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首页> 外文期刊>World Journal of Gastroenterology >A novel mouse model for colitis-associated colon carcinogenesis induced by 1,2-dimethylhydrazine and dextran sulfate sodium
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A novel mouse model for colitis-associated colon carcinogenesis induced by 1,2-dimethylhydrazine and dextran sulfate sodium

机译：1,2-二甲基肼和硫酸右旋糖酐钠诱导的结肠炎相关结肠癌的新型小鼠模型

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AIM: To develop an efficient animal colitis-associated carcinogenesis model and to detect the expression of p-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 repetitive oral administrations of 30 g/L dextran sulfate sodium to give conditions similar to the clinically observed active and remission phases. Immunohistochemical staining of β-catenin and p53 was performed on paraffin-imbedded specimens of animals with cancer and/or dysplasia, those without 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 mice that underwent 1,2-dimethylhydrazine-pretreatment with 3 cycles of 30 g/L dextran sulfate sodium-exposure. Dysplasia and/or cancer occurred as flat lesions or as dysplasia-associated lesion or mass (DALM) as observed in humans. Colorectal carcinogenesis occurred primarily on the distal portion of the large intestine. No dysplasia and/or cancer lesion was observed in the control groups with 1,2-dimethylhydrazine pretreatment or 3 cycles of 30 g/L dextran sulfate sodium exposure alone. Immunohistochemical investigation revealed that p-catenin was translocated from cell membrane to cytoplasm and/or nucleus in 100% of cases with dysplasia and neoplasm, while normal membrane staining was observed in cases without dysplasia and the normal control animals. Nuclear expression of p53 was not detected in specimens. CONCLUSION: A single dose of procarcinogen followed by induction of chronic ulcerative colitis results in a high incidence of colorectal dysplasia and cancer. Abnormal expression of β-catenin occurs frequently in dysplasia and cancer. This novel mouse model may provide an excellent vehicle for studying colitis-related colon carcinogenesis.
机译：目的：建立一种有效的动物结肠炎相关癌变模型，并检测该新模型中p-catenin和p53的表达。方法：在重复口服30 g / L硫酸右旋糖酐钠以产生类似于临床观察到的症状之前，对经20毫克/千克体重的1,2-二甲基肼单次腹膜内注射预处理的小鼠进行了发育异常和癌症研究活动和缓解阶段。对患有癌症和/或不典型增生的动物，不典型异常的动物和正常对照动物的石蜡包埋标本进行了β-catenin和p53的免疫组织化学染色。结果：在第11周时，在接受1，2-二甲基肼预处理和30 g / L硫酸右旋糖酐硫酸钠暴露3次循环的11只小鼠中，有10只（90.9％）发现了4例早期浸润性腺癌和36个不典型增生。如在人类中观察到的，不典型增生和/或癌症表现为扁平病变或不典型增生相关的病变或肿块（DALM）。大肠癌发生主要发生在大肠的远端。在对照组中，未进行1,2-二甲基肼预处理或仅暴露30 g / L右旋糖酐硫酸钠的3个周期未观察到发育异常和/或癌变。免疫组织化学研究显示，在100％的有异型增生和肿瘤的病例中，p-catenin从细胞膜转移到细胞质和/或细胞核，而在无异型增生和正常对照组的动物中，膜正常。在标本中未检测到p53的核表达。结论：单剂量的致癌物，然后诱发慢性溃疡性结肠炎，导致大肠异型增生和癌症的发生率很高。 β-catenin的异常表达经常发生在异型增生和癌症中。这种新颖的小鼠模型可能为研究结肠炎相关的结肠癌发生提供了极好的载体。

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