and downregulated CCR6. The miRNA microarray analysis against CTCL cell lines demonstrated that these pan-HDACIs commonly upregulated 161 miRNAs, including 34 known tumor suppressive miRNAs such as miR-150.

Recent in vitro and in vivo data have shown that the combination of Resminostat (HDACi) with Ruxolitinib (Jaki) acts synergistically and inhibits tumorigenesis and metastasis in CTCL experimental models.

Jul 10, 2017 · In 2006, suberoylanilide hydroxamic acid (SAHA, vorinostat) was approved by the FDA for the treatment of CTCL, representing the first histone deacetylase inhibitor (HDACi) approved for cancer treatment.

Nov 15, 2022 · These results suggest that STAT3 could be the new therapeutic target in HDACi-resistant CTCL and that gp130/STAT3 inhibition could be an important therapeutic strategy. To further elucidate the detailed mechanism of HDACi resistance, analysis of the pathways activating STAT3 without JAK and the target proteins of STAT3 is warranted.

Jul 10, 2017 · Clinical response to histone deacetylase inhibitors (HDACi) is strongly associated with a concurrent gain in chromatin accessibility. HDACi causes distinct chromatin responses in leukemic and host CD4 + T cells, reprogramming host T cells toward normalcy.

Jul 10, 2017 · In this study, we developed a systematic approach to characterize chromatin dynamics in CTCL using ATAC-seq, and addressed the regulatory dynamics in leukemic epigenomes from CTCL patients treated with HDACi.