Journal
MELANOMA RESEARCH
Volume 21, Issue 4, Pages 298-307Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/CMR.0b013e328344a003
Keywords
DNA hypermethylation; epigenetics; malignant melanoma; tumor suppressor
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Funding
- National Cancer Institute SPORE [5P50CA096784-05]
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The objective of this study was to identify novel tumor-suppressor genes in melanoma, using an integrative genomic approach. Data from: (i) earlier reports of DNA loss and gain in malignant melanoma accompanied by comparative genomic hybridization high-definition array data of the entire human genome; (ii) microarray expression data from melanoma-derived cell lines identifying genes with significantly increased expression due to methylation using a pharmacologic demethylating strategy; and (iii) publicly available RNA expression microarray data of primary tumors and benign nevi were integrated using statistical tools to define a population of candidate tumor-suppressor genes. Twenty-seven genes were identified in areas of deletion that demonstrated diminished expression in primary melanomas relative to benign nevi and were significantly increased in expression by 5-Aza treatment. Seven genes of these 27 genes demonstrated methylation and deletion in a validation cohort of 14 separate primary tumors. These were: CHRDL1, SFRP1, TMEM47, LPL, RARRES1, PLCXD1, and KOX15. All of these genes demonstrated growth-suppressive properties with transfection into melanoma-derived cell lines. Seven putative tumor-suppressor genes in malignant melanoma were identified using a novel integrative technique. Melanoma Res 21:298-307 (C) 2011 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.
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