Chronic inflammation and gastrointestinal cancer

发表时间：2015-12-03 浏览次数：1099次

引用：

Ida S, Watanabe M, Baba H. Chronic inflammation and gastrointestinal cancer. J C

关键词：

作者：

Satoshi Ida1, Masayuki Watanabe2, Hideo Baba3

作者单位：

1 Department of Gastroenterological Surgery, Cance

出版年份：

2015

期刊页数：

138-143

收录者：

其他外文数据库

摘要：

Chronic inflammation has been identified as an important risk factor in the development of the gastrointestinal (GI) tract cancers, and the underlying molecular mechanisms have been studied extensively. Chronic inflammation is able to trigger cellular events to promote malignant transformation of normal epithelial cells in the GI tract to cancer. Host inflammation responses in carcinogenesis are through multiple mechanisms such as reactive oxygen and nitration species from mononuclear phagocytes and leukocytes, immune response and pro-inflammatory cytokines. Nuclear factor-κB (NF-κB) has been considered as the central mediator of the immune response. Activation of NF-κB by phosphorylation leads to translocation of NF-κB protein to the nucleus, and in turn regulates the transcription of several pro-inflammatory cytokines and chemokines. Furthermore, chronic inflammation creates an environment for genomic and epigenetic changes. In this review, we summarize the important molecular mechanisms that link chronic inflammation and GI tract cancer, including esophageal, gastric and colonic cancers, focusing on infective and noninfective agents such as gastroesophageal reflux disease, Helicobacter pylori gastritis and inflammatory bowel disease.

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