AIM:To explore dysregulation of cyclin E in malignancies,and to further investigate the role of cyclin E in Helicobacterpylori(H.pylori)-induced gastric precancerosis.METHODS:Four-week-old specific pathogen-free maleMongolian gerbils were employed in the study.0.5 mL 1×10~8 cfu·L~(-1)suspension of H.pylori NTCC11637 in Brucellabroth was inoculated orally into each of 20 Mongolian gerbils,and a further 20 gerbils were inoculated with Brucella brothas controls.10 of the infected gerbils and 10 of the non-infected control gerbils were sacrificed at 25,45 wk afterinfection.The expression of cyclin E was analyzed by RT-PCR and immunohistochemical studies with monoclonalantibody to cyclin E in Mongolian gerbil of H.pylori-induced gastric precancerosis.RESULTS:H.pylori was constantly detected in all infectedanimals throughout the study.At 25 wk after infection of H.pylori,ulcers were observed in the antral and body ofstomach(n=6).Histological examination showed that allanimals developed severe inflammation and multifocallymphoid follicles appeared in the lamina propria andsubmucosa of gastric antrum.At 45 wk after infection of H.pylori,severe atrophic gastritis(n=10),intestinalmetaplasia(n=8)and dysplasia(n=6)could beobserved.Cyclin E mRNA levels were significantly more at25 wk after infection of H.py/ori(1.27±0.26),and at 45 wkafter infection of H.pylori(1.82±0.39)than control-animals(0.59±0.20,P<0.01);cyclin E mRNA levels wereevaluated by 2.2-fold at 25 wk(P<0.01)and 3.1-fold at 45wk(P<0.01)precancerosis induced by H.pylori,whencompared with control gastric epithelium of Mongoliangerbil.Immunohistochemical staining revealed exclusivenuclear staining of cyclin E.Furthermore,there was asequential increase in cyclin E positive cells from normalepithelium to precancerosis.CONCLUSION:Overexpression of cyclin E occurs relativelyearly in gastric tumorigenesis in this model. AIM:To explore dysregulation of cyclin E in malignancies,and to further investigate the role of cyclin E in Helicobacterpylori(H.pylori)-induced gastric precancerosis.METHODS:Four-week-old specific pathogen-free maleMongolian gerbils were employed in the study .0.5 mL 1×10~8 cfu·L -1suspension of H.pylori NTCC11637 in Brucellabroth was inoculated orally into each of 20 Mongolian gerbils,and a further 20 gerbils were inoculated with Brucella brothas controls.10 of the infection. Gerbils and 10 of the non-infected control gerbils were sacrificed at 25,45 wk afterinfection. The expression of cyclin E was analyzed by RT-PCR and immunohistochemical studies with monoclonalantibody to cyclin E in Mongolian gerbil of H.pylori-induced gastric precancerosis. RESULTS: H.pylori was constantly detected in all infectionanimals throughout the study.At 25 week after infection of H.pylori, ulcers were observed in the antral and body ofstomach (n=6).Histological examination showed that allanimals developed sev Ere inflammation and multifocallymphoid follicles appeared in the lamina propria and submucosa of gastric antrum.At 45 weeks after infection of H.pylori,severe atrophic gastritis (n=10),intestinalmetaplasia(n=8)and dysplasia(n=6)could beobserved. Cyclin E mRNA levels were significantly more at 25 weeks after infection of H.py/ori (1.27±0.26), and at 45 weeks after infection of H.pylori (1.82±0.39) than control-animals (0.59±0.20, P<0.01) Cyclin E mRNA levels wereevaluated by 2.2-fold at 25 weeks (P<0.01) and 3.1-fold at 45 weeks (P<0.01) precancerosis induced by H.pylori, whocompared with control gastric epithelium of Mongoliangerbil. Immunohistochemical staining omitted exclusive nuclear staining of Cyclin E.Furthermore,there was asequential increase in cyclin E positive cells from normal epidemic hematoma to precancerosis.CONCLUSION:Overexpression of cyclin E was given as an approximateearly in gastric tumorigenesis in this model.