No association between the XPD (Lys751G1n) polymorphism or the XRCC3 (Thr241Met) polymorphism and lung cancer risk.

Introduction DNA repair helps to protect the genome from tobacco-induced damage. Reduced DNA repair capacity may predispose individuals to lung cancer (1). Polymorphisms in genes encoding DNA repair proteins may modulate susceptibility to tobacco lung carcinogens. Bulky DNA adducts induced by chemical carcinogens in cigarette smoke are repaired through the nucleotide excision repair pathway that includes the XPD gene. An XPD variant in exon 23 leading to a Lys751G1n amino acid substitution has been associated with reduced DNA repair capacity (2). DNA strand breaks generated by reactive oxygen species in tobacco smoke may be repaired through the homology-directed doublestranded DNA break repair pathway that includes XRCC3. A nucleotide substitution in exon 7 of the XRCC3 gene results in an amino acid change Thr241Met. There are few data on these polymorphisms in relation to lung cancer (3, 4). To investigate the possible association between the XPD Lys751G1n and XRCC3 Thr241Met polymorphisms and the risk of lung cancer among Caucasians and African Americans, we analyzed DNA samples from a case-control study of 331 incident lung cancer cases and 687 population controls in Los Angeles County, California.