{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,17]],"date-time":"2026-10-17T18:06:45Z","timestamp":1792260405077,"version":"4.4.0"},"reference-count":57,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2019,8,29]],"date-time":"2019-08-29T00:00:00Z","timestamp":1567036800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Intl Journal of Cancer"],"published-print":{"date-parts":[[2020,5,15]]},"abstract":"<jats:p>\n                    <jats:italic>Helicobacter pylori<\/jats:italic>\n                    (\n                    <jats:italic>H. pylori<\/jats:italic>\n                    ) infection is considered as principal cause of gastric cancer. It is further associated with a reduced risk of esophageal adenocarcinomas. In a large prospective population\u2010based cohort study including 9,949 subjects with average observation time of 13.8 years, we assessed the risk of invasive gastric and esophageal cancer according to\n                    <jats:italic>H. pylori<\/jats:italic>\n                    infection and presence of chronic atrophic gastritis (CAG). Incidence rates and hazard ratios (HR) derived by Cox proportional hazards models and adjusted for relevant confounders were derived by seroprevalence of\n                    <jats:italic>H. pylori<\/jats:italic>\n                    and cytotoxin\u2010associated gene A (CagA) antibodies and presence of CAG based on serological markers at baseline, respectively. During follow\u2010up, 30 cases of noncardia gastric cancer and 33 cases of esophageal cancer were observed. Infection by\n                    <jats:italic>H. pylori<\/jats:italic>\n                    without and with expression of CagA was associated with a 5.2\u2010fold (95% confidence interval 1.00\u201327.1) and an 18.2\u2010fold (4.3\u201377.4) increase of noncardia gastric cancer incidence. A 0.65\u2010fold decreased risk of esophageal adenocarcinomas (HR 0.35, 0.12\u20130.97) was observed among\n                    <jats:italic>H. pylori<\/jats:italic>\n                    \u2010infected individuals. In participants infected with CagA expressed\n                    <jats:italic>H. pylori<\/jats:italic>\n                    , the presence of mild\/moderate and severe CAG was associated with a 6.4\u2010fold (1.3\u201331.0) and an 11.8\u2010fold (3.1\u201345.4) increase of gastric cancer incidence, respectively. The results of this prospective population\u2010based cohort study may contribute relevant evidence to the ongoing research of\n                    <jats:italic>H. pylori<\/jats:italic>\n                    \u2010related cancers. The results may furthermore enhance the empirical basis for risk stratification among\n                    <jats:italic>H. pylori<\/jats:italic>\n                    \u2010infected people and for recommendations regarding\n                    <jats:italic>H. pylori<\/jats:italic>\n                    screening and treatment among older adults in a Western population.\n                  <\/jats:p>","DOI":"10.1002\/ijc.32610","type":"journal-article","created":{"date-parts":[[2019,8,3]],"date-time":"2019-08-03T08:08:05Z","timestamp":1564819685000},"page":"2773-2783","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":78,"title":["<i>Helicobacter pylori<\/i>\n                    infection, chronic atrophic gastritis and risk of stomach and esophagus cancer: Results from the prospective population\u2010based ESTHER cohort 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