{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,8]],"date-time":"2026-04-08T19:52:39Z","timestamp":1775677959782,"version":"3.50.1"},"reference-count":62,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2008,10,21]],"date-time":"2008-10-21T00:00:00Z","timestamp":1224547200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Intl Journal of Cancer"],"published-print":{"date-parts":[[2009,3,15]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Genetic or epigenetic alterations in Barrett's esophagus (BE) with\/without <jats:italic>Helicobacter pylori<\/jats:italic> (<jats:italic>H. pylori<\/jats:italic>) infection remain unclear. We examined the effects of <jats:italic>H. pylori<\/jats:italic> infection on genetic instability (GIN), the CpG island methylation status and a biomarker related to BE carcinogenesis. We analyzed 113 Japanese individuals with endoscopically suspected BE. The patients included, Group CLE (<jats:italic>n<\/jats:italic> = 25): no specialized intestinal metaplasia (SIM) in a columnar lined epithelium (control); Group BE (<jats:italic>n<\/jats:italic> = 88): all had SIM. Microsatellite instability and a loss of heterozygosity as GIN, the methylation status at <jats:italic>hMLH1<\/jats:italic>, <jats:italic>E\u2010cadherin<\/jats:italic>, <jats:italic>p16<\/jats:italic> and <jats:italic>APC<\/jats:italic>, and immunoreactivity using a monoclonal antibody (mAb) Das\u20101, which specifically reacts with BE, were evaluated. Nine additional patients with BE were prospectively followed up for 2 years after successful <jats:italic>H. pylori<\/jats:italic> eradication. The frequency of GIN, methylation at <jats:italic>E\u2010cadherin<\/jats:italic> and <jats:italic>APC<\/jats:italic>, and mAb Das\u20101 reactivity in Group BE was significantly higher than that in Group CLE (<jats:italic>p<\/jats:italic> &lt; 0.0001, <jats:italic>p<\/jats:italic> &lt; 0.0001 and <jats:italic>p<\/jats:italic> &lt; 0.005, and <jats:italic>p<\/jats:italic> &lt; 0.0001, respectively). Furthermore, GIN, <jats:italic>E\u2010cadherin<\/jats:italic> methylation and mAb Das\u20101 reactivity showed a significantly higher incidence in patients with <jats:italic>H.pylori<\/jats:italic> infection than in those without <jats:italic>H. pylori<\/jats:italic> infection (<jats:italic>p<\/jats:italic> &lt; 0.01, <jats:italic>p<\/jats:italic> &lt; 0.005, and <jats:italic>p<\/jats:italic> &lt; 0.01, respectively). Interestingly, the patients from Group BE were observed to change to a stable state of molecular alterations in 60% for GIN, 42.9% for <jats:italic>E\u2010cadherin<\/jats:italic> methylation and 55.6% for <jats:italic>APC<\/jats:italic> methylation, or a reduction of mAb Das\u20101 reactivity was noted in 25% following eradication. <jats:italic>H. pylori<\/jats:italic> infection may therefore affect these molecular alterations associated with the pathogenesis of BE, to some degree, in the Japanese population. \u00a9 2008 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/ijc.24092","type":"journal-article","created":{"date-parts":[[2008,10,21]],"date-time":"2008-10-21T18:57:14Z","timestamp":1224615434000},"page":"1263-1269","source":"Crossref","is-referenced-by-count":13,"title":["Effects of <i>Helicobacter pylori<\/i> infection on genetic instability, the aberrant CpG island methylation status and the cellular phenotype in Barrett's esophagus in a Japanese population"],"prefix":"10.1002","volume":"124","author":[{"given":"Kentaro","family":"Moriichi","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jiro","family":"Watari","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kiron 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