Helicobacter pylori-induced activation-induced cytidine deaminase expression and carcinogenesis
Hiroyuki Marusawa1, Tsutomu Chiba
1Department of Gastroenterology and Hepatology, Graduate School of Medicine, Kyoto University, 54 Kawara-cho, Shogoin, Sakyo-ku, Kyoto 606-8507, Japan. maru@kuhp.kyoto-u.ac.jp
Abstract:
Tumorigenesis is a multistep process in which the accumulation of genetic alterations drives the transformation of normal cells into malignant derivatives. Activation-induced cytidine deaminase (AID) contributes to immune system diversity by inducing somatic hypermutations and class-switch recombinations of human immunoglobulin genes. The mutagenic activity of AID, however, can also induce genetic changes in various genes and may lead to the development of cancer. Helicobacter pylori, a class 1 carcinogen for human gastric cancer, affects AID expression by two different mechanisms, introduction of bacterial virulence factors into host cells and induction of inflammatory responses, thereby contributing to the accumulation of mutations in tumor-related genes. Aberrant AID activity may therefore be a novel link between infection and carcinogenesis.
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