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Type: Journal article
Title: Dclk1 defines quiescent pancreatic progenitors that promote injury-induced regeneration and tumorigenesis
Author: Westphalen, C.
Takemoto, Y.
Tanaka, T.
Macchini, M.
Jiang, Z.
Renz, B.
Chen, X.
Ormanns, S.
Nagar, K.
Tailor, Y.
May, R.
Cho, Y.
Asfaha, S.
Worthley, D.
Hayakawa, Y.
Urbanska, A.
Quante, M.
Reichert, M.
Broyde, J.
Subramaniam, P.
et al.
Citation: Cell Stem Cell, 2016; 18(4):441-455
Publisher: Elsevier
Issue Date: 2016
ISSN: 1934-5909
Statement of
C. Benedikt Westphalen, Yoshihiro Takemoto, Takayuki Tanaka, Marina Macchini, Zhengyu Jiang ... Daniel L Worthley ... et al.
Abstract: The existence of adult pancreatic progenitor cells has been debated. While some favor the concept of facultative progenitors involved in homeostasis and repair, neither a location nor markers for such cells have been defined. Using genetic lineage tracing, we show that Doublecortin-like kinase-1 (Dclk1) labels a rare population of long-lived, quiescent pancreatic cells. In vitro, Dclk1+ cells proliferate readily and sustain pancreatic organoid growth. In vivo, Dclk1+ cells are necessary for pancreatic regeneration following injury and chronic inflammation. Accordingly, their loss has detrimental effects after cerulein-induced pancreatitis. Expression of mutant Kras in Dclk1+ cells does not affect their quiescence or longevity. However, experimental pancreatitis converts Kras mutant Dclk1+ cells into potent cancer-initiating cells. As a potential effector of Kras, Dclk1 contributes functionally to the pathogenesis of pancreatic cancer. Taken together, these observations indicate that Dclk1 marks quiescent pancreatic progenitors that are candidates for the origin of pancreatic cancer.
Keywords: Carcinoma, Pancreatic Ductal
Rights: © 2016 Elsevier Inc. All rights reserved.
DOI: 10.1016/j.stem.2016.03.016
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