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Many previous studies have demonstrated that a transcriptional factor, nuclear factor (<jats:styled-content style=\"fixed-case\">NF<\/jats:styled-content>)\u2010\u03ba<jats:styled-content style=\"fixed-case\">B<\/jats:styled-content>, plays an important role in the association between inflammation and cancer development, particularly tumor promotion and tumor progression. Although it is well recognized that cancer develops via stepwise accumulation of genetic aberrations, the mechanisms underlying the generation of these genetic alterations in normal epithelial cells under inflammatory conditions are not known. We recently demonstrated that pathogenic bacterial or viral factors and the subsequent inflammatory reactions lead to the aberrant expression of a <jats:styled-content style=\"fixed-case\">DNA<\/jats:styled-content> mutator enzyme, activation\u2010induced cytidine deaminase (<jats:styled-content style=\"fixed-case\">AID<\/jats:styled-content>), in various epithelial cells via <jats:styled-content style=\"fixed-case\">NF<\/jats:styled-content>\u2010\u03ba<jats:styled-content style=\"fixed-case\">B<\/jats:styled-content> activation, which causes the accumulation of genetic alterations in tumor\u2010related genes. <jats:styled-content style=\"fixed-case\">AID<\/jats:styled-content> activation is widely observed in gastrointestinal tissues with cancer\u2010associated inflammation, such as chronic viral hepatitis, <jats:italic><jats:styled-content style=\"fixed-case\">H<\/jats:styled-content>elicobacter pylori<\/jats:italic>\u2010related gastritis, <jats:styled-content style=\"fixed-case\">B<\/jats:styled-content>arrett's esophagus and inflammatory bowel disease. Furthermore, a deficiency of endogenous <jats:styled-content style=\"fixed-case\">AID<\/jats:styled-content> expression reduces both accumulation of somatic mutations in tumor\u2010related genes and tumor incidence in a mouse model of inflammation\u2010associated cancer development. These findings strongly suggest that <jats:styled-content style=\"fixed-case\">AID<\/jats:styled-content> plays an integral role in inflammation\u2010associated carcinogenesis and is therefore a potential target molecule for the prevention and treatment of cancers. (<jats:italic>Cancer Sci<\/jats:italic> 2012; 103: 1201\u20131206)<\/jats:p>","DOI":"10.1111\/j.1349-7006.2012.02293.x","type":"journal-article","created":{"date-parts":[[2012,4,3]],"date-time":"2012-04-03T17:03:05Z","timestamp":1333472585000},"page":"1201-1206","source":"Crossref","is-referenced-by-count":92,"title":["Inflammation\u2010mediated genomic instability: roles of activation\u2010induced cytidine deaminase in carcinogenesis"],"prefix":"10.1111","volume":"103","author":[{"given":"Takahiro","family":"Shimizu","sequence":"first","affiliation":[{"name":"Department of Gastroenterology and Hepatology, Graduate School of Medicine Kyoto University Kyoto Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hiroyuki","family":"Marusawa","sequence":"additional","affiliation":[{"name":"Department of Gastroenterology and Hepatology, Graduate School of Medicine Kyoto University Kyoto 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