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We investigated genetic variation in  CYP2A6  in relation to lung cancer risk among African American smokers, a high-risk population. Previously, we found that  CYP2A6 , a nicotine/nitrosamine metabolism gene, was associated with lung cancer risk in European Americans, but smoking habits, lung cancer risk and  CYP2A6  gene variants differ significantly between European and African ancestry populations. Herein, African American ever-smokers, drawn from two independent lung cancer case–control studies, were genotyped for reduced activity  CYP2A6  alleles and grouped by predicted metabolic activity. Lung cancer risk in the Southern Community Cohort Study ( n  = 494) was lower among  CYP2A6  reduced versus normal metabolizers, as estimated by multivariate conditional logistic regression [odds ratio (OR) = 0.44; 95% confidence interval (CI) = 0.26–0.73] and by unconditional logistic regression (OR = 0.62; 95% CI = 0.41–0.94). The association was replicated in an independent study from MD Anderson Cancer Center ( n  = 407) (OR = 0.64; 95% CI = 0.42–0.98), and pooling the studies yielded an OR of 0.64 (95% CI = 0.48–0.86). Exploratory analyses revealed a significant interaction between  CYP2A6  genotype and sex on the risk for lung cancer (Southern Community Cohort Study:  P  = 0.04; MD Anderson:  P  = 0.03; Pooled studies:  P  = 0.002) with a  CYP2A6  effect in men only. These findings support a contribution of genetic variation in  CYP2A6  to lung cancer risk among African American smokers, particularly men, whereby  CYP2A6  genotypes associated with reduced metabolic activity confer a lower risk of developing lung cancer.

CYP2A6 reduced activity gene variants confer reduction in lung cancer risk in African American smokers—findings from two independent populations