{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE337nnn/GSE337536/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Homo sapiens"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE337536"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Decitabine induces innate immune gene expression in rare melanoma models","description":"Rare melanoma subtypes, including mucosal melanoma, can exhibit reduced tumor-intrinsic innate immune and interferon-associated gene expression, which may contribute to immune evasion and limited responses to immune checkpoint inhibitors. We investigated whether decitabine, a DNA methyltransferase inhibitor known to induce viral mimicry and immune-associated transcriptional programs, could restore innate immune and interferon-associated signaling in rare melanomas. Here, we report RNA-seq profiling of the MB2141 anorectal mucosal melanoma model following decitabine treatment in vitro and in vivo. Decitabine treatment resulted in robust induction of innate immune pathogen sensing, type I interferon signaling, antigen presentation, and other immune-associated gene expression programs. These data provide a transcriptional framework for understanding how DNA hypomethylating agents modulate immune gene expression in mucosal melanoma and support further investigation of decitabine as an immune-priming strategy for rare melanoma subtypes.","dates":{"publication":"2026/07/13"},"accession":"GSE337536","cross_references":{"GSM":["GSM9857587","GSM9857588","GSM9857589","GSM9857590","GSM9857591","GSM9857592","GSM9857593","GSM9857594"],"GPL":["24676"],"GSE":["337536"],"taxon":["Homo sapiens"]}}