Epigenetic marks in melanoma


  • Hunter W. Richards,

    1.  Huffington Center on Aging
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      The present address of Hunter W. Richards is the Lawrence Berkeley National Laboratory, 1 Cyclotron Rd (84-171), University of California, Berkeley, CA 94720, USA.

  • Estela E. Medrano

    1.  Huffington Center on Aging
    2.  Department of Molecular & Cellular Biology
    3.  Department of Dermatology, Baylor College of Medicine, Houston, TX, USA
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This article is corrected by:

  1. Errata: Erratum Volume 22, Issue 2, 242, Article first published online: 29 January 2009

Estela E. Medrano, e-mail: medrano@bcm.tmc.edu


Melanoma is a highly heterogeneous cancer that comes in different flavors (lentigo maligna melanoma, superficial spreading melanoma, nodular melanoma, acral lentiginous/mucosal melanoma and other less common subtypes including malignant cellular blue nevus, desmoplastic melanoma, nevoid melanoma, and animal-type melanoma) and colors (black/bluish or unpigmented). Pathologists have known for many years that melanoma displays notable changes in the nuclear architecture including thick chromatic rims, presence of mitosis, nuclear grooves, and more. It is now evident from other cancers that such changes reflect not only genomic alterations but also non-genomic changes in both the structure of DNA and the structure of chromatin to which the DNA is bound (nucleosomes). Although aberrant gene expression resulting from DNA methylation has been known for many years, genome alterations resulting from histone modifications became evident in the current decade. In prostate and other cancers, some histone marks have clinical diagnostic and/or prognostic value. Here, we review the current data on epigenetic research in melanoma skin cancers, discuss ways to modify the epigenetic landscape of melanoma for inhibiting its growth, and propose strategies for identifying novel melanoma markers.