EPIDEMIOLOGY OF ULTRAVIOLET-DNA REPAIR CAPACITY AND HUMAN CANCER

The following conclusions are derived from an epidemiological study. R educed repair of ultraviolet (UV)-induced DNA damage contributes direc tly to basal cell carcinoma (BCC) in individuals with prior sunlight o verexposure. A family history of BCC is a predictor of low DNA repair. Repair of UV-damaged DNA declines at a fixed rate of approximately 1% per annum in noncancerous controls. The DNA repair differences betwee n young BCC cases and their controls disappear as they age. Hence, BCC , in terms of DNA repair, is a premature aging disease. The persistenc e of photochemical damage because of reduced repair results in point m utations in the p53 gene and allelic loss of the nevoid BCC gene (Gorl in's syndrome) located on chromosome 9q. The fact that environmental v ulnerability is gender oriented implicates hormones in regulating DNA repair. Xeroderma pigmentosum appears to be a valid paradigm for the r ole of DNA repair in BCC in the general population.