Pancreatic DCLK1⁺ cells originate distinctly from PDX1⁺ progenitors and contribute to the initiation of intraductal papillary mucinous neoplasm in mice.

ABSTRACT: PanINs and IPMNs are the two most common precursor lesions that can progress to invasive pancreatic ductal adenocarcinoma (PDA). DCLK1 has been identified as a biomarker of progenitor cells in PDA progressed from PanINs. To explore the potential role of DCLK1-expressing cells in the genesis of IPMNs, we compared the incidence of DCLK1-positive cells in pancreatic tissue samples from genetically-engineered mouse models (GEMMs) for IPMNs, PanINs, and acinar to ductal metaplasia by immunohistochemistry and immunofluorescence. Mouse lineage tracing experiments in the IPMN GEMM showed that DCLK1⁺ cells originated from a cell lineage distinct from PDX1⁺ progenitors. The DCLK1⁺ cells shared the features of tuft cells but were devoid of IPMN tumor biomarkers. The D

SUBMITTER: Qiu W 

PROVIDER: S-EPMC6086584 | biostudies-literature | 2018 Jun

REPOSITORIES: biostudies-literature