@article {Watari921, author = {J Watari and A Tanaka and H Tanabe and R Sato and K Moriichi and A Zaky and K Okamoto and A Maemoto and M Fujiya and T Ashida and K M Das and Y Kohgo}, title = {K-ras mutations and cell kinetics in Helicobacter pylori associated gastric intestinal metaplasia: a comparison before and after eradication in patients with chronic gastritis and gastric cancer}, volume = {60}, number = {8}, pages = {921--926}, year = {2007}, doi = {10.1136/jcp.2006.041939}, publisher = {BMJ Publishing Group}, abstract = {Background:Helicobacter pylori related gastric intestinal metaplasia (IM) is considered to be a precancerous lesion. Aims: To identify the effects of H pylori eradication on K-ras mutations, cell kinetics in IM and histological changes in patients with and without gastric cancers in a one-year prospective study. Methods: Patients included group A (n = 39), chronic gastritis, and group B (n = 53), intestinal-type early gastric cancer patients who had all undergone endoscopic mucosal resection (n = 25) or surgical resection (n = 28). K-ras 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. Results: The incidence of K-ras mutations in the cancer was only 3.8\%. The mutant K-ras in IM was observed more frequently in group A (46.2\%) than in group B patients (1.9\%) (p\<0.005). After eradication, the K-ras mutations significantly declined to 12.8\% in group A (p\<0.005). The mutation pattern of K-ras 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 H pylori eradication in both groups (p\<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\<0.05); the score improved significantly after eradication. Conclusions: K-ras 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-ras mutations which are influenced by H pylori infection; some mutations may also be selected by eradication. These unstable K-ras mutations in IM may be related to lymphocyte infiltration caused by H pylori infection.}, issn = {0021-9746}, URL = {https://jcp.bmj.com/content/60/8/921}, eprint = {https://jcp.bmj.com/content/60/8/921.full.pdf}, journal = {Journal of Clinical Pathology} }