Polymorphisms in the vitamin D receptor gene and the lung cancer risk.

The relationship between the vitamin D receptor (VDR) polymorphisms and the susceptibility to lung cancer remains unclear. The present meta-analysis was performed to estimate the polymorphisms of VDR and lung cancer risk. The pooled odds ratios (ORs) and corresponding 95 % confidence intervals (CIs) were calculated. Subgroup analysis by smoking status was carried out for further elucidation. The VDR BsmI polymorphism seemed to be negatively associated with the lung cancer risk (A vs. G, OR = 0.71, 95 % CI, 0.52-0.96; GA vs. GG, OR = 0.54, 95 % CI, 0.35-0.83; AA + GA vs. GG, OR = 0.55, 95 % CI, 0.36-0.84), particularly among the smokers (AA + GA vs. GG, OR = 0.39, 95 % CI, 0.21-0.72). The VDR ApaI variant genotypes did not alter the risk of lung cancer under all gene models in overall analysis. However, smokers carrying the variant G allele were more susceptible to lung cancer (G vs. T, OR = 1.60, 95 % CI, 1.14-2.25). The polymorphism of VDR TaqI was related to a decreased risk of lung cancer (C vs. T, OR = 0.62, 95 % CI, 0.26-1.46; CC vs. TT, OR = 0.44, 95 % CI, 0.21-0.91; TC vs. TT, OR = 0.58, 95 % CI, 0.38-0.90; CC + TC vs. TT, OR = 0.55, 95 % CI, 0.36-0.84). Besides, the CC + TC carriers in the smokers were at a significantly reduced risk of lung cancer (CC + TC vs. TT, OR = 0.48, 95 % CI, 0.16-1.44). The study supports that the polymorphisms of VDR BsmI and TaqI play protective roles in the lung carcinogenesis, particularly among the smokers. The association of VDR ApaI polymorphism with the lung cancer risk needs to be further elucidated.

APE1 Asp148Glu polymorphism and lung cancer susceptibility.

Apurinic/apyrimidinic endonuclease 1 (APE1) is a key enzyme in base excision repair (BER) pathway for the removal of many oxidized and alkylated bases. Single-nucleotide polymorphisms of the APE1gene have been demonstrated to be involved in carcinogenesis. However, the association between APE1 Asp148Glu polymorphism and lung cancer risk remains inconclusive. To derive a precise estimate for this association, we carried out an updated meta-analysis by pooling data thus far published. The pooled odds ratio (OR) with 95 % confidence interval (95 % CI) was calculated to assess the role of APE1 Asp148Glu polymorphism in lung carcinogenesis. The pooled ORs suggested that variant genotypes of APE1 Asp148Glu were modestly associated with an elevated risk of lung cancer (GluGlu vs. AspAsp, OR=1.22, 95 % CI 1.01-1.48, P=0.038; GluGlu vs. AspAsp + AspGlu, OR=1.19, 95 % CI 1.02-1.39, P=0.023). The relationship was also observed in studies conducted among Asians, but not Caucasians. Sensitivity analysis further confirmed the findings. The meta-analysis shows that the polymorphism of APE1 Asp148Glu exerts risk effect on lung cancer development.