AIM To explore dysregulation of c-fos in several humanmalignancies,and to further investigate the role of c-los inHelicobacter pylori(H.pylon)-induced gastric precancerosis.METHODS:Four-week-old male Mongolian gerbils wereemployed in the study.0.5 mL 1×10~8 cfu·L~(-1)suspension ofH.pyloriNCTC 11 637 in Brucella broth were inoculatedorally into 20 Mongolian gerbils.Another 20 gerbils wereinoculated with Brucella broth as controls.10 of the infectedgerbils and 10 of the non-infected control gerbils weresacrificed at 25 and 45 weeks after infection.The stomachof each gerbil was removed and opened for macroscopicobservation.The expression of c-fos was analyzed by RT-PCR and immunohistochemical studies in H.pylori-inducedgastric precancerosis of Hongolian gerbil.Half of each gastricantrum mucosa was dissected for RNA isolation and RT-PCR.β-actin was used as the housekeeping gene andamplified with c-fosas contrast.PCR products of c-foswereanalyzed by gel image system and the level of c-los wasreflected with the ratio of c-fos/β-actin.The immunostainingfor c-foswas conducted using monoclonal antibody of c-losand the StreptAvidin-Biotin-enzyme Complex kit.RESULTS:H.pyloriwas constantly found in all infectedanimals in this study.After infection of H.Pylorifor 25 weeks,ulcers were observed in the antral and the body of stomachof 60 % infected animals(6/10).Histological examinationshowed that all animals developed severe inflammation,especially in the area close to ulcers,and multifocal lymphoidfollides appeared in the lamina propria and submucosa.Afterinfection of H.Pylorifor 45 weeks,severe atrophic gastritisin all infected animals,intestinal metaplasia in 80 % infectedanimals(8/10)and dysplasia in 60 % infected animals(6/10)could be observed.C-fos mRNA levels were significantlyhigher after infection of H.pylorifor 25 weeks(1.84±0.79),and for 45 weeks(1.59±0.37)than those in control-animals(0.74±0.22,P<0.01).C-fos mRNA levels were increased2.5-fold by 25th week(P<0.01)and 2.1-fold by 45th week(P<0.01)in precancerosis induced by H.pylori,whencompared with normal gastric epithelium of Mongolian gerbil.Immunohistochemical staining revealed exclusive nuclearstaining of c-fos.Furthermore,there was a sequentialincrease in c-fos positive cells from normal epithelium toprecancerosis. CONCLUSION:The study suggested that overexpressionof c-fos occurs relatively early in gastric tumorigenesis inthis precancerosis model induced by H.pylori. AIM To explore dysregulation of c-fos in several human malignancies, and to further investigate the role of c-los in Helicobacter pylori (H. pylon) -induced gastric precancerosis. METHODS: Four-week-old male Mongolian gerbils wereemployed in the study. 0.5 mL 1 × 10-8 cfu · L -1 suspension ofH.pylori NCTC 11 637 in Brucella broth were inoculatedorally into 20 Mongolian gerbils.Another 20 gerbils were inoculated with Brucella broth as controls.10 of the infectedgerbils and 10 of the non- infected control gerbils weresacrificed at 25 and 45 weeks after infection. The stomach of each gerbil was removed and opened for macroscopicobservation. The expression of c-fos was analyzed by RT-PCR and immunohistochemical studies in H. pylori-induced gastric precancerosis of Hongolian gerbil. Half of each gastric mucosa was dissected for RNA isolation and RT-PCR. β-actin was used as the housekeeping gene and amplified with c-fosas contrast. PCR products of c-foswere analyzed by gel image system and the level of c-lo s wasreflected with the ratio of c-fos / β-actin. the immunostaining for c-foswas conducted using monoclonal antibody of c-los and the StreptAvidin-Biotin-enzyme Complex kit.RESULTS: H. pyloriwas constantly found in all infected animals in this study. After infection of H. Pylorifor 25 weeks, ulcers were observed in the antral and the body of stomach of 60% infected animals (6/10). Histological examinationshowed that all animals developed severe inflammation, especially in the area close to ulcers, and multifocal lymphoid follides Was in the lamina propria and submucosa. Afterfection of H. Pylorifor 45 weeks, severe atrophic gastritisin all infected animals, intestinal metaplasia in 80% infected animals (8/10) and dysplasia in 60% infected animals (6/10) could be observed. C-fos mRNA levels were significantlyhigher after infection of H.pylorifor for25weeks (1.84 ± 0.79), and for45weeks (1.59 ± 0.37) than those in control-animals (0.74 ± 0.22, P <0.01) Levels were increased 2.5-fold by 25th week (P <0.01 ) and 2.1-fold by 45th week (P <0.01) in precancerosis induced by H. pylori, whencompared with normal gastric epithelium of Mongolian gerbil. Immunohistochemical staining revealed exclusive nuclearstaining of c-fos.Furthermore, there was a sequential incase in c-fos positive cells from normal epithelium toprecancerosis. CONCLUSION: The study suggested that overexpression of c-fos causing relatively early in gastric tumorigenesis in thrombastatic model induced by H. pylori.