Expression of the class 1 histone deacetylases HDAC8 and 3 are associated with improved survival of patients with metastatic melanoma View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2015-07

AUTHORS

James S Wilmott, Andrew J Colebatch, Hojabr Kakavand, Ping Shang, Matteo S Carlino, John F Thompson, Georgina V Long, Richard A Scolyer, Peter Hersey

ABSTRACT

Prior studies have shown that combinations of histone deacetylase (HDAC) and BRAF inhibitors (BRAFi) have synergistic effects on BRAFi-resistant melanoma through enhanced apoptosis and inhibition of the cAMP-dependent drug resistance pathway. However, little is known about the expression of various HDACs and their associations with BRAF/NRAS mutation status, clinicopathologic characteristics, and patient outcome. The present study extensively profiled HDAC class 1 and their targets/regulators utilizing immunohistochemistry in human melanoma samples from patients with stage IV melanoma, known BRAF/NRAS mutational status, and detailed clinicopatholgical data. HDAC8 was increased in BRAF-mutated melanoma (P=0.016), however, no association between expression of other HDACs and NRAS/BRAF status was identified. There was also a correlation between HDAC1, HDAC8 expression, and phosphorylated NFκb p65 immunoreactivity (P<0.001). Increased cytoplasmic HDAC8 immunoreactivity was independently associated with an improved survival from both diagnosis of primary melanoma and from first detection of stage IV disease to melanoma death on multivariate analysis (HR 0.992, 95% CI 0.987-0.996; P<0.001 and HR 0.993, 95% CI 0.988-0.998; P=0.009, respectively). These results suggest not only that HDAC8 may be a prognostic biomarker in melanoma, but also provide important data regarding the regulation of HDACs in melanoma and a rational basis for targeting them therapeutically. More... »

PAGES

884-894

References to SciGraph publications

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/modpathol.2015.34

    DOI

    http://dx.doi.org/10.1038/modpathol.2015.34

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1038786183

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/25836739


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    286 schema:name 1] Melanoma Institute Australia, Sydney, New South Wales, Australia [2] Departments of Melanoma and Surgical Oncology, Camperdown, New South Wales, Australia [3] Mater Hospital, North Sydney, Sydney, New South Wales, Australia [4] Discipline of Surgery, Sydney Medical School, The University of Sydney, Sydney, New South Wales, Australia.
    287 1] Melanoma Institute Australia, Sydney, New South Wales, Australia [2] Departments of Tissue Pathology and Diagnostic Oncology, Royal Prince Alfred Hospital, Camperdown, New South Wales, Australia [3] Discipline of Pathology, Sydney Medical School, The University of Sydney, Sydney, New South Wales, Australia.
    288 1] Melanoma Institute Australia, Sydney, New South Wales, Australia [2] Discipline of Medicine, Sydney Medical School, The University of Sydney, Sydney, New South Wales, Australia [3] Kolling Institute, Royal North Shore Hospital, The University of Sydney, Sydney, New South Wales, Australia.
    289 1] Melanoma Institute Australia, Sydney, New South Wales, Australia [2] Discipline of Medicine, Sydney Medical School, The University of Sydney, Sydney, New South Wales, Australia.
    290 1] Melanoma Institute Australia, Sydney, New South Wales, Australia [2] Westmead Institute for Cancer Research, The University of Sydney at Westmead Millennium Institute, Westmead, New South Wales, Australia [3] Crown Princess Mary Cancer Centre, Westmead Hospital, Westmead, New South Wales, Australia.
    291 Melanoma Institute Australia, Sydney, New South Wales, Australia.
    292 rdf:type schema:Organization
     




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