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. Author manuscript; available in PMC: 2020 Oct 1.
Published in final edited form as: J Hepatol. 2019 Jun 11;71(4):742–752. doi: 10.1016/j.jhep.2019.05.027

Figure 5. Inactivation of c-Myc completely abolishes cholangiocarcinogenesis in AKT/Fbxw7ΔF mice.

Figure 5.

(A) Study design. FVB/N mice were subjected to HTVi of either AKT/Fbxw7ΔF/pT3 (control, n=6) or AKT/Fbxw7ΔF/MadMyc (n=8) plasmids. MadMyc is a dominant negative form of c-Myc. (B) Survival curve of AKT/Fbxw7ΔF/pT3 and AKT/Fbxw7ΔF/MadMyc mice. (C) Inhibition of tumor development in AKT/Fbxw7ΔF/MadMyc mice, as revealed by macroscopic examination of the livers and histopathology of the lesions, is accompanied by immunoreactivity for the Ck19 biliary marker limited to normal biliary epithelial cells (indicated by arrows) and low/absent immunoreactivity for the proliferation marker Ki67. Scale bar: 100μm. Abbreviation: H&E, hematoxylin and eosin staining.