TP53 and cancer: In cancers that appear to retain the wild type coding sequence, p53 may be inactivated by other mechanisms (e.g., TP53 promoter or splicing alterations, MDM2 overexpression); or other genes that are regulated by TP53 may be altered obviating the need for direct inactivation of TP53. Alternatively, it is possible that the presence or absence of TP53 mutation in serous cancers may be one factor underlying the clinical heterogeneity of the disease with respect to stage, response to therapy, and outcome.