{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE317nnn/GSE317501/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Genomics"],"species":["Homo sapiens"],"gds_type":["Genome binding/occupancy profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE317501"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Divergent Roles of SPOP and CHD1 in ACSL4 Regulation Reveal Context-dependent Vulnerabilities for Targeting Ferroptosis in Prostate Cancer","description":"Genetic heterogeneity contributes to the variable therapeutic responses in prostate cancer (PCa). Frequent SPOP mutations and recurrent CHD1 deletions define distinct molecular subtypes of PCa with differential responses to anti-androgen therapy. Ferroptosis, an iron-dependent cell death driven by lipid peroxidation, has emerged as a promising anticancer strategy. Here, we identify SPOP mutations and CHD1 deletion as key genetic determinants of ferroptosis susceptibility in PCa.","dates":{"publication":"2026/04/09"},"accession":"GSE317501","cross_references":{"GSM":["GSM9473186","GSM9473185","GSM9473196","GSM9473195","GSM9473194","GSM9473193","GSM9473192","GSM9473191","GSM9473190","GSM9473189","GSM9473188","GSM9473187"],"GPL":["34281"],"GSE":["317501"],"taxon":["Homo sapiens"]}}