{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE301nnn/GSE301779/"]},"type":"primary"},"statusCodeValue":200,"statusCode":"OK"}],"scores":null,"additional":{"omics_type":["Genomics"],"species":["Mus musculus"],"gds_type":["Genome binding/occupancy profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE301779"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Examine the epigenetic consequences of KMT2D loss in melanoma using ChIP-seq profiling [CUT&Run]","description":"Cellular plasticity contributes to melanoma progression and resistance to treatment, but the epigenetic mechanisms driving these changes are not well understood. In a Braf-mutant mouse model, we show that loss of Kmt2d, an enzyme that adds H3K4me1 to enhancers, speeds up melanoma development and shifts cells toward a neural crest-like state. Using single-cell multiome analysis, we found that this shift is driven by increased activity of TFAP2 transcription factors, linked to changes at enhancer regions. Kmt2d loss also leads to a more immunosuppressive tumor environment, with higher levels of suppressive immune cells. This study provides the first genetic evidence that enhancer disruption plays a key role in cell identity changes in melanoma.","dates":{"publication":"2026/07/04"},"accession":"GSE301779","cross_references":{"GSM":["GSM9089559","GSM9089570","GSM9089571","GSM9089560","GSM9089572","GSM9089561","GSM9089577","GSM9089566","GSM9089555","GSM9089567","GSM9089556","GSM9089568","GSM9089557","GSM9089569","GSM9089558","GSM9089573","GSM9089562","GSM9089574","GSM9089563","GSM9089575","GSM9089564","GSM9089565","GSM9089554","GSM9089576"],"GPL":["19057"],"GSE":["301779"],"taxon":["Mus musculus"]}}