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Several polymorphisms in DNA repair genes have been reported to be associated with lung cancer risk includingXPA(−4G/A),XPD(Lys751Gln and Asp312Asn),XRCC1(Arg399Gln),APE1(Asp148Glu) andXRCC3(Thr241Met). As there is little information on the combined effects of these variants, polymorphisms were analyzed in a case-control study including 463 lung cancer cases [among them 204 adenocarcinoma and 212 squamous cell carcinoma (SCC)] and 460 tumor-free hospital controls. Odds ratios (OR) adjusted for age, gender, smoking and occupational exposure were calculated for the variants alone and combinations thereof. For homozygous individuals carrying the Glu variant ofAPE1, a protective effect was found (OR = 0.77, CI = 0.51–1.16). Individuals homozygous for the variantsXPA(−4A) (OR = 1.53, CI = 0.94–2.5),XPD751Gln (OR = 1.39, CI = 0.90–2.14) orXRCC3241Met (OR = 1.29, CI = 0.85–1.98) showed a slightly higher risk for lung cancer overall. In the subgroup of adenocarcinoma cases, adjusted ORs were increased for individuals homozygous forXPA(−4A) (OR = 1.62, CI = 0.91–2.88) andXRCC3241Met (OR = 1.65; CI = 0.99–2.75). When analyzing the combined effects of variant alleles, 54 patients and controls were identified that were homozygous for two or three of the potential risk alleles [i.e. the variants in nucleotide excision repair,XPA(−4A) andXPD751Gln, and in homologous recombination,XRCC3-241Met]. ORs were significantly increased when all patients (OR = 2.37; CI = 1.26–4.48), patients with SCC (OR = 2.83; CI = 1.17–6.85) and with adenocarcinoma (OR = 3.05; CI = 1.49–6.23) were analyzed. Combinations of polymorphisms in genes involved in the same repair pathway (XPA+XPDorXRCC1+APE1) affected lung cancer risk only in patients with SCC. These results indicate that lung cancer risk is only moderately increased by single DNA repair gene variants investigated but it is considerably enhanced by specific combinations of variant alleles. Analyses of additional DNA repair gene interactions in larger population-based studies are warranted for identification of high-risk subjects.

Specific combinations of DNA repair gene variants and increased risk for non-small cell lung cancer