Purpose: Nowadays, chromosomal regions containing genes associated with the risk of lung cancer are identified by a number of genome-wide association studies (GWASs). As part of the study, GWAS has identified the association of six chromosomal regions, 1q23, 4q22, 4q31, 5p15, 6p21, and 15q25, as being associated with lung cancer risk in the European population. We investigated the impact of genetic variants identified in GWASs for lung cancer susceptibility on the survival outcomes in patients

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... ith early stage non-small cell lung cancer (NSCLC). Materials and Methods: Three hundred and sixty-three patients with surgically resected NSCLC were enrolled. Eight single nucleotide polymorphisms (SNPs), rs2808630 on 1q23, rs7671167 on 4q22, rs1489759 and rs2202507 on 4q31, rs2736100 and rs402710 on 5p15, rs1052486 on 6p21 and rs16969968 on 15q25, were genotyped using a polymerase chain reaction-restriction fragment length polymorphism assay. The associations between genotypes and overall survival (OS) and disease-free survival (DFS) were analyzed. Results: None of the eight SNPs were significantly associated with OS or DFS. In addition, when the patients were categorized according to age, gender, smoking status, tumor histology and pathologic stage, there were no significant associations between the eight SNPs and the survival outcomes. Conclusion: These results suggest that the genetic variants identified by GWASs for lung cancer susceptibility may not affect the prognosis of early stage NSCLC. (J Lung Cancer 2012;11(2):66 70) DFS with genotypes and haplotypes was investigated using the Kaplan-Meier method and assessed using the log-rank test. Hazard ratios and 95% confidence intervals (CIs) were estimated using multivariate Cox proportional hazards models, with adjustment for age (≤64 years vs. >64 years), gender (male vs. female), smoking status (never-smoker vs. ever-smoker), pathologic stage (I vs. II∼IIIA) and adjuvant therapy (yes vs. no). All statistical testing was conducted with SPSS version 68 J Lung Cancer 2012;11(2):66-70 65 0.71 (0.42-1.18) 0.18 33 (49.3) 51 1.01 (0.66-1.56) 0.96 TT+TG 283 (80.9) 112 (39.6) 51 1.00 141 (49.8) 42 1.00 GG 67 (19.1) 23 (34.3) 65 0.72 (0.45-1.14) 0.16 33 (49.3) 51 0.96 (0.65-1.43) 0.85 CLPTM1L/rs402710 GG 186 (53.8) 78 (41.9) 55 1.00 98 (52.7) 43 1.00 GA 134 (38.7) 47 (35.1) 54 0.80 (0.56-1.16) 0.24 60 (44.8) 48 0.80 (0.58-1.11) 0.18 AA 26 (7.5) 11 (42.3) 47 1.08 (0.57-2.04) 0.82 14 (53.9) 34 1.00 (0.57-1.75) 0.99 BAT3/rs1052486 AA 97 (27.3) 34 (35.1) 58 1.00 47 (48.5) 45 1.00 AG 164 (46.2) 63 (38.4) 55 0.97 (0.64-1.47) 0.88 82 (50.0) 43 1.02 (0.71-1.46) 0.94 GG 94 (26.5) 42 (44.7) 48 1.10 (0.69-1.75) 0.69 48 (51.1) 43 1.00 (0.67-1.52) 0.98 CHRNA5/rs16969968 GG 326 (91.8) 129 (39.6) 54 1.00 165 (50.6) 43 1.00 GA 28 (7.9) 11 (39.3) 52 1.14 (0.62-2.12) 0.67 15 (53.6) 42 1.17 (0.69-1.99) 0.56 AA 1 (0.3) 0 (0.00) 100 0 (0.00) 100 *Column percentage, † Row percentage, ‡ Five year-overall survival rate (5Y-OSR) and 5 year-disease free survival rate (5Y-DFSR), proportion of survival derived from Kaplan-Meier analysis, § Hazard ratios (HRs), 95% confidence intervals (CIs) and corresponding p-values were calculated using multivariate Cox proportional hazard models, adjusted for age, gender, smoking status, tumor histology, pathologic stage and adjuvant therapy.