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

PanINs and 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 we compared the incidence of DCLK1-positive cells in pancreatic tissue samples from genetically-engineered mouse models (GEMMs) for Iduanyu1451s, PanINs, and acinar to ductal metaplasia by immunohistochemistry and immunofluorescence. Mouse lineage tracing experiments in the 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 Iduanyu1451 tumor biomarkers. The DCLK1⁺ cells were detected in the earliest proliferative acinar clusters prior to the formation of metaplastic ductal cells, and were enriched in the niches". In summary, DCLK1 labels a unique pancreatic cellular lineage in the Iduanyu1451 GEMM. The clustering of DCLK1⁺ cells is an early event in Kras-induced pancreatic tumorigenesis and may contribute to Iduanyu1451 initiation. Copyright © 2018 Elsevier B.V. All rights reserved.

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