PO.IM02.07 · 免疫学
一种用于评估MYC驱动型肝癌靶向治疗和免疫治疗疗效的新型同基因模型
A novel syngeneic model for evaluating the efficacy of MYC-driven liver cancer targeted and immunotherapy
作者与单位 Authors & Affiliations
摘要 Abstract
中文摘要
在肝癌中，MYC及其信号通路发生显著变化，对肝癌进展产生深远影响。这些影响包括肿瘤增殖、转移、去分化、代谢、免疫微环境以及对综合治疗的耐药。这使得MYC成为极具吸引力的治疗靶点。我们实验室构建了C57BL/6背景、肝细胞特异性表达小鼠c-Myc的小鼠，导致快速、自发的肝细胞癌（简称c-Myc/ALB模型）。收获原发肿瘤并进行培养，以建立一种新型的自发肿瘤细胞系。在免疫功能健全的C57BL/6小鼠的c-Myc/ALB同基因肿瘤模型中，c-Myc抑制剂10058-F4以剂量依赖的方式显著抑制肿瘤生长。PD-1抗体与10058-F4以及免疫检查点抑制剂PD-1抗体联合使用，显示出更好的抗肿瘤效力。
查看英文原文 English abstract
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.
利益披露 Disclosure
L. Ci,
Shanghai Model Organisms Center, Inc. Other, Parent Company.
K. Zhou,
Shanghai Model Organisms Center, Inc. Other, Parent Company.
J. Liu,
Shanghai Model Organisms Center, Inc. Other, Parent Company.
R. Sun,
Shanghai Model Organisms Center, Inc. Other, Parent Company.