{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,11]],"date-time":"2026-02-11T15:12:15Z","timestamp":1770822735241,"version":"3.50.1"},"reference-count":0,"publisher":"Hindawi Limited","issue":"3","license":[{"start":{"date-parts":[[1999,1,1]],"date-time":"1999-01-01T00:00:00Z","timestamp":915148800000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Canadian Journal of Gastroenterology"],"published-print":{"date-parts":[[1999]]},"abstract":"<jats:p>The pathology of gastritis associated with<jats:italic>Helicobacter pylori<\/jats:italic>infection is summarized. The literature is reviewed regarding the role of<jats:italic>H pylori<\/jats:italic>in the pathogenesis of gastric carcinoma and mucosa-associated lymphoid tissue (MALT) lymphoma. The potential mechanisms of gastric carcinogenesis include transformation of the gastric mucosa by metabolic products of<jats:italic>H pylori<\/jats:italic>, transformation of the host cell by incorporation of<jats:italic>H pylori<\/jats:italic>DNA and genotoxic effects of the inflammatory response to the organism. A model for gastric carcinogenesis is proposed in which<jats:italic>H pylori<\/jats:italic>causes cell proliferation, and the risk of DNA damage is increased, leading to inadequate repair and malignant transformation. Investigation of early gastric carcinomas concluded that two main pathways operated in gastric carcinogenesis, both starting from<jats:italic>H pylori<\/jats:italic>gastritis and leading to phenotypically variable gastric or intestinal tumour growth. The histological features and molecular genetics of MALT lymphoma are briefly reviewed. There is evidence that tumour cells of low grade B cell MALT lymphoma proliferate specifically in response to<jats:italic>H pylori<\/jats:italic>. This response is dependent on T cell activation by<jats:italic>H pylori<\/jats:italic>. A proposed model for the pathogenesis of MALT lymphoma postulates that B lymphocytes with a genetic change acquire a growth advantage resulting in a monoclonal proliferation in response to<jats:italic>H pylori<\/jats:italic>-activated T cells. Further genetic changes may result in escape from T cell dependency.<\/jats:p>","DOI":"10.1155\/1999\/487098","type":"journal-article","created":{"date-parts":[[2016,3,28]],"date-time":"2016-03-28T21:01:22Z","timestamp":1459198882000},"page":"224-227","source":"Crossref","is-referenced-by-count":9,"title":["Role of<i>Helicobacter pylori<\/i>in the Pathogenesis of Gastric Carcinoma and Progression of Lymphoid Nodules to Lymphoma"],"prefix":"10.1155","volume":"13","author":[{"given":"M","family":"Guindi","sequence":"first","affiliation":[{"name":"Department of Laboratory Medicine, Ottawa Hospital, Civic Site, Ottawa, Ontario, Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"98","container-title":["Canadian Journal of Gastroenterology"],"original-title":[],"language":"en","link":[{"URL":"http:\/\/downloads.hindawi.com\/journals\/cjgh\/1999\/487098.pdf","content-type":"application\/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"http:\/\/downloads.hindawi.com\/journals\/cjgh\/1999\/487098.pdf","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2016,8,23]],"date-time":"2016-08-23T09:42:12Z","timestamp":1471945332000},"score":1,"resource":{"primary":{"URL":"http:\/\/www.hindawi.com\/journals\/cjgh\/1999\/487098\/abs\/"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1999]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1999]]}},"alternative-id":["487098"],"URL":"https:\/\/doi.org\/10.1155\/1999\/487098","relation":{},"ISSN":["0835-7900"],"issn-type":[{"value":"0835-7900","type":"print"}],"subject":[],"published":{"date-parts":[[1999]]}}}