Effect of cigarette smoke exposure and mutant Kras overexpression on pancreatic cell proliferation

Howard P. Glauert, R. Scott Elliott, Sung Gu Han, Mark Athey, Eun Y. Lee, C. Gary Gairola

Research output: Contribution to journalArticlepeer-review

4 Scopus citations


Pancreatic cancer is the fourth leading cause of cancer-associated mortality. The major risk factor for pancreatic cancer is cigarette smoking. Kras mutations are commonly observed in human pancreatic cancers. The present study examined the hypothesis that exposure to cigarette smoke and overexpression of a mutant Kras gene in the pancreas affects pancreatic cell proliferation in mice. Mice overexpressing the mutant Kras gene (KRasG12D) in the pancreas as well as wild-type mice were exposed to environmental tobacco smoke for 2 weeks. Overexpression of mutant Kras increased cell proliferation in pancreatic ductal, acinar and islet cells. Notably, cigarette smoke exposure decreased cell proliferation in pancreatic ductal and acinar cells, and had no effect in islet cells. Cigarette smoke did not affect pancreatic protein levels of tumor necrosis factor (TNF)α, p53, or cyclin D1, but mutant Kras overexpression slightly decreased TNFα and p53 protein levels. Therefore, pancreatic cell proliferation in mice overexpressing mutant Kras is associated with the later development of pancreatic tumors, but effects of cigarette smoke on pancreatic cell proliferation do not provide a good model for human pancreatic carcinogenesis.

Original languageEnglish
Pages (from-to)1939-1943
Number of pages5
JournalOncology Letters
Issue number3
StatePublished - Mar 2017

Bibliographical note

Publisher Copyright:
© 2017, Spandidos Publications. All rights reserved.


  • Cell proliferation
  • Cigarette smoke
  • Kras
  • Pancreas

ASJC Scopus subject areas

  • Oncology
  • Cancer Research


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