GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE317nnn/GSE317501/primaryOK200GenomicsHomo sapiensGenome binding/occupancy profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE317501GEOGSEfalseDivergent Roles of SPOP and CHD1 in ACSL4 Regulation Reveal Context-dependent Vulnerabilities for Targeting Ferroptosis in Prostate CancerGenetic 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.2026/04/09GSE317501GSM9473186GSM9473185GSM9473196GSM9473195GSM9473194GSM9473193GSM9473192GSM9473191GSM9473190GSM9473189GSM9473188GSM947318734281317501Homo sapiens