19 × 10−3 (αcorrect = 2.38 × 10−3/2). Spearman’s r test was used to analyze the correlation between XRCC4 genotypes and XRCC4 protein expression. Kaplan-Meier’s survival analysis with the log-rank test was used to evaluate the relationship between this polymorphism and HCC Selleck Copanlisib prognosis. Risk factors for HCC prognosis were first selected using Cox’s multivariate regression model (including age, sex, race, HBV and HCV infection, AFB1 exposure information, tumor size, tumor TNM stage, and all possible multiplicatively interactive variables)

with step-wise forward selection based on the likelihood ratio test. Hazard ratios (HRs) and 95% CIs for risk factors were next calculated in the same multivariate Cox’s regression model (simultaneously including all risk variables and multiplicatively interactive variables). Our final analysis included 1,499 HCC cases and 2,045 controls (Supporting Table 3). There were no significant differences between cases and controls in terms of distribution of age, sex, race, and HBV and HCV status as a result of individual matching (P > 0.05). These results suggest that HCC patient data were comparable to control data. The AFB1 exposure information for the entire study population is shown in Supporting BMS-354825 solubility dmso Table 4. We observed that the AFB1 exposure years were associated with

an increased risk for HCC (OR = 2.53 for medium-exposure years; OR = 5.85 for long-exposure years). We also found that MCE HCC cases (28.38 fmol/mg) had higher serum levels of AFB1 ALB adducts than controls (11.57 fmol/mg).

For statistical analysis, values were logarithmically transformed and then were divided into three stratus: low (<2.18 ln fmol/mg), medium (2.18-2.98 ln fmol/mg), and high (>2.98 ln fmol/mg), according to the mean logit value of serum AFB1 ALB adducts among controls and cases (Supporting Table 4). Regression analysis showed that HCC risk gradually increased with an increasing number of exposure levels (adjusted OR = 2.10-6.52; P < 0.01). XRCC4 genotypes from all peripheral blood DNA samples are listed in Table 1. For these SNPs, the genotype distribution of controls was consistent with those expected from Hardy-Weinberg's equilibrium (Supporting Table 5; P > 0.05). Among 21 SNPs, only rs28383151 (no. 3) was observed to modify HCC risk. Logistic regression analyses exhibited that the adjusted OR for HCC for those individuals carrying the heterozygotes of rs28383151 G and A allele (rs28383151-GA) versus those with the homozygotes of the rs28383151 G alleles (rs28383151-GG) was 1.94 (95% CI: 1.54-2.43); the corresponding OR for those featuring the homozygotes of rs28383151 A alleles (rs28383151-AA) was 3.10 (95% CI: 2.10-4.58).