The role of DNA repair capacity in susceptibility to lung cancer: a review

Abstract

Human cancer risk assessment has relied largely on animal experiments and use of short-term biological tests based on chemical-DNA interaction. The recent introduction of biomarkers to molecular epidemiologic studies has provided another means of assessing risk for tobacco-related cancer. Several biomarkers for genetic susceptibility to lung cancer have been developed and validated in pilot studies that have demonstrated their association with increased risk of lung cancer. For instance, metabolic enzymes responsible for bioactivation and detoxification of environmental chemicals, carcinogen-induced DNA adducts and chromosomal aberrations, and host DNA repair capacity have been measured in human peripheral lymphocytes. These markers allow estimation of interindividual variation in response to carcinogen exposure and thus assessment of cancer risk. Therefore, epidemiological studies of exposure and of molecular etiology of human carcinogenesis provide a new avenue of cancer risk assessment.