Skip to main content
. 2020 Sep 21;12(9):2695. doi: 10.3390/cancers12092695

Figure 1.

Figure 1

Conditional loss of Arid1a in mouse pancreas restricts growth of Kras-driven early premalignant lesions. (A,B) Representative gross macroscopic images and H&E stained histological sections from “KC” and “KAC” pancreata at early ages showing normal parenchyma replaced by mucinous cysts resembling human IPMNs. Representative images from at least 7 mice per age group are shown. (C) Quantification of immunohistochemical (IHC) staining for Ki-67 on pancreata from age-matched mice revealed lower percentage of proliferating PanINs lesions in “KAC” than “KC” group. For Ki67 quantification, % of Pos = (number of cells positive for Ki67 staining in PanINs)/(total number of cells in PanINs) from at least 5 mice per age group. (D) IHC staining for cleaved caspase-3 on 28-week old pancreata from “KC” and “KAC” mice showed stronger and widespread staining in acini and precursor lesions of “KAC” mice. (E) Kaplan-Meier survival curve for “KC” and “KAC” mice showing overall shorter median survival of “KAC” mice (38 weeks versus 58 weeks for “KC”) with p value of < 0.0001 based on Log-rank (Mantel-Cox) test. (F) Representative histopathological section from “KAC” mice characterized by foci of well-differentiated PDAC surrounded by areas of LG-IPMNs, ADMs and LG-PanINs (arrows). (G) Representative gross necropsy image and H&E stained sections from 48-week “KAC” mice showing well-differentiated PDAC (Pancreas), which metastasized to liver and lung, although majority of pancreas was still populated by IPMN lesions (IPMN). Scale bar is 100 µm.