Northwestern University Feinberg School of Medicine

Beatriz Sosa-Pineda Lab

Acinar Cell Plasticity

Under certain pathologic conditions (e.g., pancreatitis), acinar cells can dedifferentiate into a progenitor/duct-like lesion called acinar-to-ductal metaplasia (ADM). We found that Prox1 is transiently re-activated in acinar cells undergoing dedifferentiation and acinar-to-ductal metaplastic conversion. We also uncovered that Prox1-heterozygosis markedly increases the formation of ADMs and early neoplasias in mouse pancreatic tissues expressing oncogenic Kras. We will use our mouse models, ex-vivo protocols of ADM formation and other methodologies, to identify novel regulators of acinar cell plasticity and their possible role in neoplastic transformation. 


Transient dedifferentiation


Persistent dedifferentiation