title: HDAC inhibitors for the treatment of cutaneous T-cell lymphomas.
abstract: Epigenetic modification by small-molecule histone deacetylase inhibitors (HDAC-Is) has been a promising new antineoplastic approach for various solid and hematological malignancies, particularly for cutaneous T-cell lymphoma (CTCL). Vorinostat, a pan-HDAC-I and, most recently, romidepsin, a bicyclic pan-HDAC-I, have been US FDA approved for treatment of relapsed or refractory CTCL. However, because many patients do not reach the 50% partial response mark and response is not always sustainable, overcoming HDAC-I resistance by adding other agents or finding more selective molecules is an important clinical problem in realizing the full clinical potential of HDAC-Is. In this review, we discuss the molecular basis for HDAC-I function in cancer, the clinical response and side-effect profile experienced by CTCL patients, and the progress made in attempting to identify biomarkers of response and resistance, as well as synergistic combination therapies.
authors.affiliation: Department of Dermatology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
authors.forename: Sophia
authors.initials: S
authors.lastname: Rangwala
authors.forename: Chunlei
authors.initials: C
authors.lastname: Zhang
authors.forename: Madeleine
authors.initials: M
authors.lastname: Duvic
mesh_terms: D000970:Antineoplastic Agents / Q000627:therapeutic use*; D002986:Clinical Trials as Topic; D004359:Drug Therapy, Combination; D044127:Epigenesis, Genetic; D056572:Histone Deacetylase Inhibitors / Q000627:therapeutic use*; D006655:Histone Deacetylases / Q000737:chemistry* / Q000235:genetics / Q000378:metabolism; D006801:Humans; D016410:Lymphoma, T-Cell, Cutaneous / Q000188:drug therapy*; D012878:Skin Neoplasms / Q000188:drug therapy*
chemical_list: D000970:Antineoplastic Agents; D056572:Histone Deacetylase Inhibitors; D006655:Histone Deacetylases