KRas, ROS and the initiation of pancreatic cancer

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

Oncogenic mutations of KRAS are the most frequent driver mutations in pancreatic cancer. Expression of an oncogenic allele of KRAS leads to metabolic changes and altered cellular signaling that both can increase the production of intracellular reactive oxygen species (ROS). Increases in ROS have been shown to drive the formation and progression of pancreatic precancerous lesions by upregulating survival and growth factor signaling. A key issue for precancerous and cancer cells is to keep ROS at levels where they are beneficial for tumor development and progression, but below the threshold that leads to induction of senescence or cell death. In KRas-driven neoplasia aberrantly increased ROS levels are therefore balanced by an upregulation of antioxidant genes.

Original languageEnglish (US)
Pages (from-to)1-5
Number of pages5
JournalSmall GTPases
DOIs
StateAccepted/In press - Jun 15 2016

Fingerprint

Pancreatic Neoplasms
Reactive Oxygen Species
Cell signaling
Neoplasms
Mutation
Cell death
Tumors
Intercellular Signaling Peptides and Proteins
Cell Death
Up-Regulation
Antioxidants
Genes
Alleles
Cells

Keywords

  • KRas
  • mitochondria
  • oxidative stress
  • pancreatic cancer
  • PanIN
  • ROS

ASJC Scopus subject areas

  • Biochemistry
  • Cell Biology

Cite this

KRas, ROS and the initiation of pancreatic cancer. / Storz, Peter.

In: Small GTPases, 15.06.2016, p. 1-5.

Research output: Contribution to journalArticle

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