Mutations in the p53 tumor suppressor gene occur in about 50% of all human tumors,
making it the most frequent target for genetic alterations in cancer (for recent reviews on p53
see Refs. 1–5). Such mutations probably facilitate carcinogenesis primarily through
abrogating the tumor suppressor activities of the wild type p53 protein, although at least
some forms of tumor-associated mutant p53 proteins may also contribute overt oncogenic
activities (gain of function). Excessive wild type p53 activity gives rise to a variety of cellular …