Helicobacter pylori-Induced Signaling Pathways Contribute to Intestinal Metaplasia and Gastric Carcinogenesis

被引：56
作者：
Sue, Soichiro [1 ]
Shibata, Wataru [1 ]
Maeda, Shin [1 ]
机构：
[1] Yokohama City Univ, Dept Gastroenterol, Kanazawa Ku, Yokohama, Kanagawa 2360004, Japan
来源：
BIOMED RESEARCH INTERNATIONAL | 2015年 / 2015卷
关键词：
NF-KAPPA-B; ABERRANT DNA METHYLATION; TUMOR-NECROSIS-FACTOR; EPITHELIAL-CELLS; CYTIDINE DEAMINASE; SONIC HEDGEHOG; P53; MUTATIONS; GENE; EXPRESSION; CANCER;
D O I：
10.1155/2015/737621
中图分类号：
Q81 [生物工程学（生物技术）]; Q93 [微生物学];
学科分类号：
071005 ; 0836 ; 090102 ; 100705 ;
摘要：
Helicobacter pylori (H. pylori) induces chronic gastric inflammation, atrophic gastritis, intestinal metaplasia, and cancer. Although the risk of gastric cancer increases exponentially with the extent of atrophic gastritis, the precise mechanisms of gastric carcinogenesis have not been fully elucidated. H. pylori induces genetic and epigenetic changes in gastric epithelial cells through activating intracellular signaling pathways in a cagPAI-dependent manner. H. pylori eventually induces gastric cancer with chromosomal instability (CIN) or microsatellite instability (MSI), which are classified as two major subtypes of gastric cancer. Elucidation of the precise mechanisms of gastric carcinogenesis will also be important for cancer therapy.
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页数：9
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