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Special Report

Epigenomic Landscape of Melanoma Progression to Brain Metastasis: Unexplored Therapeutic Alternatives

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Pages 1303-1311 | Received 01 Jun 2015, Accepted 04 Aug 2015, Published online: 07 Dec 2015
 

Abstract

Melanoma brain metastasis is a complication with rising incidence. Despite the high rate of somatic mutations driving the initial stages of melanocyte transformation, the brain colonization requires a phenotypic reprogramming that is, in part, influenced by epigenomic modifications. This special report summarizes recent findings in the epigenomic landscape of melanoma progression to brain metastasis, with particular emphasis on the clinical utility of DNA methylation, chromatin modifications and ncRNA expression as theragnostic markers, as well as the significance of the metastatic microenvironment on melanoma brain metastasis epigenome.

Disclaimer

The content is solely the responsibility of the authors and does not necessarily represent the official view of the National Cancer Institute or the National Institutes of Health.

Acknowledgements

The authors would like to thank Nousha Javanmardi for her critical editorial assistance for the manuscript.

Financial & competing interest disclosure

Relevant research in the authors’ laboratory is supported by the NIH, National Cancer Institute (grant number R01CA167967 to D Hoon); the Dr Miriam and Sheldon G Adelson Medical Research Foundation (D Hoon, I Witz); the Leslie and Susan Gonda (Goldschmied) Foundation (D Hoon), and the Ruth and Martin H Weil Foundation (D Hoon). The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed. The content is solely the responsibility of the authors and does not necessarily represent the official view of the National Cancer Institute or the National Institutes of Health.

No writing assistance was utilized in the production of this manuscript.

Additional information

Funding

Relevant research in the authors’ laboratory is supported by the NIH, National Cancer Institute (grant number R01CA167967 to D Hoon); the Dr Miriam and Sheldon G Adelson Medical Research Foundation (D Hoon, I Witz); the Leslie and Susan Gonda (Goldschmied) Foundation (D Hoon), and the Ruth and Martin H Weil Foundation (D Hoon). The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed. The content is solely the responsibility of the authors and does not necessarily represent the official view of the National Cancer Institute or the National Institutes of Health. No writing assistance was utilized in the production of this manuscript.

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