TP53 and carcinoma: In addition, the involvement of TP53 mutations in the intestinal type is well-demonstrated by mouse genetic experiments in which precancerous lesions (polyps) and carcinomas following the exogenous overexpression of the intestinal differentiation transcription factor CDX2 are favored by the inactivation of tp53 (50 weeks, 50% penetrance vs. 80–100 weeks) [46].