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. Author manuscript; available in PMC: 2012 Sep 15.
Published in final edited form as: Cancer Res. 2012 Jan 20;72(6):1557–1567. doi: 10.1158/0008-5472.CAN-11-3596

Figure 1.

Figure 1

KrasG12D and p53 mutation in the hepatic epithelium cooperate to cause cholangiocarcinoma. A) Modeling strategy; compound mutant mice harboring albumin-Cre transgene, LSL-KrasG12D, and p53L/L were created to conditionally activate KrasG12D and delete p53 in the hepatic epithelium. Lox P sites are indicated with red triangles. B) Kaplan-Meier survival analysis of cohorts of compound mutant animals. The p53 status is indicated; all of the mice have the LSL–KrasG12D allele. C) Gross tumor nodules in the Kras-p53 model. Arrowheads indicate tumor nodules seen in an animal with three distinct tumors. The arrow in image ii indicates enlarged lymph nodes. The tumor in the lower aspect of image ii is cystic and fluid- filled and was found to be an IPBN.

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