{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,11]],"date-time":"2026-06-11T00:13:27Z","timestamp":1781136807621,"version":"3.54.1"},"reference-count":46,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2015,1,12]],"date-time":"2015-01-12T00:00:00Z","timestamp":1421020800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Helicobacter"],"published-print":{"date-parts":[[2015,4]]},"abstract":"<jats:sec><jats:title>Background<\/jats:title><jats:p>Patients with duodenal ulcer have a reduced risk of developing gastric cancer compared to those without. Recently, the <jats:italic>prostate stem cell antigen<\/jats:italic> (<jats:italic><jats:styled-content style=\"fixed-case\">PSCA<\/jats:styled-content><\/jats:italic>) rs2294008 C&gt;T polymorphism was found to be associated with different pathogenesis of duodenal ulcer and gastric cancer developments. However, whether <jats:italic><jats:styled-content style=\"fixed-case\">PSCA<\/jats:styled-content><\/jats:italic> rs2294008 C&gt;T polymorphism is associated with severity of gastric mucosal atrophy is unclear. We examined the influence of the <jats:italic><jats:styled-content style=\"fixed-case\">PSCA<\/jats:styled-content><\/jats:italic> rs2294008 C&gt;T polymorphism on susceptibility to <jats:italic>H.\u00a0pylori\u2010<\/jats:italic>related diseases and the relationships between <jats:italic><jats:styled-content style=\"fixed-case\">PSCA<\/jats:styled-content><\/jats:italic> polymorphism and gastric mucosal atrophy.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p><jats:italic><jats:styled-content style=\"fixed-case\">PSCA<\/jats:styled-content><\/jats:italic> rs2294008 C&gt;T polymorphism was assessed in <jats:italic>H.\u00a0pylori<\/jats:italic>\u2010positive Japanese patients (n\u00a0=\u00a0488) with noncardia gastric cancer (n\u00a0=\u00a0193), gastric ulcer (n\u00a0=\u00a084), duodenal ulcer (n\u00a0=\u00a061), and atrophic gastritis (n\u00a0=\u00a0150), as well as in <jats:italic>H.\u00a0pylori<\/jats:italic>\u2010negatives (n\u00a0=\u00a0266).<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Frequency of <jats:italic><jats:styled-content style=\"fixed-case\">PSCA<\/jats:styled-content><\/jats:italic> rs2294008 C\/C genotype in duodenal ulcer was 36.1%, which was significantly higher than those with gastric cancer (12.4%), gastric ulcer (19.0%), gastritis (10.7%), and <jats:italic>H.\u00a0pylori<\/jats:italic>\u2010negatives (19.5%) (<jats:italic>p<\/jats:italic>\u00a0&lt;\u00a0.001). Compared with duodenal ulcer, having the T allele significantly increased the risk of gastric cancer (<jats:styled-content style=\"fixed-case\">OR<\/jats:styled-content>: 3.97, 95% <jats:styled-content style=\"fixed-case\">CI<\/jats:styled-content>: 2.02\u20137.80; <jats:italic>p<\/jats:italic>\u00a0&lt;\u00a0.001), gastric ulcer (2.40, 1.13\u20135.10; <jats:italic>p<\/jats:italic>\u00a0=\u00a0.023), and gastritis (4.72, 2.26\u20139.86; <jats:italic>p<\/jats:italic>\u00a0&lt;\u00a0.001). Mean pepsinogen (<jats:styled-content style=\"fixed-case\">PG<\/jats:styled-content>) I\/<jats:styled-content style=\"fixed-case\">PG II<\/jats:styled-content> ratio in T allele carriers (2.17\u00a0\u00b1\u00a00.75) was significantly lower than that in C\/C genotype (3.39\u00a0\u00b1\u00a01.27, <jats:italic>p\u00a0<\/jats:italic>&lt;\u00a0.001).<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>The <jats:italic><jats:styled-content style=\"fixed-case\">PSCA<\/jats:styled-content><\/jats:italic> rs2294008 C&gt;T polymorphism is associated with differing susceptibilities to <jats:italic>H.\u00a0pylori<\/jats:italic>\u2010associated diseases. The <jats:italic><jats:styled-content style=\"fixed-case\">PSCA<\/jats:styled-content><\/jats:italic> rs2294008 C&gt;T polymorphism may be acting through induction of gastric mucosal atrophy, finally leading to development of gastric ulcer and gastric cancer in <jats:italic><jats:styled-content style=\"fixed-case\">PSCA<\/jats:styled-content><\/jats:italic> rs2294008 T allele carriers, but not duodenal ulcer.<\/jats:p><\/jats:sec>","DOI":"10.1111\/hel.12183","type":"journal-article","created":{"date-parts":[[2015,1,13]],"date-time":"2015-01-13T01:42:59Z","timestamp":1421113379000},"page":"106-113","source":"Crossref","is-referenced-by-count":14,"title":["Influence of Prostate Stem Cell Antigen Gene Polymorphisms on Susceptibility to <i>Helicobacter pylori<\/i>\u2010associated Diseases: A Case\u2010control Study"],"prefix":"10.1111","volume":"20","author":[{"given":"Hitomi","family":"Ichikawa","sequence":"first","affiliation":[{"name":"First Department of Medicine Hamamatsu University 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