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Unless treated,\n                    <jats:italic>H. pylori<\/jats:italic>\n                    causes life-long acute and chronic gastric inflammation resulting in progressive gastric mucosal damage that may result in gastric cancer. The rate of progression from superficial gastritis, to an atrophic metaplastic mucosa, and ultimately to cancer relates to the virulence of the infecting\n                    <jats:italic>H. pylori<\/jats:italic>\n                    as well as host and environmental factors.\n                    <jats:italic>H. pylori<\/jats:italic>\n                    virulence is a reflection of its propensity to cause severe gastric inflammation. Both mucosal inflammation and\n                    <jats:italic>H. pylori<\/jats:italic>\n                    can cause host genomic instability, including dysregulation of DNA mismatch repair, stimulation of expression of activation-induced cytidine deaminase, abnormal DNA methylation and dysregulation of \u00a0micro RNAs, which may result in an accumulation of mutations and loss of normal regulation of cell growth. The difference in cancer risk between the most and least virulent\n                    <jats:italic>H. pylori<\/jats:italic>\n                    strain is only approximately 2-fold. Overall, none of the putative virulence factors identified to date have proved to be disease-specific. The presence, severity, extent and duration of inflammation appear to be the most important factors and current evidence suggests that any host, environmental or bacterial factor that reliably enhances the inflammatory response to the\n                    <jats:italic>H. pylori<\/jats:italic>\n                    infection increases the risk of gastric cancer.\n                  <\/jats:p>","DOI":"10.1017\/erm.2017.4","type":"journal-article","created":{"date-parts":[[2017,3,21]],"date-time":"2017-03-21T05:11:45Z","timestamp":1490073105000},"source":"Crossref","is-referenced-by-count":71,"title":["<i>Helicobacter pylori<\/i>\n                    as an oncogenic pathogen, revisited"],"prefix":"10.1017","volume":"19","author":[{"given":"Muhammad","family":"Miftahussurur","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yoshio","family":"Yamaoka","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David Y.","family":"Graham","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"56","published-online":{"date-parts":[[2017,3,21]]},"reference":[{"key":"S1462399417000047_ref37","doi-asserted-by":"publisher","DOI":"10.1111\/j.1349-7006.2004.tb02196.x"},{"key":"S1462399417000047_ref2","doi-asserted-by":"publisher","DOI":"10.3748\/wjg.v20.i18.5191"},{"key":"S1462399417000047_ref4","doi-asserted-by":"publisher","DOI":"10.1136\/gut.50.4.568"},{"key":"S1462399417000047_ref113","doi-asserted-by":"publisher","DOI":"10.1099\/00222615-25-4-253"},{"key":"S1462399417000047_ref104","doi-asserted-by":"publisher","DOI":"10.1007\/s00535-013-0808-z"},{"key":"S1462399417000047_ref117","doi-asserted-by":"publisher","DOI":"10.1016\/j.gie.2006.03.013"},{"key":"S1462399417000047_ref112","doi-asserted-by":"crossref","first-page":"1331","DOI":"10.7326\/0003-4819-34-6-1331","article-title":"Gastric acidity before and after development of gastric cancer: its etiologic, diagnostic and prognostic significance","volume":"34","author":"Comfort","year":"1951","journal-title":"Annals of Internal Medicine"},{"key":"S1462399417000047_ref111","doi-asserted-by":"publisher","DOI":"10.1111\/hel.12146"},{"key":"S1462399417000047_ref105","doi-asserted-by":"publisher","DOI":"10.1007\/s10620-011-1916-3"},{"key":"S1462399417000047_ref116","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.01271-12"},{"key":"S1462399417000047_ref6","unstructured":"IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, Schistosomes, Liver Flukes and Helicobacter pylori (1994) Infection with Helicobacter pylori. 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