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Notch and Kras reprogram pancreatic acinar cells to ductal intraepithelial neoplasia.
Proc Natl Acad Sci U S A. 2008 Dec 2;105(48):18907-12. doi: 10.1073/pnas.0810111105. Epub 2008 Nov 21.
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Spontaneous induction of murine pancreatic intraepithelial neoplasia (mPanIN) by acinar cell targeting of oncogenic Kras in adult mice.
Proc Natl Acad Sci U S A. 2008 Dec 2;105(48):18913-8. doi: 10.1073/pnas.0810097105. Epub 2008 Nov 21.
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Hedgehog signaling is required for effective regeneration of exocrine pancreas.
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Notch signaling is required for exocrine regeneration after acute pancreatitis.
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In vivo lineage tracing defines the role of acinar-to-ductal transdifferentiation in inflammatory ductal metaplasia.
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Acinar cells contribute to the molecular heterogeneity of pancreatic intraepithelial neoplasia.
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Preexisting pancreatic acinar cells contribute to acinar cell, but not islet beta cell, regeneration.
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The Nestin progenitor lineage is the compartment of origin for pancreatic intraepithelial neoplasia.
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Chronic pancreatitis is essential for induction of pancreatic ductal adenocarcinoma by K-Ras oncogenes in adult mice.
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