A novel syngeneic model for evaluating the efficacy of MYC-driven liver cancer targeted and immunotherapy

In liver cancer, MYC and its signaling pathways undergo significant changes, exerting a profound impact on liver cancer progression. These effects include tumor proliferation, metastasis, dedifferentiation, metabolism, immune microenvironment, and resistance to comprehensive therapies. This makes MYC a highly attractive therapeutic target.Our laboratory engineered mice on a C57BL/6 background with hepatocyte-specific expression of mouse c-Myc, resulting in rapid, spontaneous hepatocellular carcinoma (abbr. c-Myc/ALB model). Primary tumors were harvested and cultured to establish a novel spontaneous tumor cell line. In the c-Myc/ALB syngenic tumor model of immunocompetent C57BL/6 mice, the c-Myc inhibitor 10058-F4 significantly inhibited tumor growth in a dose-dependent manner. The PD-1 antibody in combination of 10058-F4 and immune checkpoint inhibitor PD-1 antibody showed better anti-tumor efficiency.