Notch1 functions as a tumor suppressor in a model of K-ras-induced pancreatic ductal adenocarcinoma

Linda Hanlon, Jacqueline L. Avila, Renée M. Demarest, Scott Troutman, Megan Allen, Francesca Ratti, Anil K. Rustgi, Ben Z. Stanger, Fred Radtke, Volkan Adsay, Fenella Long, Anthony J. Capobianco, Joseph L. Kissil

Research output: Contribution to journalArticlepeer-review

118 Scopus citations


K-ras is the most commonly mutated oncogene in pancreatic cancer and its activation in murine models is sufficient to recapitulate the spectrum of lesions seen in human pancreatic ductal adenocarcinoma (PDAC). Recent studies suggest that Notch receptor signaling becomes reactivated in a subset of PDACs, leading to the hypothesis that Notch1 functions as an oncogene in this setting. To determine whether Notch1 is required for K-ras-induced tumorigenesis, we used a mouse model in which an oncogenic allele of K-ras is activated and Notch1 is deleted simultaneously in the pancreas. Unexpectedly, the loss of Notch1 in this model resulted in increased tumor incidence and progression, implying that Notch1 can function as a tumor suppressor gene in PDAC.

Original languageEnglish (US)
Pages (from-to)4280-4286
Number of pages7
JournalCancer Research
Issue number11
StatePublished - Jun 1 2010
Externally publishedYes

ASJC Scopus subject areas

  • Oncology
  • Cancer Research


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