Abstract
Epidemiological, clinical, and biological studies convincingly demonstrate that chronic inflammation predisposes to the development of human cancers. In digestive organs, inflammation-associated cancers include colitis-associated colorectal cancers, Helicobacter pylori-associated gastric cancer, as well as Barrett’s esophagus and esophageal adenocarcinoma associated with chronic duodenogastric-esophageal reflux. Cancer is a genomic disease, and stepwise accumulation of genetic and epigenetic alterations of tumor-related genes leads to the development of tumor cells. Recent genome analyses show that genetic alterations, which are evoked by inflammation, are latently accumulated in inflamed epithelial cells of digestive organs. Production of reactive oxygen and aberrant expression of activation-induced cytidine deaminase, a nucleotide-editing enzyme, could be induced in inflamed gastrointestinal epithelial cells and play a role as a genomic modulator of inflammation-associated carcinogenesis. Understanding the molecular linkage between inflammation and genetic alterations will open up a new field of tumor biology and provide a novel strategy for the prevention of inflammation-associated tumorigenesis.
Highlights
Cancer is induced by factors such as chemical carcinogens, infection, and chronic inflammation
Numerous epidemiological studies show that chronic inflammation predisposes to tumor formation, including colorectal cancer caused by inflammatory bowel disease (IBD), gastric cancer caused by Helicobacter pylori (H. pylori) infection, and esophageal cancer associated with gastro-esophageal reflux disease (GERD)
Such evidence was acquired by numerous epidemiological studies that convincingly demonstrate that the suppression of chronic inflammation is closely associated with the prevention of the development of inflammation-associated cancer in certain organs other than the gastrointestinal tract
Summary
Cancer is induced by factors such as chemical carcinogens, infection, and chronic inflammation. European Crohn’s and Colitis Organisation guidelines refer that patients with high risk factors, such as extensive colitis with severe active inflammation, stricture or dysplasia detected within the past five years, primary sclerosing cholangitis, should have their surveillance colonoscopy scheduled for one year. Patients with intermediate risk factors, such as extensive colitis with mild or moderate active inflammation, should have their surveillance colonoscopy scheduled for two to three years [7]. These findings suggest that chronic inflammation of the colonic epithelium plays a critical role in tumorigenesis
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
