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X. Zhang



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    P3.22 - Poster Session 3 - Epidemiology, Etiology (ID 168)

    • Event: WCLC 2013
    • Type: Poster Session
    • Track: Prevention & Epidemiology
    • Presentations: 1
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      P3.22-005 - XPA gene rs1800975 single nucleotide polymorphism and lung cancer risk: a meta-analysis (ID 2359)

      09:30 - 09:30  |  Author(s): X. Zhang

      • Abstract

      Background
      No clear consensus has been reached on the XPA gene A23G (rs1800975) polymorphism and lung cancer risk. We performed a meta-analysis in an effort to systematically explore the possible association.

      Methods
      Case-control studies in English and Chinese publications performed with human subjects were identified by searching MEDLINE, EMBASE, Wanfang and CNKI databases prior to June 2013. References of retrieved articles were also screened. According to the inclusion criteria, 10 articles (12 studies) were finally included. The fixed-effects model and the random-effects model were applied for dichotomous outcomes to combine the results of the individual studies.

      Results
      Overall, statistical association could be found between A23G polymorphism and lung cancer risk in recessive genetic model (AA vs. (AG+GG)) (P=0.001, OR=1.21, 95%CI [1.08–1.35], P~heterogeneity~=0.11, fixed-effects model) and in the homozygote comparison (AA vs. GG) (P=0.03, OR=1.15, 95%CI [1.01–1.31], P~heterogeneity~=0.14, fixed-effects model). In East Asians, significant association was found in allele comparison model (A vs. G) (P=0.03, OR=1.13, 95%CI [1.01–1.26], P~heterogeneity~=0.39, fixed-effects model), in recessive genetic model (AA vs. (AG+GG)) (P=0.005, OR=1.30, 95%CI [1.08–1.56], P~heterogeneity~=0.58, fixed-effects model) and in the homozygote comparison (AA vs. GG) (P=0.02, OR=1.30, 95%CI[1.04–1.63], P~heterogeneity~=0.39, fixed-effects model). No evidence suggested that A23G polymorphism might associate with lung cancer risk in the Caucasians or African-Americans. Stratification analysis was performed by histologic types and indicated that AA genotype might represent a risk factor for squamous cell carcinoma (AA vs. (AG+GG)) (P=0.01, OR=1.42, 95%CI [1.08–1.86], P~heterogeneity~=0.27, fixed-effects model); (AA vs. GG) (P=0.03, OR=1.43, 95%CI[1.04–1.96], P~heterogeneity~=0.21, fixed-effects model). No association was observed in adenocarcinoma subgroup. Stratification analysis performed by gender shown that A allele might increase the lung cancer risk in male (A vs. G) (P=0.02, OR=1.18, 95%CI [1.02–1.37], P~heterogeneity~=0.48, fixed-effects model), but did not found association in female subgroup. Figure 1 Figure – Meta-analysis for the association between XPA gene rs1800975 polymorphism and lung cancer risk in the contrast of AA vs. (AG+GG) in overall. “Events” indicates the number of the AA genotype; “Total” indicates the total number of the AG+GG genotype plus the AA genotype.

      Conclusion
      XPA gene A23G polymorphism might associate with lung cancer risk in Overall and East Asians. This polymorphism might also associate with lung cancer risk in male and in the squamous cell carcinoma subgroup.