GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE329nnn/GSE329231/primaryOK200GenomicsHomo sapiensGenome binding/occupancy profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE329231GEOGSEfalseEpigenomic profiling of H3K9me3 and H3K27ac across melanoma cell lines with different mutational backgroundsMelanoma is a genetically and phenotypically heterogeneous cancer, and changes in chromatin state have been implicated in melanoma progression, phenotypic plasticity, and tumor behavior. To investigate the epigenetic landscape associated with melanoma aggressiveness and mutational background, we performed ChIP-seq for the active chromatin mark H3K27ac and the repressive chromatin mark H3K9me3 in five human melanoma cell lines: SK-Mel-19, SK-Mel-29, SK-Mel-103, UACC-62, and UACC-257. These cell lines represent melanomas with different degrees of aggressiveness and distinct mutation profiles. Our analysis revealed differential patterns of H3K27ac across the cell lines, suggesting that enhancer-associated chromatin states are linked to mutation-dependent transcriptional regulation in melanoma.2026/05/01GSE329231GSM9699690GSM9699709GSM9699708GSM9699707GSM9699717GSM9699716GSM9699715GSM9699714GSM9699713GSM9699712GSM9699679GSM9699711GSM9699699GSM9699710GSM9699698GSM9699697GSM9699696GSM9699695GSM9699694GSM9699693GSM9699692GSM9699691GSM9699719GSM9699718GSM9699706GSM9699705GSM9699704GSM9699703GSM9699702GSM9699723GSM9699701GSM9699700GSM9699689GSM9699722GSM9699721GSM9699688GSM9699720GSM9699687GSM9699686GSM9699685GSM9699684GSM9699683GSM9699682GSM9699681GSM969968023227329231Homo sapiens