GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE311nnn/GSE311404/primary200OKGenomicsMus musculusGenome binding/occupancy profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE311404GEOGSEfalseCombined BET Bromodomain and DNMT Inhibition Targets Lineage Plasticity in Prostate Cancer [ChIP-seq]Lineage plasticity is increasingly recognized as a resistance mechanism to androgen receptor (AR) inhibition in prostate cancer. Loss of the tumor suppressors TP53 and RB1 is common in tumors exhibiting lineage plasticity; however, mechanisms by which TP53/RB1 loss promotes this phenotype remain poorly understood, and effective treatments are limited. To identify the histone acetylation alterations that occur with TP53/RB1 loss chromatin reprogramming, we performed H3K27Ac ChIP-seq on TP53/RB1-deficient vs. TP53/RB1-intact cell lines.2026/06/22GSE311404GSM9324566GSM9324567GSM9324568GSM9324569GSM9324564GSM9324565GSM9324570GSM9324571GSM932457224247311404Mus musculus