Acute pancreatitis markedly accelerates pancreatic cancer progression in mice expressing oncogenic Kras

Catherine Carrière, Alison L. Young, Jason R. Gunn, Daniel S. Longnecker, Murray Korc

Research output: Contribution to journalArticle

118 Citations (Scopus)

Abstract

Chronic pancreatitis increases by 16-fold the risk of developing pancreatic ductal adenocarcinoma (PDAC), one of the deadliest human cancers. It also appears to accelerate cancer progression in genetically engineered mouse models. We now report that in a mouse model where oncogenic Kras is activated in all pancreatic cell types, two brief episodes of acute pancreatitis caused rapid PanIN progression and accelerated pancreatic cancer development. Thus, a brief inflammatory insult to the pancreas, when occurring in the context of oncogenic KrasG12D, can initiate a cascade of events that dramatically enhances the risk for pancreatic malignant transformation.

Original languageEnglish (US)
Pages (from-to)561-565
Number of pages5
JournalBiochemical and Biophysical Research Communications
Volume382
Issue number3
DOIs
StatePublished - May 8 2009
Externally publishedYes

Fingerprint

Pancreatic Neoplasms
Pancreatitis
Chronic Pancreatitis
Pancreas
Neoplasms
Adenocarcinoma

Keywords

  • Acute pancreatitis
  • Kras
  • PDAC

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Cell Biology
  • Molecular Biology

Cite this

Acute pancreatitis markedly accelerates pancreatic cancer progression in mice expressing oncogenic Kras. / Carrière, Catherine; Young, Alison L.; Gunn, Jason R.; Longnecker, Daniel S.; Korc, Murray.

In: Biochemical and Biophysical Research Communications, Vol. 382, No. 3, 08.05.2009, p. 561-565.

Research output: Contribution to journalArticle

Carrière, Catherine ; Young, Alison L. ; Gunn, Jason R. ; Longnecker, Daniel S. ; Korc, Murray. / Acute pancreatitis markedly accelerates pancreatic cancer progression in mice expressing oncogenic Kras. In: Biochemical and Biophysical Research Communications. 2009 ; Vol. 382, No. 3. pp. 561-565.
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