Abstract
Oxidative stress and aberrant activation-induced cytidine deaminase (AID) expression induced by chronic inflammation play an important role in inflammation-associated carcinogenesis. While AID plays a physiological role in B lymphocytes to induce somatic hypermutation and class switch recombination of immunoglobulin gene, it appears to promote mutagenesis in other cells than B lymphocytes. The impact of AID on carcinogenesis has been reported in numerous studies on colon, liver, lung, and gastric cancers, as well as hematologic malignancies. Chronic active gastritis by Helicobacter pylori (H. pylori) infection leads to aberrant AID expression, followed by mutations of tumor-related genes such as p53 and CDKN2B-CDKN2A, which suggests one possible mechanism how H. pylori infection induces gastric carcinogenesis.
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