{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,10]],"date-time":"2026-03-10T13:39:39Z","timestamp":1773149979199,"version":"3.50.1"},"reference-count":41,"publisher":"BMJ","issue":"8","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J Clin Pathol"],"published-print":{"date-parts":[[2007,8]]},"abstract":"<jats:p>\n                  <jats:bold>Background:<\/jats:bold>\n                  <jats:italic>Helicobacter pylori<\/jats:italic> related gastric intestinal metaplasia (IM) is considered to be a precancerous lesion.<\/jats:p>\n               <jats:p>\n                  <jats:bold>Aims:<\/jats:bold> To identify the effects of <jats:italic>H pylori<\/jats:italic> eradication on K-<jats:italic>ras<\/jats:italic> mutations, cell kinetics in IM and histological changes in patients with and without gastric cancers in a one-year prospective study.<\/jats:p>\n               <jats:p>\n                  <jats:bold>Methods:<\/jats:bold> Patients included group A (n\u200a=\u200a39), chronic gastritis, and group B (n\u200a=\u200a53), intestinal-type early gastric cancer patients who had all undergone endoscopic mucosal resection (n\u200a=\u200a25) or surgical resection (n\u200a=\u200a28). K-<jats:italic>ras<\/jats:italic> codon 12 mutations in IM were examined, followed by DNA sequencing analysis. Proliferating and apoptotic cells were detected with anti-Ki-67 antibody and using the TUNEL method, respectively.<\/jats:p>\n               <jats:p>\n                  <jats:bold>Results:<\/jats:bold> The incidence of K-<jats:italic>ras<\/jats:italic> mutations in the cancer was only 3.8%. The mutant K-<jats:italic>ras<\/jats:italic> in IM was observed more frequently in group A (46.2%) than in group B patients (1.9%) (p&lt;0.005). After eradication, the K-<jats:italic>ras<\/jats:italic> mutations significantly declined to 12.8% in group A (p&lt;0.005). The mutation pattern of K-<jats:italic>ras<\/jats:italic> codon 12 before eradication was that GGT was mainly changed to AGT (50%) in group A. AGT transformation was not affected by treatment. Apoptosis in IM showed an increase after <jats:italic>H pylori<\/jats:italic> eradication in both groups (p&lt;0.05 in group A) although no histological improvement in IM was observed. The monocyte score was significantly higher in group A than in group B (p&lt;0.05); the score improved significantly after eradication.<\/jats:p>\n               <jats:p>\n                  <jats:bold>Conclusions:<\/jats:bold> K-<jats:italic>ras<\/jats:italic> mutations in IM do not always play a role in gastric carcinogenesis but cell kinetics, especially apoptosis, in IM may contribute to it. There are early events in K-<jats:italic>ras<\/jats:italic> mutations which are influenced by <jats:italic>H pylori<\/jats:italic> infection; some mutations may also be selected by eradication. These unstable K-<jats:italic>ras<\/jats:italic> mutations in IM may be related to lymphocyte infiltration caused by <jats:italic>H pylori<\/jats:italic> infection.<\/jats:p>","DOI":"10.1136\/jcp.2006.041939","type":"journal-article","created":{"date-parts":[[2006,9,22]],"date-time":"2006-09-22T20:52:44Z","timestamp":1158958364000},"page":"921-926","source":"Crossref","is-referenced-by-count":13,"title":["K-<i>ras<\/i> mutations and cell kinetics in <i>Helicobacter pylori<\/i> associated gastric intestinal metaplasia: a comparison before and after eradication in patients with chronic gastritis and gastric cancer"],"prefix":"10.1136","volume":"60","author":[{"given":"J","family":"Watari","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"A","family":"Tanaka","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"H","family":"Tanabe","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"R","family":"Sato","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"K","family":"Moriichi","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"A","family":"Zaky","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"K","family":"Okamoto","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"A","family":"Maemoto","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M","family":"Fujiya","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"T","family":"Ashida","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"K M","family":"Das","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Y","family":"Kohgo","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"239","published-online":{"date-parts":[[2006,9,22]]},"reference":[{"key":"2025092502004078000_60.8.921.1","doi-asserted-by":"publisher","DOI":"10.1002\/1097-0142(19901215)66:12<2569::AID-CNCR2820661220>3.0.CO;2-I"},{"key":"2025092502004078000_60.8.921.2","first-page":"3","volume":"196","year":"1993","journal-title":"Scand J Gastroenterol"},{"key":"2025092502004078000_60.8.921.3","first-page":"177","volume":"61","year":"1994","journal-title":"IARC monographs on the evaluation of carcinogenic risks to humans. 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