KRas, ROS and the initiation of pancreatic cancer
Open accessAbstract
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.
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Oncogenic KRAS mutation plays a crucial role in initiation and progression of PDAC by inducing ROS generation through metabolic changes.
“Oncogenic KRAS mutation plays a crucial role in the initiation and progression of PDAC by inducing reactive oxygen species (ROS) generation through metabolic changes.”
From Significance of TP53, CDKN2A, SMAD4 and KRAS in Pancreatic Cancer (2024) · cites this paper as [122]
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- Authors
- Storz, P.
- Venue
- Small GTPases
- Publisher
- Informa UK Limited
- Published
- 2016-05-24
- Volume
- 8
- Issue
- 1
- Pages
- 38-42
- ISSN
- 2154-1248 (ISSN-L)
- 2154-1256
- PMC
- PMC5331894
- OpenAlex
- W2397520720
- Cited by
- 82
- References
- 42
- Citations by year
- 2026: 4 · 2025: 12 · 2024: 5 · 2023: 8 · 2022: 11 · 2021: 15 · 2020: 14 · 2019: 4 · 2018: 3 · 2017: 3 · 2016: 3
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Small GTPases (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Pancreatic Cancer Action Network
- National Institutes of Health (CA200572)
- National Cancer Institute (R01CA200572, R01CA140182, CA200572, CA140182)
- Topics
- Health Sciences › Medicine › Oncology › Pancreatic and Hepatic Oncology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Keywords
- KRAS mutation, reactive oxygen species, pancreatic cancer initiation, pancreatic precancerous lesions, oncogenic KRAS, antioxidant genes, cellular senescence, growth factor signaling, tumor progression, oxidative stress
- MeSH terms
- Humans, Mitochondria, Mutation, Pancreatic Neoplasms, Signal Transduction, Proto-Oncogene Proteins p21(ras), Reactive Oxygen Species, Disease Progression
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