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Enhancer activation during tumor progression in the KrasLSLG12D/+; Trp53LSLR172H/+; Pdx1-Cre (KPC) mouse model of pancreatic ductal adenocarcinoma.

GSE144704 Mus musculus Genome binding/occupancy profiling by high throughput sequencing 8 samples Submitted 2020/06/16 Platform GPL19057
Summary
Murine pancreatic ductal adenocarcinoma tumor organoids (T6 and T23) were generated from primary tumors from KrasLSL-G12D/+; Trp53LSL-R172H/+; Pdx1-Cre mice. At the first passage, cells in Matrigel were overlaid with mouse complete medium alone or supplemented with 10 uM Nutlin-3a to select for cells that have undergone loss-of-heterozygosity (LOH) for the wild-type (wt, "+") allele of Trp53. Organoids were cultured for 3 passages in the presence or absense of Nutlin-3a, and then culturing was continued in unsupplemented mouse complete medium. H3K27ac ChIP-sequencing (ChIP-seq) was performed to identify regions differentially enriched for H3K27ac binding in Trp53-LOH vs. wt tumor organoids.
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Also filed as BioProject PRJNA604612 and SRA study SRP246948. Searching any of these in the dataset finder brings you back here.

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