GEO series
Divergent roles of SPOP and CHD1 in ACSL4 regulation reveal context-dependent vulnerabilities for targeting ferroptosis
GSE317501
Homo sapiens
Genome binding/occupancy profiling by high throughput sequencing
12 samples
2026/04/09
GPL34281
Summary
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.
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Paper (PMID 42380152) ↗
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