Skip to main content
. Author manuscript; available in PMC: 2022 Jun 1.
Published in final edited form as: Cancer Discov. 2021 Dec 1;11(12):3158–3177. doi: 10.1158/2159-8290.CD-21-0209

Figure 2. Expression of oncogenic Pik3caH1047R but not KrasG12D induces extrahepatic cholangiocarcinoma (ECC).

Figure 2

(A) Representative in situ images of 12-month-old wildtype (control), Pdx1-Cre;LSL-Pik3caH1047R/+ and Pdx1-Cre;LSL-KrasG12D/+ mice. The common bile duct is outlined by a white dashed line. Scale bars, 1cm. (B) Representative H&E stainings and immunohistochemical analyses of PI3K/AKT pathway activation in the common bile duct of aged Pdx1-Cre;LSL-Pik3caH1047R/+ mice with invasive ECC. Scale bars, 50 μm for micrographs and 20 μm for insets. (C) Kaplan-Meier survival curves of the indicated genotypes (n.s., not significant; *** p<0.001, log rank test). (D) Tumor type distribution in % according to histological analysis of the extrahepatic bile duct and the pancreas from Pdx1-Cre;LSL-KrasG12D/+ and Pdx1-Cre;LSL-Pik3caH1047R/+ mice. ECC, extrahepatic cholangiocarcinoma, PDAC, pancreatic ductal adenocarcinoma.