Omics analyses of a somatic Trp53 R245W/+ breast cancer model identify cooperating driver events activating PI3K/Akt/mTOR signaling

Alterations of the tumor suppressor TP53, one of the most common events in cancer, alone are insufficient for tumor development but serve as drivers of transformation. We sought to identify cooperating events through genomic analyses of a novel somatic Trp53 R245W mouse model (equivalent to the TP53 R248W hot spot mutation in human cancers) that recapitulates metastatic breast cancer development and performed whole genome sequencing (WGS) on 9 Trp53 R245W/+ tumors with two tails as controls.