AIM:To develop an efficient animal colitis-associatedcarcinogenesis model and to detect the expression ofβ-catenin and p53 in this new model.METHODS:Dysplasia and cancer were investigated in micepretreated with a single intraperitoneal injection of 20 mg/kgbody mass of 1,2-dimethylhydrazine prior to three repetitiveoral administrations of 30 g/L dextran sulfate sodium togive conditions similar to the clinically observed active andremission phases.Immunohistochemical staining of β-catenin and p53 was performed on paraffin-imbeddedspecimens of animals with cancer and/or dysplasia,thosewithout dysplasia and the normal control animals.RESULTS:At wk 11,four early-invasive adenocarcinomasand 36 dysplasia were found in 10(90.9%)of the 11 micethat underwent 1,2-dimethylhydrazine-pretreatment with3 cycles of 30 g/L dextran sulfate sodium-exposure.Dysplasiaand/or cancer occurred as flat lesions or as dysplasia-associatedlesion or mass(DALM)as observed in humans.Colorectalcarcinogenesis occurred primarily on the distal portion ofthe large intestine.No dysplasia and/or cancer lesion wasobserved in the control groups with 1,2-dimethylhydrazinepretreatment or 3 cycles of 30 g/L dextran sulfate sodiumexposure alone.Immunohistochemical investigationrevealed that β-catenin was translocated from cellmembrane to cytoplasm and/or nucleus in 100% of caseswith dysplasia and neoplasm,while normal membranestaining was observed in cases without dysplasia and thenormal control animals.Nuclear expression of p53 was notdetected in specimens.CONCLUSION:A single dose of procarcinogen followedby induction of chronic ulcerative colitis results in a highincidence of colorectal dysplasia and cancer.Abnormalexpression of β-catenin occurs frequently in dysplasia andcancer.This novel mouse model may provide an excellentvehicle for studying colitis-related colon carcinogenesis. AIM: To develop an efficient animal colitis-associatedcarcinogenesis model and to detect the expression of β- catenin and p53 in this new model. METHODS: Dysplasia and cancer were investigated in mice pretreated with a single intraperitoneal injection of 20 mg / kg body mass of 1, 2 -dimethylhydrazine prior to three repetitiveoral administrations of 30 g / L dextran sulfate sodium togive conditions similar to the clinically observed active andreproducing phases. Immunohistochemical staining of β-catenin and p53 was performed on paraffin-imbeddedspecimens of animals with cancer and / or dysplasia, thosewithout dysplasia and the normal control animals.RESULTS: At wk 11, four early-invasive adenocarcinomas and 36 dysplasia were found in 10 (90.9%) of the 11 micethat underwent 1,2-dimethylhydrazine-pretreatment with 3 cycles of 30 g / L dextran sulfate sodium -exposure.Dysplasiaand / or cancer occurred as flat lesions or as dysplasia-associated lesions or mass (DALM) as observed in humans. Colorectalcarcinogenesis occurre d in on the distal portion of the large intestine. No dysplasia and / or cancer lesion wasobserved in the control groups with 1,2-dimethylhydrazine treatment or 3 cycles of 30 g / L dextran sulfate sodiumexposure alone. Immunohistochemical investigationrevealed that β-catenin was translocated from cellmembrane to cytoplasm and / or nucleus in 100% of cases with dysplasia and neoplasm, while normal membrane staining was observed in cases without dysplasia and then normal control animals. Nuclear expression of p53 was not detected in specimens. CONCLUSION: A single dose of procarcinogen followed by induction of chronic The novel mouse model may provide an excellent vein for studying colitis-related colon carcinogenesis.