DNA repair gene xeroderma pigmentosum group D 751 polymorphism and the risk on esophageal cancer:a Meta-analysis / 中华流行病学杂志
Chinese Journal of Epidemiology
; (12): 281-285, 2009.
Article
de Zh
| WPRIM
| ID: wpr-266551
Bibliothèque responsable:
WPRO
ABSTRACT
Objective To explore the association between XPD codon 751 polymorphism and esophageal cancer (EC) by systematically reviewing the risk of the original studies. Methods A comprehensive search was conducted to identify all case-control studies of XPD codon 751 polymorphism and EC risk. Meta-analysis was applied with Rev Man 4.2 software for calculation of pooled OR value (with 95%C1)of EC, esophageal squamous cell carcinoma (ESCC)and esophageal adenocarcinoma (EAC). Results Of the 12 case-control studies selected for this Meta-analysis, a total of 2558 EC cases and 5122 controls were included. Compared with the wild-type homozygote Lys/Lys, the pooled Odds Ratios (with 95% CI) of Lys/Gln, Gin/Gin, (Lys/Gln + Gln/Gln) genotypes of XPD codon 751 polymorphism for EC risk were 1.19(1.05, 1.34), 1.22(0.86, 1.74), 1.20(1.01,1.42), respectively. In a stratified analysis, a total of 1417 ESCC cases and 2312 controls were included, and individuals carrying Lys/Gln genotype or (Lys/Gln+Gln/Gln) had 1.22-fold or 1.24-fold excess risks for ESCC compared with those carrying Lys/Lys genotype. A total of 935 EAC cases and 2604 controls were included, and none of the genotype of XPD codon 751 genetic polymorphism was found to be related to EAC. Conclusion Both heterogyzote Lys/Gln and (Lys/Gln + Gln/Gln) for XPD codon 751 genetic polymorphism were associated with an increased risk of developing esophageal cancer. Furthermore, heterogyzote Lys/Gln and (Lys/Gln + Gln/Gln) for XPD codon 751 genetic polymorphism might have increased the risk of ESCC, but have no association with EAC.
Texte intégral:
1
Base de données:
WPRIM
Type d'étude:
Etiology_studies
/
Observational_studies
/
Risk_factors_studies
/
Systematic_reviews
Langue:
Zh
Journal:
Chinese Journal of Epidemiology
Année:
2009
Type de document:
Article