Chronic inflammation and gastrointestinal cancer

Satoshi Ida , Masayuki Watanabe , Hideo Baba

Journal of Cancer Metastasis and Treatment ›› 2015, Vol. 1 : 138 -43.

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Journal of Cancer Metastasis and Treatment ›› 2015, Vol. 1:138 -43. DOI: 10.4103/2394-4722.166994
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Chronic inflammation and gastrointestinal cancer

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Abstract

Chronic inflammation has been identified as an important risk factor in 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 gastrointestinal 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 transcription of several pro-inflammatory cytokines and chemokines. Furthermore, chronic inflammation creates an environment forgenomic and epigenetic changes. In this review, we summarize 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.

Keywords

Cancer / gastrointestinal tract / immune response / inflammation

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Satoshi Ida, Masayuki Watanabe, Hideo Baba. Chronic inflammation and gastrointestinal cancer. Journal of Cancer Metastasis and Treatment, 2015, 1: 138-43 DOI:10.4103/2394-4722.166994

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