DNA repair and epidemiology of basal cell carcinoma

Abstract

Abstract In a molecular epidemiological study of DNA repair, host reactivation assay was used to measure the DNA repair capacity of cryopreserved lymphocytes from 88 primary basal cell carcinoma (BCC) patients and 135 cancer-free controls. In this study population, reduced repair of ultraviolet radiation-induced DNA damage contributed to the risk of sunlight-induced BCC. A family history of BCC is associated with low DNA repair. Repair of ultraviolet radiation-damaged DNA declines at a rate of approximately 1%/year in noncancerous controls. Reduced DNA repair is more likely seen in young BCC patients, indicating that BCC is a premature aging disease of the skin. The persistence of photochemical damage because of reduced repair results in point mutations in the p53 gene and allelic loss of the nevoid BCC gene located on chromosome 9q. Xeroderma pigmentosum appears to be a valid paradigm for the role of DNA repair in BCC in the general population.