Understanding the genetic alterations accompanying radiation-induced cancers may permit the development of ways to prevent or retard disease progression. Alterations in the p53 gene of human skin basal-cell carcinomas have been found, indicating probable deletions or translocations involving exon 8. That some individuals exhibit multiple cancers suggests a subpopulation with unusual sensitivity to ultraviolet (UV) light or x-rays. Also, some UV-induced basal-cell cancers exhibit CC to TT mutations consistent with UV action on DNA. These results suggest that cancer origin can be deduced from the type of molecular damage in the DNA from induced cancers. Deficient knowledge about cancer mechanisms inhibits estimation of cancer risk, especially at low doses of an inducing agent. To better understand radiation carcinogenesis, we use discrete genetic steps and cellular proliferation in animals to predict quantitative cancer risks. We 'calibrate' cancer models with data from individuals exposed to ionizing radiation.