{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,1]],"date-time":"2026-09-01T18:08:07Z","timestamp":1788286087327,"version":"build-2803163510"},"reference-count":43,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2002,12,6]],"date-time":"2002-12-06T00:00:00Z","timestamp":1039132800000},"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":[[2003,3]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Infection with <jats:italic>Helicobacter pylori (H. pylori),<\/jats:italic> especially CagA+ strains, has been associated with an increased risk of noncardia gastric adenocarcinoma. The relationship with junctional cancer (adenocarcinomas of the esophagus and gastric cardia combined) has not been adequately investigated, although some studies have reported a reduced risk associated with <jats:italic>H. pylori<\/jats:italic> and CagA seroseropositivity. We investigated this question in a subset of cases and controls from a recently completed, large population\u2010based case\u2010control study of gastric and esophageal adenocarcinomas in Los Angeles County. Using established antigen\u2010specific ELISAs, serum IgG antibodies to <jats:italic>H. pylori<\/jats:italic> whole\u2010cell antigens (Helico\u2010G) and CagA were measured in population controls (<jats:italic>n<\/jats:italic> = 356) and patients with incident esophageal adenocarcinoma (<jats:italic>n<\/jats:italic> = 80), gastric cardia cancer (<jats:italic>n<\/jats:italic> = 87) or distal gastric cancers (noncardia gastric adenocarcinoma) (<jats:italic>n<\/jats:italic> = 127). After controlling for demographic characteristics (age, gender, race, birthplace, education), smoking and body mass index, seropositivity for <jats:italic>H. pylori<\/jats:italic> was associated with a statistically significant increased risk of distal gastric cancer (adjusted odds ratio [OR] = 1.85, 95% confidence interval [CI] = 1.03, 3.32) but the risk of junctional cancer was not increased (adjusted OR = 1.26, 95% CI = 0.82, 1.94). The risk of junctional cancer was not changed when CagA and <jats:italic>H. pylori<\/jats:italic> were both considered, but the risk of distal gastric cancer was further increased. Subjects who were seropositive for both CagA and <jats:italic>H. pylori<\/jats:italic> compared to those who were seronegative for <jats:italic>H. pylori<\/jats:italic> showed a risk of 2.20 (95% CI = 1.13, 4.26) for distal gastric cancer and 0.86 (95% CI = 0.47, 1.59) for junctional cancer. Although tests for interaction between smoking and <jats:italic>H. pylori<\/jats:italic> were not statistically significant for junctional or distal gastric cancers, risk for both tumor types tended to be higher among current smokers who were also <jats:italic>H. pylori<\/jats:italic> seropositive. In conclusion, we find no evidence that infection with CagA+ strains of <jats:italic>H. pylori<\/jats:italic> reduces risk of esophageal and gastric cardia adenocarcinoma in this population. Our findings confirm the positive association between risk of distal gastric cancer and infection with <jats:italic>H. pylori<\/jats:italic> infection, especially CagA+ strains. \u00a9 2002 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/ijc.10887","type":"journal-article","created":{"date-parts":[[2003,1,7]],"date-time":"2003-01-07T21:16:01Z","timestamp":1041974161000},"page":"815-821","source":"Crossref","is-referenced-by-count":128,"title":["Role of <i>Helicobacter pylori<\/i> CagA+ strains and risk of adenocarcinoma of the stomach and esophagus"],"prefix":"10.1002","volume":"103","author":[{"given":"Anna H.","family":"Wu","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jean 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