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. 2013 Oct 8;123(11):4681–4694. doi: 10.1172/JCI65764

Figure 5. ICMT deficiency accelerates the development of PDA but does not significantly affect the survival of mice expressing oncogenic KRASG12D and dominant-negative p53R172H in the pancreas.

Figure 5

(A) Percentage of Icmtflx/+;Pdx1-Cre;LSL-KrasG12D (Icmtflx/+) versus Icmtflx/flx;Pdx1-Cre;LSL-KrasG12D (Icmtflx/flx) mice of the indicated ages that had PDA upon histological examination of the pancreas at necropsy (cohort size = 17). (B) H&E staining of paraffin sections of the pancreas (left) and liver (right) of a 6-month-old Icmtflx/flx;Pdx1-Cre;LSL-KrasG12D mouse that developed metastatic disease. Scale bars: 100 μm. (C) Kaplan-Meier survival curves for mice of the genotypes Icmtflx/+;Pdx1-Cre;LSL-KrasG12D;LSL-p53R172H (Icmtflx/+, n = 15) and Icmtflx/flx;Pdx1-Cre;LSL-KrasG12D;LSL-p53R172H (Icmtflx/flx, n = 13). The curves did not differ significantly. (D) Gross pathology of tumors found in a 6-month-old Icmtflx/+;Pdx1-Cre;LSL-KrasG12D;LSL-p53R172H mouse. Clearly visible are a large tumor at the head of the pancreas (asterisk), liver metastases (arrows), and an enlarged spleen (arrowhead).