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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 4. Deletion of Notch2 retards, without impairing, cholangiocarcinogenesis in AKT/Fbxw7ΔF mice.

Figure 4.

(A) Study design. Notch2lox/flox conditional knockout mice were subjected to HTVi of either AKT/Fbxw7ΔF/pCMV (control, n=8) or AKT/Fbxw7ΔF/Cre (n=10) plasmids. (B) Delay of tumor development in AKT/Fbxw7ΔF mice, as revealed by macroscopic examination of the livers and histopathology of the lesions, is accompanied by reduction of the Ck19 biliary marker and increase of the Hnf-4α hepatocellular marker. (C) Survival curve showing the delay of intrahepatic cholangiocarcinoma development following deletion of Notch2. (D) Analysis of Ck19-positive areas in control (pCMV) and Notch2-depleted (Cre) livers. (E) Western blotting of AKT/Fbxw7ΔF livers from control and Notch2 deleted mice. Scale bar: 200μm. Abbreviations: H&E, hematoxylin and eosin staining; NL, normal liver. *** p <0.001.