Uehara Takeki, Pogribny Igor P, Rusyn Ivan
Department of Environmental Sciences and Engineering, University of North Carolina, Chapel Hill, North Carolina.
Strategic Development Department, Shionogi & Co, Osaka, Japan.
Curr Protoc Pharmacol. 2014 Sep 2;66:14.30.1-14.30.10. doi: 10.1002/0471141755.ph1430s66.
Human hepatocellular carcinoma (HCC) develops most often as a complication of fibrosis or cirrhosis. While most human studies of HCC provide crucial insights into the molecular signatures of HCC, seldom do they address the etiology of HCC. Mouse models are essential tools for investigating the pathogenesis of HCC; however, the overwhelming majority of cancer models in rodents do not feature liver fibrosis. Detailed in this unit is a protocol for an experimental mouse model of HCC that arises in association with advanced liver fibrosis. The disease model is induced by a single injection of N-nitrosodiethylamine (DEN) followed by repeated administration of carbon tetrachloride (CCl4 ). A dramatic potentiation of liver tumor incidence is observed following administration of DEN and CCl4 , with 100% of mice developing liver tumors at 5 months of age. This model can be employed for studying the molecular mechanisms of fibrogenesis and HCC development, and in cancer hazard/chemotherapy testing of drug candidates.
人类肝细胞癌(HCC)最常作为纤维化或肝硬化的并发症出现。虽然大多数关于HCC的人体研究为HCC的分子特征提供了关键见解,但它们很少涉及HCC的病因。小鼠模型是研究HCC发病机制的重要工具;然而,绝大多数啮齿动物癌症模型没有肝纤维化特征。本单元详细介绍了一种与晚期肝纤维化相关的HCC实验小鼠模型的方案。该疾病模型通过单次注射N-亚硝基二乙胺(DEN),随后反复给予四氯化碳(CCl4)诱导。在给予DEN和CCl4后,观察到肝肿瘤发生率显著升高,100%的小鼠在5月龄时发生肝肿瘤。该模型可用于研究纤维化形成和HCC发展的分子机制,以及候选药物的癌症风险/化疗测试。