TP53 and neoplasm: We have shown here that failure to suppress A3B expression following mutational or viral inactivation of p53, results in elevated A3B expression and activity, with attendant increase in potential genetic mutations, as demonstrated by the ability of activated WT, but not mutant, p53 to suppress abasic site generation in genomic DNA and through the demonstration that the frequency of mutations ascribed to A3B activity in diverse cancer types is elevated in p53 mutant tumours.