The roles of cellular protooncogenes that are activated to transforming genes by point mutation and by other mechanisms consistent with the actions of carcinogenic agents continue to be investigated in both experimental neoplasms in animals and in human cancers of the prostate, stomach, and female reproductive tract. Transforming genes of current interest include the ras and receptor tyrosine kinase families. The work is being extended to suppressor genes, especially p53, that are inacti- vated by mechanisms comparable to the activation processes for trans- forming genes. Novel mechanisms of c-Kras-2 have been identified in experimental tumors; patterns of c-Kras-2 activation have been found to vary in cohorts of human gastric carcinomas from geographically and culturally distinct high risk regions; and evidence has been obtained that latent carcinoma of the prostate may evolve by a mechanism that includes c-Kras-2 activation and is different in this regard from clinical and prostatic carcinoma in which this pathway does not appear to be involved.
