Emerging evidences from preclinical and clinical studies have shown that epidermal growth factor (EGF) has some effectiveness against endogenously arising carcinogenesis. Functional + 61A > G polymorphism (rs4444903 A > G) in the promoter region of the EGF gene was observed to modulate EGF levels, thus affecting the susceptibility to gastrointestinal cancer; but individually published studies showed inconclusive results. The aim of this Human Genome Epidemiology (HuGE) review and meta-analysis was to derive a more precise estimation of the association between EGF + 61A > G polymorphism and gastrointestinal cancer risk. A literature search of Pubmed, Embase, Web of Science and Chinese BioMedical databases from inception through July 2012 was conducted. Twelve studies were assessed with a total of 2868 gastrointestinal cancer cases and 4278 healthy controls. When all the eligible studies were pooled into the meta-analysis, the results showed that the G allele and GG genotype of EGF + 61A > G polymorphism might increase the risk of gastrointestinal cancer. In the stratified analysis by cancer types, the G allele and GG genotype of EGF + 61A > G polymorphism showed displayed significant correlations with increased risk of esophageal cancer. We also found significant correlations between the G carrier (GG. +. AG) and GG genotype of EGF + 61A > G polymorphism and colorectal cancer risk. However, EGF + 61A > G polymorphism did not appear to have an influence on gastric cancer susceptibility. Results from the current meta-analysis indicate that EGF + 61A > G polymorphism might increase the risk of esophageal and colorectal cancers. Nevertheless, further studies are needed to determine whether genetic associations between EGF + 61A > G polymorphism and susceptibility to gastric cancer are significant. © 2013 Elsevier B.V.
CITATION STYLE
Piao, Y., Liu, Z., Ding, Z., Xu, L., Guo, F., Sun, Q., & Xie, X. (2013). EGF +61A>G polymorphism and gastrointestinal cancer risk: A HuGE review and meta-analysis. Gene, 519(1), 26–33. https://doi.org/10.1016/j.gene.2013.01.057
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