Helicobacter pylori-Mediated Genetic Instability and Gastric Carcinogenesis

被引：23

作者：

Shimizu, Takahiro ^{[1
]}

Chiba, Tsutomu ^{[1
]}

Marusawa, Hiroyuki ^{[1
]}

机构：

[1] Kyoto Univ, Dept Gastroenterol & Hepatol, Grad Sch Med, Sakyo Ku, 54 Kawara Cho, Kyoto 6068507, Japan

来源：

MOLECULAR PATHOGENESIS AND SIGNAL TRANSDUCTION BY HELICOBACTER PYLORI | 2017年 / 400卷

关键词：

INDUCED CYTIDINE DEAMINASE; POLYPEPTIDE-EXPRESSING METAPLASIA; DOUBLE-STRAND BREAKS; DNA MISMATCH REPAIR; ESOPHAGEAL ADENOCARCINOMA; MICROSATELLITE INSTABILITY; MUTATIONAL LANDSCAPE; SOMATIC MUTATIONS; CHIEF CELLS; CANCER;

D O I：

10.1007/978-3-319-50520-6_13

中图分类号：

R57 [消化系及腹部疾病];

学科分类号：

摘要：

Helicobacter pylori infection is the most important cause of human gastric cancer worldwide. Gastric cancer develops over a long time after H. pylori infection via stepwise accumulation of genetic alterations and positive selection of cells with growth advantages. H. pylori itself and the resultant chronic inflammation lead to the emergence of genetic alterations in gastric epithelial cells via increased susceptibility of these cells to DNA damage. Reactive oxygen species (ROS) and reactive nitrogen species (RNS) in inflammatory and gastric epithelial cells, as well as the expression of cytidine deaminase in gastric epithelial cells, may link H. pylori-related inflammation and DNA damage. Recent comprehensive analyses of gastric cancer genomes provide clues for the possible molecular mechanisms of gastric carcinogenesis. In this chapter, we describe how genetic alterations emerge during gastric carcinogenesis related to H. pylori infection.

引用

页码：305 / 323

页数：19

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