Gastric Carcinogenesis and Underlying Molecular Mechanisms: Helicobacter pylori and Novel Targeted Therapy

被引：29

作者：

Nishizawa, Toshihiro ^{[1
,2
]}

Suzuki, Hidekazu ^{[1
]}

机构：

[1] Keio Univ, Sch Med, Dept Internal Med,Div Gastroenterol & Hepatol, Shinjuku Ku, Tokyo 1608582, Japan

[2] Keio Univ, Sch Med, Ctr Canc,Div Res & Dev Minimally Invas Treatment, Shinjuku Ku, Tokyo 1608582, Japan

来源：

BIOMED RESEARCH INTERNATIONAL | 2015年 / 2015卷

关键词：

INDUCED CYTIDINE DEAMINASE; OPEN-LABEL; PREDICTIVE MARKER; EPITHELIAL-CELLS; CANCER; ERADICATION; EXPRESSION; TUMOR; INFECTION; CAGA;

D O I：

10.1155/2015/794378

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：

The oxygen-derived free radicals that are released from activated neutrophils are one of the cytotoxic factors of Helicobacter pylori-induced gastric mucosal injury. Increased cytidine deaminase activity in H. pylori-infected gastric tissues promotes the accumulation of various mutations and might promote gastric carcinogenesis. Cytotoxin-associated gene A (CagA) is delivered into gastric epithelial cells via bacterial type IV secretion system, and it causes inflammation and activation of oncogenic pathways. H. pylori infection induces epigenetic transformations, such as aberrant promoter methylation in tumor-suppressor genes. Aberrant expression of microRNAs is also reportedly linked to gastric tumorogenesis. Moreover, recent advances in molecular targeting therapies provided a new interesting weapon to treat advanced gastric cancer through anti-human epidermal growth factor receptor 2 (HER-2) therapies. This updated review article highlights possible mechanisms of gastric carcinogenesis including H. pylori-associated factors.

引用

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