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    HDAC Inhibitors Finally Open Up: Chromatin Accessibility Signatures of CTCL.
    Cancer Cell 2017 07;32(1):1-3
    Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. Electronic address:
    In this issue of Cancer Cell, Qu et al. describe the chromatin accessibility profiles of cutaneous T cell lymphoma, with dynamic assessments of response and resistance to histone deacetylase inhibitor therapy. Their "personal regulome" analysis framework reveals chromatin features that may be predictive of clinical response to epigenetic therapy.

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    Chromatin Accessibility Landscape of Cutaneous T Cell Lymphoma and Dynamic Response to HDAC Inhibitors.
    Cancer Cell 2017 Jul 15;32(1):27-41.e4. Epub 2017 Jun 15.
    Center for Personal Dynamic Regulomes and Program in Epithelial Biology, Stanford University School of Medicine, CCSR 2155c, 269 Campus Drive, Stanford, CA 94305-5168, USA; Department of Dermatology, Stanford University School of Medicine, Stanford, CA 94305, USA. Electronic address:
    Here, we define the landscape and dynamics of active regulatory DNA in cutaneous T cell lymphoma (CTCL) by ATAC-seq. Analysis of 111 human CTCL and control samples revealed extensive chromatin signatures that distinguished leukemic, host, and normal CD4(+) T cells. We identify three dominant patterns of transcription factor (TF) activation that drive leukemia regulomes, as well as TF deactivations that alter host T cells in CTCL patients. Read More
    HDAC inhibitors for the treatment of cutaneous T-cell lymphomas.
    Future Med Chem 2012 Mar;4(4):471-86
    Department of Dermatology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
    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. Read More
    Inhibition of histone deacetylase 3 causes replication stress in cutaneous T cell lymphoma.
    PLoS One 2013 22;8(7):e68915. Epub 2013 Jul 22.
    Department of Biochemistry, Vanderbilt University School of Medicine, Nashville, Tennessee, USA.
    Given the fundamental roles of histone deacetylases (HDACs) in the regulation of DNA repair, replication, transcription and chromatin structure, it is fitting that therapies targeting HDAC activities are now being explored as anti-cancer agents. In fact, two histone deacetylase inhibitors (HDIs), SAHA and Depsipeptide, are FDA approved for single-agent treatment of refractory cutaneous T cell lymphoma (CTCL). An important target of these HDIs, histone deacetylase 3 (HDAC3), regulates processes such as DNA repair, metabolism, and tumorigenesis through the regulation of chromatin structure and gene expression. Read More
    Prognostic significance of the therapeutic targets histone deacetylase 1, 2, 6 and acetylated histone H4 in cutaneous T-cell lymphoma.
    Histopathology 2008 Sep;53(3):267-77
    Department of Pathology, Experimental Pathology Unit, Copenhagen Biocentre, Copenhagen University Hospital, Copenhagen.
    Aims: Aberrant histone acetylation has been associated with malignancy and histone deacetylase (HDAC) inhibitors are currently being investigated in numerous clinical trials. So far, the malignancy most sensitive to HDAC inhibitors has been cutaneous T-cell lymphoma (CTCL). The reason for this sensitivity is unclear and studies on HDAC expression and histone acetylation in CTCL are lacking. Read More