DNA repair capacity as a risk factor for non-melanocytic skin cancer--a molecular epidemiological study.

Capacity to repair UV-induced DNA damage was studied by use of host cell reactivation assay in T lymphocytes isolated from 86 cases and 87 controls (aged 44-68 years) who were participants in a population-based case-control study of basal cell (BCC) or squamous cell (SCC) carcinoma of the skin in Geraldton, Western Australia. Lymphocytes were cultured and transfected with either control or UV-irradiated plasmids (254 nm, 350 J/m2) containing a reporter gene [the chloramphenicol-acetyltransferase (CAT) gene], and the repair capacity was determined by measuring CAT gene expression in protein extracts prepared from the transfected cells. DNA repair activity was 1.07 (95% confidence interval 0.94-1.26) times greater in BCC cases than in controls for each 350 J/m2 increment in UV dose to the plasmids, and 1.04 (95% confidence interval 0.85-1.26) times greater in SCC cases than in controls, though the differences were not statistically significant. DNA repair activity showed little association with age, sex and viability of the lymphocytes, though it was positively associated with their blastogenic rate (p = 0.055).