Prevention and Reversion of Pancreatic Tumorigenesis through a Differentiation-Based Mechanism

Nathan M. Krah, Shuba M. Narayanan, Deanne E. Yugawa, Julie A. Straley, Christopher V.E. Wright, Raymond J MacDonald, L. Charles Murtaugh

Research output: Contribution to journalArticle

1 Scopus citations

Abstract

Pancreatic cancer arises from mutations in exocrine acinar cells. Krah et al. demonstrate that preserving acinar cell identity protects these cells from oncogenic Kras-induced tumorigenesis. Furthermore, re-expressing the acinar differentiation gene Ptf1a in existing precancerous lesions in vivo, or human pancreatic cancer cells in vitro, induces quiescence and re-differentiation.

Original languageEnglish (US)
Pages (from-to)744-754.e4
JournalDevelopmental Cell
Volume50
Issue number6
DOIs
StatePublished - Sep 23 2019

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Keywords

  • acinar cell
  • differentiation
  • Kras
  • pancreas
  • pancreatic cancer
  • Ptf1a

ASJC Scopus subject areas

  • Molecular Biology
  • Biochemistry, Genetics and Molecular Biology(all)
  • Developmental Biology
  • Cell Biology

Cite this

Krah, N. M., Narayanan, S. M., Yugawa, D. E., Straley, J. A., Wright, C. V. E., MacDonald, R. J., & Murtaugh, L. C. (2019). Prevention and Reversion of Pancreatic Tumorigenesis through a Differentiation-Based Mechanism. Developmental Cell, 50(6), 744-754.e4. https://doi.org/10.1016/j.devcel.2019.07.012