Yin Ming, Hu Zhibin, Tan Dongfeng, Ajani Jaffer A, Wei Qingyi
Am J Transl Res. 2009 Jan 1;1(1):44-54.
Gastric cancer is a disease of gene-environment interactions, as suggested by the varying geographic patterns of its incidence. Even in areas with high rates of Helicobacter pylori infection, only a small proportion of infected individuals develop gastric cancer. Genetic susceptibility to gastric cancer can be investigated by common genetic variants, such as single nucleotide polymorphisms (SNPs), in various genes that regulate multiple biological pathways. The susceptibility to gastric carcinogenesis has a substantial influence on the population attributable risk by modulating the effects of environmental risk factors. Despite recent progress in the field of the molecular epidemiology of cancer, a re-evaluation of gastric cancer susceptibility and potentially functional SNPs in candidate genes is necessary, given the inconsistency of previous reported studies. This review focuses on genetic variants that contribute to the etiology of gastric cancer, particularly those SNPs involved in inflammatory response, metabolism of chemical carcinogens, DNA repair, and tumor suppression. In the future, well-designed large multicenter population-based studies will be needed to validate current findings and provide the rationale for identifying at-risk subpopulations for primary prevention of gastric cancer.
胃癌是一种基因与环境相互作用的疾病，其发病率的地理分布差异表明了这一点。即使在幽门螺杆菌感染率高的地区，也只有一小部分感染者会患上胃癌。可以通过常见的基因变异，如单核苷酸多态性（SNP），在调节多种生物学途径的各种基因中研究胃癌的遗传易感性。胃癌发生的易感性通过调节环境风险因素的作用，对人群归因风险有重大影响。尽管癌症分子流行病学领域最近取得了进展，但鉴于先前报道的研究结果不一致，有必要重新评估胃癌易感性以及候选基因中潜在的功能性SNP。本综述重点关注导致胃癌病因的基因变异，特别是那些参与炎症反应、化学致癌物代谢、DNA修复和肿瘤抑制的SNP。未来，需要精心设计的大型多中心人群研究来验证当前的发现，并为识别胃癌一级预防的高危亚人群提供理论依据。
