TP53 and cancer: Mutant p53-R175H inhibits wild-type p53 interaction with promoter elements,49 advances angiogenesis,50 and promotes epithelial–mesenchymal transition.51 Genotype–phenotype analysis of Li-Fraumeni families revealed that patients carrying such a mutation in the core p53 DNA-binding domain show more highly penetrant cancer phenotypes with higher incidence and earlier onset than those with TP53 inactivation mutations.52, 53 These observations are also reflected in mouse studies.