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[…] The candidate SNPs (single nucleotide polymorphisms) were selected from 3 public databases: the International HapMap Project database (, the Functional Element SNPs database ( [], and the SNPinfo Web Server ( The selection criteria were as follows: (i) haplotype-tagging SNPs with an R-square cutoff of 0.9 and minimum minor allele frequency in CHB and JPT population of 0.05; (ii) SNPs located in functional regions, such as the promoter, start codon, splice site, coding exon, and stop codon; and (iii) non-synonymous SNPs. Finally, we selected seven SNPs (rs662, rs13306698, rs854572, rs854573, rs854552, rs854565, and rs854568) in the PON1 gene for genotyping.Genomic DNA was isolated from peripheral blood using the QuickGene-810 Nucleic Acid Isolation System (Fujifilm, Tokyo, Japan) and the QuickGene DNA Whole Blood Kit in accordance with the manufacturer’s protocol; the DNA samples were stored at-70°C until analysis. SNP genotyping was performed using the VeraCode GoldenGate assay (Illumina, San Diego, CA, USA). All SNPs were in Hardy-Weinberg equilibrium in cases and controls, and the call rate for the seven SNPs was 100%. presents detailed information on the seven SNPs and allele frequencies. [...] Statistical power was calculated using Genetic Power Calculator ( []. The parameters were set as follows: risk allele frequency of less than 0.15, alpha error of less than 0.05, and a disease prevalence of less than 0.1%. The power of a dominant model was 72.4% when the odds ratio for a genotype with one or two risk allele(s) was taken as 1.5.Student’s t-test was used to compare continuous variables between the patients and control subjects. Associations between lung cancer and putative risk factors were estimated by odds ratios (ORs) and their corresponding 95% confidence intervals (95% CI) derived from multivariate conditional logistic regression models after adjusting for potential confounding factors, such as age, sex, smoking history, and occupational history. A stratified analysis was used to estimate the combined effects of genotypes and smoking status. The P-values for the interactions between the genotypes and smoking status were assessed using the Wald test for the cross-product term in a model containing the main effects of genotype and exposure variable. Multiple testing corrections were carried out using the Benjamini-Hochberg procedure for controlling the false discovery rate (FDR) []. All of the statistical analyses were performed using SAS Version 9.2 (SAS Institute, Cary, NC, USA). Linkage disequilibrium statistics and haplotype blocks were obtained using the Haploview program ( []. Haplotype frequency estimation and the analysis of the association of haplotypes with lung cancer risk were conducted with SNPStats ( []. […]

Pipeline specifications

Software tools SNPinfo, Haploview, snpStats
Databases International HapMap Project FESD
Application GWAS
Organisms Homo sapiens, Nicotiana tabacum
Diseases Lung Neoplasms