The tumor suppressor gene, p53, lies on chromosome 17p, and has been examined in a wide variety of primary tumors, xenografts, and cell lines derived from tumors. Point mutations in the evolutionally conserved codons of p53 have appeared to be the most common genetic alterations in human cancers (1 ). The p53 mutational spectrum differs among those of cancers of the colon, lungs, esophagus, breast, liver, brain, reticuloendothelial tissues, and hemophoietic tissues. In particular, 75–80% of colon carcinomas exhibit a loss of both p53 alleles, one through deletion and the other through point mutation (1 ).
