Chronic infl ammation and gastrointestinal cancer

Chronic infl ammation has been identifi ed as an important risk factor in the development of the gastrointestinal (GI) tract cancers, and the underlying molecular mechanisms have been studied extensively. Chronic infl ammation is able to trigger cellular events to promote malignant transformation of normal epithelial cells in the GI tract to cancer. Host infl ammation responses in carcinogenesis are through multiple mechanisms such as reactive oxygen and nitration species from mononuclear phagocytes and leukocytes, immune response and pro-infl ammatory 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-infl ammatory cytokines and chemokines. Furthermore, chronic infl ammation creates an environment for genomic and epigenetic changes. In this review, we summarize the important molecular mechanisms that link chronic infl ammation and GI tract cancer, including esophageal, gastric and colonic cancers, focusing on infective and noninfective agents such as gastroesophageal refl ux disease, Helicobacter pylori gastritis and infl ammatory bowel disease.