【摘要】 目的:建立小鼠结直肠自发肿瘤模型。方法:用雄性Ap^Mn/+基因突变小鼠与雌性BubR1^+/-基因敲除小鼠交配。得到的子代小鼠,按基因型分为Wild Type,BubR1^+/-,Apc（Mn/+）,和BubR^1+/-Apc（Mn/+4）组,每组7只,观察各组肠组织肿瘤数目、大小和位置,行HE染色后观察病理学改变,并用免疫组化染色法研究各组结直肠β-catenin的表达。结果:①BubR1^+/-Apc（Mn/+）组小鼠结直肠肿瘤的发病率显著增加,较Apc（Mn/+）组有显著差异（P=0．008）。②BubR1或Apc单独缺失组小鼠结直肠中β-catenin蛋白除在细胞膜表达外,在细胞质也有弱阳性表达;而BubR1^+/-Apc（Mn/+）组小鼠结直肠β-catenin的表达水平明显增高,且多为细胞质表达和（或）膜浆共表达,部分合并细胞核表达。结论建立小鼠结直肠自发肿瘤模型对于筛选抗肿瘤药物和研究肿瘤发生机制具一定的应用价值。更多还原

【Abstract】 Objective:To establish a spontaneous colorectal neoplasm model in mice for experimental studies.Methods: We mated ApcMin/+ male mice with BubR1^+/- female mice to get littermates.The mice were divided into 4 groups（7 mice per group）according to the genotype:Wild Type,BubRl^+/-z Apc^Min/+,BubR1^+/-Apc^Min/+.The amount,volume,localization of the intestinal tumors were analyzed,and the pathology was observed by HE staining.The expression ofβ-catenin in colons from mice of various genotypes were detected by immunohistochemistry.The incidence of tumor was analyzed by statistics.Results:In BubR1+ /-ApcMin/+mice,the incidence of the colorectal neoplasm was significantly higher than that in ApcMird+group（P=0.008）.In colon tissues of BubR1^+/-or Ape^Min/+ mice,β-catenin protein was observed to have low expression on cell membrane and/or in cytoplasma.Whereas,in that of BubR1^+/-Ape^Min/+ mice,β-catenin protein was accumulated much more in cytoplasma and/or nudeus.Conclusions:The spontaneous colorectal neoplasm model was established and it provides a useful tool for selecting antineoplastic drug and for studying the mechanism of the colon carcinoma.更多还原