Statistical analysis All statistical analyses were performed with

Statistical analysis All statistical analyses were performed with Statistical Product and Service Solutions (SPSS) v13.0, if not otherwise specified. All of the tests were two-sided, and statistical significance was defined as P < 0.05. Pearson's chi-square test was used

to compare the distribution of the demographic variables and examine differences in risk factors and genotypes, alleles and haplotypes between cases and controls. Hardy-Weinberg equilibrium (HWE) of the genotypes was tested by performing a goodness-of-fit χ2 test. Unconditional logistic regression analysis was performed to calculate the AZD5363 clinical trial odds ratios (ORs) with 95% confidence intervals (CIs) for estimating the association between certain genotypes and lung cancer. The stratified analyses and gene-environment interaction were evaluated by logistic regression Selleckchem Bafilomycin A1 models. On the basis of the observed frequencies of three SNPs, we used the SHEsis analysis platform to calculate linkage disequilibrium index (D’ and r2) and infer haplotype frequencies [6, 7]. Results Selected demographic

variables and environmental risk factors for the 285 patients and 285 controls were listed in Table 1. All subjects were females and all cases were lung adenocarcinoma patients. Mean ages of cases and controls (mean ± S.D.) were almost identical (53.9 ± 12.0 and 54.1 ± 9.1 years, respectively). There were no significant differences in the distribution of family history of cancer, passive smoking, fuel smoke exposure, occupational exposures,

and dietary habits between cases and controls. However the cases were more likely than the controls to report cooking oil fume Sitaxentan exposure (OR 1.61, 95%CI 1.13-2.30, P = 0.009). Table 1 Selected variable in cases and controls Variable Cases n (%) Controls n (%) P value Female 285 285   Age (years) 53.9 ± 12.0 54.1 ± 9.1 0.750 Income(yuan/month) 619.34 ± 374.59 557.11 ± 390.61 0.071 Education     0.779    Never 27 (9.5) 26 (9.1)      Elementary school 133 (46.7) 145 (50.9)      Junior school 85 (29.8) 76 (26.7)      Senior school and upwards 40 (14.0) 38 (13.3)   Family history of cancer 39 (13.7) 27 (9.5) 0.116 Passive smoking 174 (61.1) 162 (56.8) 0.307 Fuel smoke exposure 84 (29.5) 78 (27.4) 0.577 Cooking oil fume exposure 104 (36.5) 75 (26.3) 0.009 Table 2 presents the distribution of ERCC2 751, 312 and ERCC1 118 polymorphisms in cases and controls. The frequencies of the 751C, 312A and 118T allele in the controls were 0.08, 0.05 and 0.21, respectively. All allele distributions were consistent with Hardy-Weinberg equilibrium. Among these SNPs, heterozygous carriers of the ERCC2 751AC genotype had a 1.66-fold risk of lung adenocarcinoma compared with those Protein Tyrosine Kinase inhibitor carrying the homozygous wild genotype (95%CI 1.07-2.59, P = 0.024). Individuals carrying ERCC1 118TT homozygote genotype had a 2.

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