Abstract

Abstract Hepatocellular carcinoma is a fatal liver cancer, and there are limited treatment options for this cancer. c-Myc is a key oncogene in liver cancer, but the specific mechanism of carcinogenesis in liver is unknown. Animal models are widely used to explore the molecular pathogenesis of HCC and test new drug candidates. In this poster, we reported a c-Myc conditional over-expression mouse model (LSL-Myc), which inserts the CAG-Loxp-stop-Loxp-c-Myc-polyA expression cassette into the H11 site. The expression of the Myc gene in this mouse model is regulated by Cre recombinase, which is not normally expressed, but only expressed in Cre-expressing tissue cells. LSL-Myc / Alb-cre double-positive mice were produced by crossing LSL-Myc hybrid mice with Alb-cre mice. In this mouse model, c-Myc was specifically expressed in liver cells. LSL-Myc / Alb-cre double-positive mice show a typical HCC phenotype and show accelerated tumor initiation and rapid HCC progression. Mice can detect significant liver tumorigenesis at 2 months of age, and 100% mice can occur hepatocellular carcinoma. The liver cancer tissues from LSL-Myc / Alb-cre double-positive mice can be transplanted to C57BL/6 mice to establish a mouse-derived PDX model. In summary, this model has the advantages of rapid oncogenesis and high incidence of liver cancer. It is an ideal model for studying the mechanism of c-Myc-driven liver cancer and c-Myc targeted therapy. Citation Format: Jinjin Wang, Dan Feng, Haiyan Zhu, Lei Ci, Zhipeng Wan, Ruilin Sun. A novel mouse model of hepatocellular carcinoma induced by c-myc overexpression [abstract]. In: Proceedings of the Annual Meeting of the American Association for Cancer Research 2020; 2020 Apr 27-28 and Jun 22-24. Philadelphia (PA): AACR; Cancer Res 2020;80(16 Suppl):Abstract nr 1626.

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