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. Author manuscript; available in PMC: 2015 Jan 1.
Published in final edited form as: Gastroenterology. 2013 Oct 2;146(1):245–256. doi: 10.1053/j.gastro.2013.09.050

Figure 1. Histological analysis of mPanIN progression model after activation of oncogenic Kras in the acinar cell compartment.

Figure 1

(A) Schematic illustrating tamoxifen induction of CreERT2 activity with and without concomitant cerulein-induced chronic pancreatitis in Mist1:CreERT2; LSL-Kras; LSL-YFP (KCiMist1Y) and Mist1:CreERT2; LSL-Kras; mTmG (KCiMist1G) mice. (B–E) Progressive PanIN formation with and without concomitant chronic pancreatitis. (B) No PanIN are detected in either the absence of KrasG12D activation or 1 week following KrasG12D activation. (C) Representative section depicting mPanIN three weeks after oncogenic Kras expression, at which point mPanINs typically occupy ~5% of cross sectional area. (D) Increased PanIN density 6 weeks following KrasG12D activation, at which point mPanINs typically occupy ~10–15% of cross sectional area. (E) Accelerated PanIn formation following KrasG12D activation in combination with cerulein-mediated chronic pancreatitis; PanIN lesions occupy greater than 70% of the pancreas. (F) Antibody labeling for GFP and tdTomato in pancreatic tissue harvested from KCiMist1G mice confirms acinar cell origin of ADM and PanIN.