{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,11,3]],"date-time":"2025-11-03T09:01:49Z","timestamp":1762160509313,"version":"3.44.0"},"reference-count":35,"publisher":"BMJ","issue":"12","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J Clin Pathol"],"published-print":{"date-parts":[[2006,12]]},"abstract":"<jats:p>\n                  <jats:bold>Background:<\/jats:bold> The cadherin\u2013catenin complex is the key component of the adherens junction in epithelial cells, and changes in this complex are implicated in gastric adenocarcinoma. Germline mutations in E-cadherin have been described in diffuse-type gastric adenocarcinoma. <jats:italic>Helicobacter pylori<\/jats:italic> infection is the first stage in gastric carcinogenesis.<\/jats:p>\n               <jats:p>\n                  <jats:bold>Aims:<\/jats:bold> To determine whether <jats:italic>H pylori<\/jats:italic> was associated with changes in the complex, and whether this was affected by virulence of the strain.<\/jats:p>\n               <jats:p>\n                  <jats:bold>Methods:<\/jats:bold> Epithelial cell lines were cultured with <jats:italic>H pylori<\/jats:italic> using the wild-type pathogenic and non-pathogenic strains and <jats:italic>CagE<\/jats:italic> null and <jats:italic>VacA<\/jats:italic> null isogenic mutants. Gastric biopsy specimens at endoscopy were obtained from patients with (n\u200a=\u200a17) and without (n\u200a=\u200a15) <jats:italic>H pylori<\/jats:italic> infection, and E-cadherin and \u03b2\u2013catenin expression was assessed by immunohistochemistry. <jats:italic>H pylori<\/jats:italic> was typed by polymerase chain reaction from these patients for <jats:italic>CagE<\/jats:italic> and <jats:italic>VacA<\/jats:italic>.<\/jats:p>\n               <jats:p>\n                  <jats:bold>Results:<\/jats:bold> In vitro studies showed that coculture with a pathogenic strain of <jats:italic>H pylori<\/jats:italic> led to disruption of epithelial junctional \u03b2-catenin expression, but without evidence of nuclear translocation or signalling. This effect was independent of a functional <jats:italic>Cag<\/jats:italic> pathogenicity island and vacuolating activity, but dependent on live bacteria. No marked differences in \u03b2-catenin or E-cadherin expression were seen in gastric biopsy specimens in patients with and without <jats:italic>H pylori<\/jats:italic> infection.<\/jats:p>\n               <jats:p>\n                  <jats:bold>Conclusion:<\/jats:bold> Acute <jats:italic>H pylori<\/jats:italic> infection disrupts junctional \u03b2-catenin in vitro, but chronic infection by <jats:italic>H pylori<\/jats:italic> has no effect on E-cadherin and \u03b2-catenin expression, as seen in gastric biopsy specimens at the initial gastritis stage of the proposed Correa pathway of gastric carcinogenesis. A later effect at the later stages of atrophy or intestinal metaplasia cannot be ruled out.<\/jats:p>","DOI":"10.1136\/jcp.2006.036772","type":"journal-article","created":{"date-parts":[[2006,5,5]],"date-time":"2006-05-05T20:32:00Z","timestamp":1146861120000},"page":"1261-1266","source":"Crossref","is-referenced-by-count":28,"title":["Effects of <i>Helicobacter pylori<\/i> on the cadherin\u2013catenin complex"],"prefix":"10.1136","volume":"59","author":[{"given":"J R","family":"Bebb","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"L","family":"Leach","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"A","family":"Zaitoun","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"N","family":"Hand","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"D 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