Murine models for familial pancreatic cancer: Histopathology, latency and drug sensitivity among cancers of Palb2, Brca1 and Brca2 mutant mouse strains
Fig 2
Concomitant expression of mutant KrasG12D and p53R270H cooperates with Palb2, Brca1 or Brca2 loss in pancreatic ductal cells to promote PDAC tumorigenesis.
(A) Kaplan-Meier survival curves of KPC, Brca1-KPC, Palb2-KPC and Brca2-KPC. Higher rates of death were observed in Brca1-KPC, Palb2-KPC and Brca2-KPC compared with KPC (****P<0.0001 compared with KPC). Palb2-KPC animals showed slightly, but significantly worse survival rates than Brca1-KPC and Brca2-KPC (****P<0.0001, **P = 0.0022). (B) Gross appearance of pancreatic tumor of Palb2-KPC mouse. Large solid tumor in the head of pancreas growing into bile duct (T: tumor, L: Liver, B: Bile duct and D: Duodenum). (C) H&E (Hematoxylin and eosin) analysis of the histopathology of KPC, Brca1-KPC, Palb2-KPC and Brca2-KPC tissues (D) Detection of acinar ductal metaplasia (ADM) lesions by immunohistochemical double staining of amylase and cytokeratin 19. (E) Quantification of acinar ductal metaplasia (ADM) lesions in the mouse strain pancreata (Means ± SEM; *P<0.05).