AIM To establish a model system for studying gastric carcinogenesis of MNNG, a gastric cancer relatedcarcinogen.METHODS Cell culture transformation, PCR-restriction fragment length polymorphism (PCR-RFLP),DNA blotting and immunochemical techniques and analysis of LDH isozyme and chromosome wereperformed.RESULTS GES-1 cells surviving by MNNG treatment were named MC (2 × 105M for 24 hours) and MC-B(2 × 10-7M for 7 days). The two cell lines treated by MNNG showed more malignant than maternal cell GES-1 with the evidences of more chromosome aberrations, abnormal morphology and eytoskeleton and alsogained the ability of colony formation on soft agar. C-Ha-ras gene point mutation in the 12th codon and LDHisoenzyme abnormal express were found in MC-B cells. In addition, C-met gene rearrangement was revealedby Southern blot analysis in MC-B and MC.CONCLUSION This gastric epithelial cell system is an important model system for further study of stomachcancer, MNNG had a selective effect on the cytoskeleton mierofilament in human gastric epithelial cells andintimately associated with the activation of certain oncogenes and some protein.

AIM To observe the therapeutic effect of Welcome on gastric mucosal dysplasia in rats.METHODS Rats with gastric mucosal dysplasia induced by MMNG and heat-damage were treated withWelcome, a kind of traditional Chinese medicine compound which has the functions of replenishing qi toinvigorate the spleen, and of nourishing the liver and kidney and clearing away heat and toxic materials, thecontrol rats were treated with saline and tretinoin.RESULTS AND CONCLUSION The results showed Welcome could obviously block the mutagenic action ofMNNG and prevent the occurrence of gastric mucosal dysplasia of rats.

AIM To establish an ideal model of gastric precancerous lesions for rats.METHODS Fifty rats were fed with carcinogen MNNG for 35 wk and heat-plaste at 60C for 20 wk, thepathological changes were observed. Data in the groups were analyzed by Ridit test.RESULTS The occurrence rate of dysplasia in rats due to MNNG and heat-damage was 65%, which wasobviously higher than that due to MNNG only. The differences between the two groups were significant.CONCLUSION The animal model made by MNNG and heat-damage was an ideal one which could be usedto investigate the pathologic mechanism of gastric precancerous lesions.