Zender L, Xue W, Cordón-Cardo C, Hannon G J, Lucito R, Powers S, Flemming P, Spector M S, Lowe S W
Cold Spring Harbor Laboratory, New York 11724, USA.
Cold Spring Harb Symp Quant Biol. 2005;70:251-61. doi: 10.1101/sqb.2005.70.059.
Hepatocellular carcinoma is a chemoresistant cancer and a leading cause of cancer mortality; however, the molecular mechanisms responsible for the aggressive nature of this disease are poorly understood. In this study, we developed a new liver cancer mouse model that is based on the ex vivo genetic manipulation of embryonic liver progenitor cells (hepatoblasts). After retroviral gene transfer of oncogenes or short hairpin RNAs targeting tumor suppressor genes, genetically altered liver progenitor cells are seeded into the liver of otherwise normal recipient mice. We show that histopathology of the engineered liver carcinomas reveals features of the human disease. Furthermore, representational oligonucleotide microarray analysis (ROMA) of murine liver tumors initiated by two defined genetic hits revealed spontaneously acquired genetic alterations that are characteristic for human hepatocellular carcinoma. This model provides a powerful platform for applications like cancer gene discovery or high-throughput preclinical drug testing.
肝细胞癌是一种化疗耐药性癌症,也是癌症死亡的主要原因;然而,导致这种疾病侵袭性的分子机制却知之甚少。在本研究中,我们基于胚胎肝祖细胞(成肝细胞)的体外基因操作开发了一种新的肝癌小鼠模型。在将癌基因或靶向肿瘤抑制基因的短发夹RNA进行逆转录病毒基因转移后,将基因改变的肝祖细胞接种到原本正常的受体小鼠肝脏中。我们发现,工程化肝癌的组织病理学显示出人类疾病的特征。此外,对由两种明确的基因打击引发的小鼠肝肿瘤进行代表性寡核苷酸微阵列分析(ROMA),揭示了人类肝细胞癌特有的自发获得性基因改变。该模型为癌症基因发现或高通量临床前药物测试等应用提供了一个强大的平台。