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- Title
Genetic polymorphisms of VEGF, interactions with cigarette smoking exposure and esophageal adenocarcinoma risk.
- Authors
Rihong Zhai; Geoffrey Liu; Kofi Asomaning; Li Su; Matthew H. Kulke; Rebecca S. Heist; Norman S. Nishioka; Thomas J. Lynch; John C. Wain; Xihong Lin; David C. Christiani
- Abstract
Vascular endothelial growth factor (VEGF) is a major regulator of angiogenesis in the process of tumor growth and metastasis in esophageal adenocarcinoma (EA). Polymorphisms in the VEGF gene have been associated with altered VEGF expression and plasma VEGF levels. We hypothesized that polymorphisms of VEGF may contribute to EA risk. Functional polymorphisms in the VEGF gene (â460C/T, 䋼 and 苽) were determined in 308 patients with EA and 546 healthy controls. Logistic regression analysis was employed to assess the associations between genotypes, haplotypes of VEGF and EA risk, adjusting for multiple confounding factors. Compared with the genotype, the combined 艏 genotypes were significantly associated with increased risk of developing EA, with adjusted odds ratio (OR)â=â1.49 [95% confidence interval (CI), 1.05â2.12; Pâ=â0.027]. The â460CT were associated with increased risk of EA in smokers (adjusted ORâ=â1.57; 95% CI, 1.07â2.30; Pâ=â0.021), whereas the â460CT/CC were associated with decreased risk of EA (adjusted ORâ=â0.47; 95% CI, 0.25â0.91; Pâ=â0.025) in non-smokers. Compared with non-smokers with the , smokers with the ɏ had significantly higher risk of EA (adjusted ORâ=â3.32; 95% CI, 1.56â7.10; Pâ=â0.002). No overall or interacting association with EA risk was found for the 䋼 polymorphism. Haplotype CGT (â460C/䛿) was significantly associated with higher risk of EA (adjusted ORâ=â1.70; 95% CI, 1.04â2.73; Pâ=â0.034). These results suggested that cigarette smoking modifies the association between VEGF polymorphisms and EA risk among Caucasians.
- Subjects
VASCULAR endothelial growth factor antagonists; TUMOR growth; METASTASIS; ESOPHAGEAL cancer risk factors; GENETIC polymorphisms; LOGISTIC regression analysis
- Publication
Carcinogenesis, 2008, Vol 29, Issue 12, p2330
- ISSN
0143-3334
- Publication type
Article
- DOI
10.1093/carcin/bgn210