GEO series
Combined BET Bromodomain and DNMT Inhibition Targets Lineage Plasticity in Prostate Cancer [ATAC-seq]
GSE311400
Mus musculus
Genome binding/occupancy profiling by high throughput sequencing
15 samples
2026/06/22
GPL24247
Summary
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.
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