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. Author manuscript; available in PMC: 2018 Jul 9.
Published in final edited form as: Nat Rev Gastroenterol Hepatol. 2017 Mar 8;14(5):296–304. doi: 10.1038/nrgastro.2017.12

Figure 1. Acinar cell plasticity and metaplasia to duct-like cells in the adult pancreas.

Figure 1

In response to pancreatic injury, the loss of cell–cell and cell–matrix contacts (contact-mediated signalling), loss of polarity, KRAS hyperactivity and increased inflammatory signalling can drive acinar cells to undergo dedifferentiation and transdifferentiation to a duct-like phenotype that is needed for pancreatic regeneration. Acinar-to-ductal metaplasia becomes irreversible in the presence of an oncogenic Kras mutation and persistent growth factor signalling, leading to metabolic and signalling changes that lock the duct-like cells in their transdifferentiated state and initiate further progression to low-grade precancerous lesions.