炎症细胞因子对胃癌发生的调控
Regulation of Gastric Carcinogenesis by Inflammatory Cytokines.
作者信息
Bockerstett Kevin A, DiPaolo Richard J
机构信息
Department of Molecular Microbiology and Immunology, Saint Louis University School of Medicine, St Louis, Missouri.
出版信息
Cell Mol Gastroenterol Hepatol. 2017 Mar 14;4(1):47-53. doi: 10.1016/j.jcmgh.2017.03.005. eCollection 2017 Jul.
Abstract
Chronic inflammation caused by infection with and autoimmune gastritis increases an individual's risk of developing gastric cancer. More than 90% of gastric cancers are adenocarcinomas, which originate from epithelial cells in the chronically inflamed gastric mucosa. However, only a small subset of chronic gastritis patients develops gastric cancer, implying a role for genetic and environmental factors in cancer development. A number of DNA polymorphisms that increase gastric cancer risk have mapped to genes encoding cytokines. Many different cytokines secreted by immune cells and epithelial cells during chronic gastritis have been identified, but a better understanding of how cytokines regulate the severity of gastritis, epithelial cell changes, and neoplastic transformation is needed. This review summarizes studies in both human and mouse models, describing a number of different findings that implicate various cytokines in regulating the development of gastric cancer.
摘要
由幽门螺杆菌感染和自身免疫性胃炎引起的慢性炎症会增加个体患胃癌的风险。超过90%的胃癌是腺癌，起源于慢性炎症胃黏膜中的上皮细胞。然而，只有一小部分慢性胃炎患者会发展为胃癌，这意味着遗传和环境因素在癌症发展中起作用。一些增加胃癌风险的DNA多态性已定位到编码细胞因子的基因。在慢性胃炎期间，免疫细胞和上皮细胞分泌的许多不同细胞因子已被鉴定出来，但需要更好地了解细胞因子如何调节胃炎的严重程度、上皮细胞变化和肿瘤转化。本综述总结了人类和小鼠模型中的研究，描述了一些不同的发现，这些发现表明各种细胞因子在调节胃癌发展中起作用。
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