{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T11:08:03Z","timestamp":1791198483606,"version":"4.1.0"},"reference-count":25,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2011,3,3]],"date-time":"2011-03-03T00:00:00Z","timestamp":1299110400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Molecular Carcinogenesis"],"published-print":{"date-parts":[[2011,10]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>We tested whether <jats:italic>cagL<\/jats:italic> amino acid sequence polymorphisms of <jats:italic>Helicobacter pylori<\/jats:italic> correlated to clinico\u2010histological outcomes and gastric \u03b15\u03b21 integrin expressions. One hundred forty five patients with <jats:italic>H. pylori<\/jats:italic> infection and 47 noninfected controls were enrolled to check gastric integrin \u03b15\u03b21 intensities topographically. The collected isolates were screened for <jats:italic>cagL<\/jats:italic>\u2010genotype by polymerase chain reaction (PCR), and assessed for amino acid sequence polymorphisms using sequence translation. Our <jats:italic>H. pylori<\/jats:italic> isolates were predominantly (98.6%) <jats:italic>cagL<\/jats:italic>\u2010genopositive, 95.8% of which had the RGD motif in their amino acid sequences. The isolates from the gastric cancer (GCA) patients indicated a higher rate of amino acid sequence polymorphisms\u2014Y58 and E59\u2014than those of the non\u2010GCA patients (<jats:italic>P<\/jats:italic>\u2009&lt;\u20090.05). The polymorphisms as Y58E59 noted with increased risk of GCA up to 4.6\u2010fold (95%CI: 1.8\u201311.9). <jats:italic>H. pylori<\/jats:italic>\u2010infected patients had higher integrin \u03b15\u03b21 than noninfected patients (<jats:italic>P<\/jats:italic>\u2009&lt;\u20090.05). Furthermore, <jats:italic>cagL<\/jats:italic>\u2010Y58E59 <jats:italic>H. pylori<\/jats:italic> infection predisposed an upward shift in integrin \u03b15\u03b21 (<jats:italic>P<\/jats:italic>\u2009=\u20090.007) in the corpus, leading to more severe corpus chronic inflammation (<jats:italic>P<\/jats:italic>\u2009&lt;\u20090.05). <jats:italic>H. pylori<\/jats:italic> CagL amino acid polymorphisms like Y58E59 correlate with a higher risk of GCA, and may regulate a corpus shift of gastric integrin \u03b15\u03b21 to lead to severe corpus gastritis during gastric carcinogenesis. Mol. Carcinog. \u00a9 2011 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/mc.20753","type":"journal-article","created":{"date-parts":[[2011,3,3]],"date-time":"2011-03-03T21:22:20Z","timestamp":1299187340000},"page":"751-759","source":"Crossref","is-referenced-by-count":44,"title":["<i>H. pylori cagL<\/i> amino acid sequence polymorphism Y58E59 induces a corpus shift of gastric integrin \u03b15\u03b21 related with gastric carcinogenesis"],"prefix":"10.1002","volume":"50","author":[{"given":"Yi\u2010Chun","family":"Yeh","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wei\u2010Lun","family":"Chang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hsiao\u2010Bai","family":"Yang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hsiu\u2010Chi","family":"Cheng","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jiunn\u2010Jung","family":"Wu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bor\u2010Shyang","family":"Sheu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2011,3,3]]},"reference":[{"key":"e_1_2_7_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0016-5085(99)70575-5"},{"key":"e_1_2_7_3_2","doi-asserted-by":"publisher","DOI":"10.1136\/gut.2006.101634"},{"key":"e_1_2_7_4_2","first-page":"1903","article-title":"Key importance of the Helicobacter pylori adherence factor blood group antigen binding adhesin during chronic gastric inflammation","volume":"61","author":"Prinz C","year":"2001","journal-title":"Cancer Res"},{"key":"e_1_2_7_5_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.96.22.12778"},{"key":"e_1_2_7_6_2","doi-asserted-by":"publisher","DOI":"10.1128\/JCM.39.7.2463-2465.2001"},{"key":"e_1_2_7_7_2","first-page":"1316","article-title":"Genetic analysis of the cytotoxin\u2010associated gene and the vacuolating toxin gene in Helicobacter pylori strains isolated from Taiwanese patients","volume":"92","author":"Yang JC","year":"1997","journal-title":"Am J Gastroenterol"},{"key":"e_1_2_7_8_2","doi-asserted-by":"publisher","DOI":"10.1136\/gut.52.7.927"},{"key":"e_1_2_7_9_2","first-page":"18","article-title":"The Presence of iceA1 but not cagA, cagC, cagE, cagF, cagN, cagT, or orf13 genes of Helicobacter pylori is associated with more severe gastric inflammation in 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