Epigenetic Markers in Melanoma

Abstract

Melanoma, one of the most virulent forms of human malignancy, is the primary cause of mortality from cancers arising from the skin. The prognosis of metastatic melanoma remains dismal despite targeted therapeutic regimens that exploit our growing understanding of cancer immunology and genetic mutations that drive oncogenic cell signaling pathways in cancer. Epigenetic mechanisms, including DNA methylation/demethylation, histone modifications and noncoding RNAs recently have been shown to play critical roles in melanoma pathogenesis. Current evidence indicates that imbalance of DNA methylation and demethylation, dysregulation of histone modification and chromatin remodeling, and altered translational control by noncoding RNAs contribute to melanoma tumorigenesis. Here, we summarize the most recent insights relating to epigenetic markers, focusing on diagnostic potential as well as novel therapeutic approaches for more effective treatment of advanced melanoma.

What Is Epigenetic Change and What Do We Know About Its Impact on Molecular Pathologic Mechanisms of the Diseases?

“…It has been shown that a large group of genes are methylated in melanomas [54]. Among the TSGs that are reported to be hypermethylated most frequently in the process of melanoma development and progression are retinoic acid receptor-beta2 (RARbeta 2), RASSF1A, CDKN2A, PTEN genes [55].…”