{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,21]],"date-time":"2026-09-21T23:48:36Z","timestamp":1790034516553,"version":"4.0.1"},"reference-count":30,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2001,11,8]],"date-time":"2001-11-08T00:00:00Z","timestamp":1005177600000},"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":[[2002,2,10]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Mutations of an oncogene, K\u2010<jats:italic>ras<\/jats:italic>, are associated with the development and progression of many types of human cancer. To elucidate the significance of K\u2010<jats:italic>ras<\/jats:italic> mutations in gastric carcinogenesis, we examined K\u2010<jats:italic>ras<\/jats:italic> mutations in gastric cancers and in <jats:italic>Helicobacter pylori<\/jats:italic>\u2010associated chronic gastritis (<jats:italic>H. pylori<\/jats:italic><jats:italic>\u2010<\/jats:italic>CG), which is associated with an increased risk for the gastric cancer development. Specimens of gastric cancer and <jats:italic>H. pylori<\/jats:italic><jats:italic>\u2010<\/jats:italic>CG were obtained from 64 gastric cancer patients with <jats:italic>H. pylori<\/jats:italic>\u2010CG, 99 cancer\u2010free <jats:italic>H. pylori<\/jats:italic>\u2010CG patients and 30 <jats:italic>H. pylori<\/jats:italic>\u2010negative healthy subjects. K\u2010<jats:italic>ras<\/jats:italic> mutations were examined by polymerase chain reaction\u2010single strand conformation polymorphism (PCR\u2010SSCP), followed by DNA sequencing analysis. K\u2010<jats:italic>ras<\/jats:italic> mutations were detected in 4 of 48 (8.3%) gastric cancers, in 10 of 163 (6.1%) <jats:italic>H. pylori<\/jats:italic>\u2010CG and none of the 30 <jats:italic>H. pylori<\/jats:italic>\u2010negative healthy subjects. In the gastric cancer patients, mutated K\u2010<jats:italic>ras<\/jats:italic> was detected in differentiated type cancers but not in any of the undifferentiated type cancers. K\u2010<jats:italic>ras<\/jats:italic> mutations in <jats:italic>H. pylori<\/jats:italic>\u2010CG were significantly more frequent in gastric cancer patients than in cancer\u2010free patients (10.9% <jats:italic>vs.<\/jats:italic> 3.0%, <jats:italic>p<\/jats:italic> = 0.044). In addition, K\u2010<jats:italic>ras<\/jats:italic> mutations in <jats:italic>H. pylori<\/jats:italic>\u2010CG were significantly more frequent in patients with K\u2010<jats:italic>ras<\/jats:italic> mutated gastric cancer than in patients with K\u2010<jats:italic>ras<\/jats:italic> unmutated gastric cancer (50.0% <jats:italic>vs.<\/jats:italic> 3.7%, <jats:italic>p<\/jats:italic> = 0.037). These data suggest that the genetic mechanism(s) of carcinogenesis differs between the differentiated type and the undifferentiated type of gastric cancer and that K\u2010<jats:italic>ras<\/jats:italic> mutations may be involved in the early stages of gastric carcinogenesis of the differentiated type. \u00a9 2001 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/ijc.1644","type":"journal-article","created":{"date-parts":[[2004,11,9]],"date-time":"2004-11-09T08:36:08Z","timestamp":1099989368000},"page":"562-566","source":"Crossref","is-referenced-by-count":57,"title":["K\u2010<i>ras<\/i> mutation in <i>h<\/i><i>elicobacter pylori<\/i>\u2010associated chronic gastritis in patients with and without gastric cancer"],"prefix":"10.1002","volume":"97","author":[{"given":"Toru","family":"Hiyama","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ken","family":"Haruma","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yasuhiko","family":"Kitadai","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hiroshi","family":"Masuda","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Masaki","family":"Miyamoto","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shinji","family":"Tanaka","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Masaharu","family":"Yoshihara","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fumio","family":"Shimamoto","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kazuaki","family":"Chayama","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2001,11,8]]},"reference":[{"key":"e_1_2_5_2_2","first-page":"1731","article-title":"Detection of K\u2010ras mutations by denaturing gradient gel electrophoresis (DGGE): a study on pancreatic cancer","volume":"12","author":"Pellegata NS","year":"1992","journal-title":"Anticancer Res"},{"key":"e_1_2_5_3_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1349-7006.1993.tb00148.x"},{"key":"e_1_2_5_4_2","doi-asserted-by":"publisher","DOI":"10.1002\/1097-0142(19950615)75:12<2794::AID-CNCR2820751203>3.0.CO;2-F"},{"key":"e_1_2_5_5_2","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1096-9896(1998100)186:2<131::AID-PATH158>3.0.CO;2-1"},{"key":"e_1_2_5_6_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0016-5085(00)70357-X"},{"key":"e_1_2_5_7_2","doi-asserted-by":"publisher","DOI":"10.1038\/304507a0"},{"key":"e_1_2_5_8_2","doi-asserted-by":"publisher","DOI":"10.3322\/canjclin.48.1.6"},{"key":"e_1_2_5_9_2","doi-asserted-by":"publisher","DOI":"10.1016\/0016-5085(90)90019-W"},{"key":"e_1_2_5_10_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1349-7006.1993.tb02850.x"},{"key":"e_1_2_5_11_2","first-page":"6735","article-title":"Human gastric carcinogenesis: a multistep and multifactorial process. 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