{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,14]],"date-time":"2026-07-14T02:37:56Z","timestamp":1783996676512,"version":"3.55.0"},"reference-count":27,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2008,10,10]],"date-time":"2008-10-10T00:00:00Z","timestamp":1223596800000},"content-version":"vor","delay-in-days":2415,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J of Gastro and Hepatol"],"published-print":{"date-parts":[[2002,3]]},"abstract":"<jats:sec><jats:title>Abstract<\/jats:title><\/jats:sec><jats:sec><jats:title>Background and Aim:<\/jats:title><jats:p>Debate that <jats:italic>Helicobacter pylori<\/jats:italic> might play a causative role in gastric carcinogenesis still exists in spite of the World\n Health Organization\u2019s definition of <jats:italic>H. pylori<\/jats:italic> as a class I carcinogen.\n In order to define the exact role of <jats:italic>H. pylori<\/jats:italic> infection in gastric carcinogenesis,\n we established a mice model of <jats:italic>H. pylori<\/jats:italic> infection.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods:<\/jats:title><jats:p>One hundred and forty\u2010four female C57BL\/6 mice were divided into nine groups according to <jats:italic>N<\/jats:italic>\u2010methyl\u2010<jats:italic>N<\/jats:italic>\u2010nitrosourea (MNU) treatment\n and <jats:italic>H. pylori<\/jats:italic> infection. All mice were killed at the 50th or 80th week after treatment, and their histopathological changes were evaluated according to group.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results:<\/jats:title><jats:p>The incidence of gastric adenocarcinoma at the 50th week was 80% in mice treated with both MNU 240 \u03bcg\/L and <jats:italic>H. pylori<\/jats:italic> infection,\n whereas the incidence was only 27% in mice treated with only MNU 240 \u03bcg\/L.\n Although <jats:italic>H. pylori<\/jats:italic> caused marked expansion of the proliferative zone at the\n surface epithelium, <jats:italic>H. pylori<\/jats:italic> infection alone caused only chronic atrophic\n gastritis without any evidence of carcinomas until 80 weeks. The combination of MNU\n and <jats:italic>H. pylori<\/jats:italic> infection also resulted in a significantly higher incidence\n of gastric adenoma and adenocarcinoma. Significantly higher expressions of proliferating\n cell nuclear antigen were noted in the gastric mucosa infected with <jats:italic>H. pylori<\/jats:italic> compared to controls.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions:<\/jats:title><jats:p>These results clearly demonstrated the role of <jats:italic>H. pylori<\/jats:italic> infection, rather than direct carcinogens, in promoting gastric carcinogenesis in a mice model.<\/jats:p><jats:p>\u00a9 2002 Blackwell Science Asia Pty Ltd<\/jats:p><\/jats:sec>","DOI":"10.1046\/j.1440-1746.2002.02684.x","type":"journal-article","created":{"date-parts":[[2003,3,12]],"date-time":"2003-03-12T05:21:57Z","timestamp":1047446517000},"page":"253-261","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":61,"title":["<i>Helicobacter pylori<\/i> infection promotes gastric carcinogenesis in a mice model"],"prefix":"10.1111","volume":"17","author":[{"given":"SANG\u2010UK","family":"HAN","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"YOUNG\u2010BAE","family":"KIM","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"HEE\u2010JAE","family":"JOO","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"KI\u2010BAIK","family":"HAHM","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"WON\u2010HEUNG","family":"LEE","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"YONG\u2010KWAN","family":"CHO","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"DAE\u2010YONG","family":"KIM","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"MYUNG\u2010WOOK","family":"KIM","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2008,10,10]]},"reference":[{"key":"e_1_2_6_2_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199110173251603"},{"key":"e_1_2_6_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/0016-5085(93)90954-B"},{"key":"e_1_2_6_4_2","first-page":"16","article-title":"Helicobacter pylori and gastric cancer: what is the real risk?","volume":"6","author":"Crespi M","year":"1998","journal-title":"Gastroenterologist"},{"key":"e_1_2_6_5_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1746.1997.tb00391.x"},{"key":"e_1_2_6_6_2","doi-asserted-by":"publisher","DOI":"10.3109\/00365529609036884"},{"key":"e_1_2_6_7_2","first-page":"4255","article-title":"Development of Helicobacter pylori\u2010induced gastric carcinoma in Mongolian\n Gerbils.","volume":"58","author":"Honda S","year":"1998","journal-title":"Cancer Res."},{"key":"e_1_2_6_8_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0016-5085(98)70143-X"},{"key":"e_1_2_6_9_2","doi-asserted-by":"publisher","DOI":"10.1093\/carcin\/20.4.669"},{"key":"e_1_2_6_10_2","first-page":"2067","article-title":"Helicobacter pylori infection enhances N\u2010methyl\u2010N\u2010nitrosourea\u2010induced\n stomach carcinogenesis in the Mongolian gerbil.","volume":"58","author":"Sugiyama A","year":"1998","journal-title":"Cancer Res."},{"key":"e_1_2_6_11_2","doi-asserted-by":"publisher","DOI":"10.1093\/carcin\/20.7.1261"},{"key":"e_1_2_6_12_2","first-page":"645","article-title":"The pathology of the Mongolian Gerbil (Meriones unguiculatus): a review.","volume":"29","author":"Vincent AL","year":"1979","journal-title":"Lab. 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IARC working group on the evaluation of carcinogenic risks to humans.","volume":"61","author":"International Agency for Research on Cancer.","year":"1994","journal-title":"Monogr. Eval. Carcinog. 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