GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE311nnn/GSE311400/primaryOK200GenomicsMus musculusGenome binding/occupancy profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE311400GEOGSEfalseCombined BET Bromodomain and DNMT Inhibition Targets Lineage Plasticity in Prostate Cancer [ATAC-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 promote this phenotype remain poorly understood, and effective treatments are limited. Thus we used multi-omic profiling of TP53/RB1 loss prostate cancer models to identify alterations in chromatin accessibility, DNA methylation, and gene expression associated with lineage plasticity.2026/06/22GSE311400GSM9324508GSM9324509GSM9324504GSM9324505GSM9324506GSM9324507GSM9324500GSM9324501GSM9324502GSM9324503GSM9324496GSM9324497GSM9324498GSM9324499GSM932449524247311400Mus musculus