Zhang Xiao-Ying, Zhang Pei-Ying, Aboul-Soud Mourad A M
Nanjing University of Chinese Medicine, Information Institute, Nanjing, Jiangsu 221009, P.R. China.
Department of Cardiology, Xuzhou Central Hospital, The Affiliated Xuzhou Hospital of Medical College of Southeast University, Xuzhou, Jiangsu 221009, P.R. China.
Oncol Lett. 2017 Feb;13(2):543-548. doi: 10.3892/ol.2016.5506. Epub 2016 Dec 15.
Gastric cancer is a multifactorial disease and a leading cause of mortality and the risk factors for this include environmental factors and factors that influence host-pathogen interaction and complex interplay between these factors. Gastric adenocarcinomas are of two types, namely intestinal and diffuse type, and () infection has been suspected of being causally linked to the initiation of chronic active gastritis, which leads to adenocarcinoma of the intestinal type. Even though most individuals with infection do not show any clinical symptoms, long-term infection leads to inflammation of gastric epithelium and approximately 10% of infected patients develop peptic ulcers and 1-3% of patients develop gastric adenocarcinoma. Among the several mechanisms involved in tumorigenesis, CagA and peptidoglycan of , which enter the infected gastric epithelial cells play an important role by triggering oncogenic pathways. Inflammation induced by in gastric epithelium, which involves the cyclooxygenase-2/prostaglandin E2 pathway and IL-1β, is also an important factor that triggers chronic active gastritis and adenocarcinoma. infection induced oxidative stress and dysregulated E-cadherin/β-catenin/p120 interactions and function also play a critical role in tumorigenesis. Environmental and dietary factors, in particular salt intake, are known to modify the pathogenesis induced by . Gastric cancer induced by appears to involve several mechanisms, making this mode of tumorigenesis a highly complicated process. Nevertheless, there are many events in this tumorigenesis that remain to be clarified and investigated.
胃癌是一种多因素疾病，是导致死亡的主要原因，其风险因素包括环境因素、影响宿主与病原体相互作用的因素以及这些因素之间的复杂相互作用。胃腺癌有两种类型，即肠型和弥漫型，（）感染被怀疑与慢性活动性胃炎的发生存在因果关系，而慢性活动性胃炎会导致肠型腺癌。尽管大多数感染（）的个体没有任何临床症状，但长期感染会导致胃上皮炎症，约10%的感染患者会发展为消化性溃疡，1%-3%的患者会发展为胃腺癌。在肿瘤发生的几种机制中，进入受感染胃上皮细胞的（）的CagA和肽聚糖通过触发致癌途径发挥重要作用。（）在胃上皮中诱导的炎症，涉及环氧合酶-2/前列腺素E2途径和白细胞介素-1β，也是引发慢性活动性胃炎和腺癌的重要因素。（）感染诱导的氧化应激以及E-钙黏蛋白/β-连环蛋白/p120相互作用和功能失调在肿瘤发生中也起关键作用。环境和饮食因素，特别是盐的摄入量，已知会改变（）诱导的发病机制。（）诱导的胃癌似乎涉及多种机制，使得这种肿瘤发生模式成为一个高度复杂的过程。然而，在这种肿瘤发生过程中有许多事件仍有待阐明和研究。
