In a bi-transgenic mouse in which endogenous p53 is functionally inactivated by constitutive expression of SV40 T-antigen and a mutated p53-R172H protein is expressed the former induces formation of mammary adenocarcinomas and the latter increases the rate of transition from intraepithelial neoplasma to invasive carcinoma. This evidence concerns the gene TP53 and breast adenocarcinoma.