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Regenerative Medicine

Acinar cell reprogramming: a clinically important target in pancreatic disease

    Christopher L Pin

    *Author for correspondence:

    E-mail Address: cpin@uwo.ca

    Department of Paediatrics, Physiology & Pharmacology, & Oncology, University of Western Ontario, London, ON N6C 2V5, Canada

    Department of Physiology & Pharmacology, University of Western Ontario, London, ON N6C 2V5, Canada

    Department of Oncology, University of Western Ontario, London, ON N6C 2V5, Canada

    Children's Health Research Institute, London, ON, Canada

    ,
    Joanna F Ryan

    Department of Paediatrics, Physiology & Pharmacology, & Oncology, University of Western Ontario, London, ON N6C 2V5, Canada

    Department of Physiology & Pharmacology, University of Western Ontario, London, ON N6C 2V5, Canada

    Department of Oncology, University of Western Ontario, London, ON N6C 2V5, Canada

    Children's Health Research Institute, London, ON, Canada

    &
    Rashid Mehmood

    Department of Paediatrics, Physiology & Pharmacology, & Oncology, University of Western Ontario, London, ON N6C 2V5, Canada

    Department of Physiology & Pharmacology, University of Western Ontario, London, ON N6C 2V5, Canada

    Department of Oncology, University of Western Ontario, London, ON N6C 2V5, Canada

    Children's Health Research Institute, London, ON, Canada

    Published Online:https://doi.org/10.2217/epi.14.83

    Acinar cells of the pancreas produce the majority of enzymes required for digestion and make up >90% of the cells within the pancreas. Due to a common developmental origin and the plastic nature of the acinar cell phenotype, these cells have been identified as a possible source of β cells as a therapeutic option for Type I diabetes. However, recent evidence indicates that acinar cells are the main source of pancreatic intraepithelial neoplasias (PanINs), the predecessor of pancreatic ductal adenocarcinoma (PDAC). The conversion of acinar cells to either β cells or precursors to PDAC is dependent on reprogramming of the cells to a more primitive, progenitor-like phenotype, which involves changes in transcription factor expression and activity, and changes in their epigenetic program. This review will focus on the mechanisms that promote acinar cell reprogramming, as well as the factors that may affect these mechanisms.

    Papers of special note have been highlighted as: • of interest; •• of considerable interest

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