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To explore the potential role for estrogen in lung cancer susceptibility, candidate single-nucleotide polymorphism (SNPs) in tobacco and estrogen metabolism genes were evaluated. Population-based cases (n = 504) included women aged 18–74, diagnosed with NSCLC in metropolitan Detroit between November 2001 and October 2005. Population-based controls (n = 527) were identified through random digit dialing and matched on race and age. Eleven SNPs in 10 different genes were examined in relation to risk:CYP1A1 Msp1,CYP1A1 Ile462Val,CYP1B1 Leu432Val,CYP17,CYP19A1,XRCC1 Gln399Arg,COMT Val158Met,NQO1 Pro187Ser,GSTM1,GSTT1andGSTP1 Ile105Val. Lung cancer risk associated with individual SNPs was seen forGSTP1[A allele; odds ratio (OR) = 1.85; 95% confidence interval (CI), 1.04–3.27] andXRCC1(A/A genotype; OR = 1.68; 95% CI, 1.01–2.79) in white women andCYP1B1(G allele; OR = 11.1; 95% CI, 1.18–104) in black women smokers. White women smokers carrying two risk genotypes at the following loci were at increased risk of lung cancer compared with individuals not carrying risk alleles at these loci:CYP17andGSTM1,COMTandGSTM1,CYP17andGSTT1,XRCC1andGSTP1,CYP1B1andXRCC1andCOMTandXRCC1. The most parsimonious model of lung cancer risk in white smoking women included age, family history of lung cancer, history of chronic lung disease, pack-years, body mass index,XRCC1 A/Agenotype,GSTM1 nullandCOMT A/GorG/Ggenotype. These findings support the need for continued study of estrogen in relation to lung cancer risk. Polymorphisms in the tobacco metabolism, estrogen metabolism and DNA repair pathways will be useful in developing more predictive models of individual risk.

Tobacco and estrogen metabolic polymorphisms and risk of non-small cell lung cancer in women