GSE158221
Oncogenic KRAS recruits an  expansive transcriptional network through mutant p53
We utilized genetically engineered mouse models that do and do not express mutant p53 to identify gain of function mechanisms in pancreatic cancer. Human pancreatic cancer (PDAC) patient derived xenografts with high and low p53 levels underwent transcriptional profiling Overall design: Bulk RNA-sequencing was performed on 4 KPC tumors that express mutant p53 and 4 KPC tumors that are p53 null. DE analysis was performed. 19 PDAC PDX tumors were identified that express high levels of mutant p53 and 11 PDAC PDX tumors were identified that do not express any p53. Differential gene expression analysis was performed.