ReviewFrontiers in physiology2013
Overview on how oncogenic Kras promotes pancreatic carcinogenesis by inducing low intracellular ROS levels.
Review in Frontiers in physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.
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Who cites it
41 citing papers in PubMed, 1 synthesis or guideline pooled it, 71 citations in OpenAlex.
- Dual roles and therapeutic potential of Keap1-Nrf2 pathway in pancreatic cancer: a systematic review.Cell communication and signaling : CCS · 2019Pooled it
- HypoxamiRs in pancreatic cancer: master regulators of the hypoxic tumor microenvironment.Cell biology and toxicology · 2025Review
- Mitophagy's impacts on cancer and neurodegenerative diseases: implications for future therapies.Journal of hematology & oncology · 2025Review
- Recent Anti-KRASCancers · 2025Review
- The Role of Nrf2 in the Regulation of Mitochondrial Function and Ferroptosis in Pancreatic Cancer.Antioxidants (Basel, Switzerland) · 2024Review
- KRAS Mutation Detection with (2Molecular pharmaceutics · 2024Article
- STAG2 inactivation reprograms glutamine metabolism of BRAF-mutant thyroid cancer cells.Cell death & disease · 2023Article
- An update of Nrf2 activators and inhibitors in cancer prevention/promotion.Cell communication and signaling : CCS · 2022Review
- Therapeutic Targeting of the NRF2 Signaling Pathway in Cancer.Molecules (Basel, Switzerland) · 2021Review
- [A Review of Metabolic Stress and Development of Pancreatic Cancer].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2021Review
- Lipid Metabolism Regulates Oxidative Stress and Ferroptosis in RAS-Driven Cancers: A Perspective on Cancer Progression and Therapy.Frontiers in molecular biosciences · 2021Review
- Beyond the Genomic Mutation: Rethinking the Molecular Biomarkers of K-RAS Dependency in Pancreatic Cancers.International journal of molecular sciences · 2020Review
- The GTPase KRAS suppresses the p53 tumor suppressor by activating the NRF2-regulated antioxidant defense system in cancer cells.The Journal of biological chemistry · 2020Article
- Ferroptosis: Final destination for cancer?Cell proliferation · 2020Review
- Metabolism remodeling in pancreatic ductal adenocarcinoma.Cell stress · 2019Review
- Silencing of Glutathione S-Transferase Pi Inhibits Cancer Cell Growth via Oxidative Stress Induced by Mitochondria Dysfunction.Scientific reports · 2019Article
- ENO1 silencing impaires hypoxia-induced gemcitabine chemoresistance associated with redox modulation in pancreatic cancer cells.American journal of translational research · 2019Article
- Comparison of redox parameters in ovarian endometrioma and its malignant transformation.Oncology letters · 2018Article
- Novel Methylselenoesters Induce Programed Cell Death via Entosis in Pancreatic Cancer Cells.International journal of molecular sciences · 2018Article
- The Nrf2 inhibitor brusatol is a potent antitumour agent in an orthotopic mouse model of colorectal cancer.Oncotarget · 2018Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is a devastating disease without clearly known disease causes. Recent epidemiological and animal studies suggest that the supplementation of dietary antioxidants (e.g., vitamins C and E) decreases cancer risk, implying that increased reactive oxygen species (ROS) may play a role in pancreatic carcinogenesis. However, oncogenic Kras mutations (e.g., Kras(G12D)), which are present in more than 90% of PDAC, have been proven to foster low intracellular ROS levels. Here, oncogenic Kras activates expression of a series of anti-oxidant genes via Nrf2 (nuclear factor, erythroid derived 2, like 2) and also mediates an unusual metabolic pathway of glutamine to generate NADPH. This can then be used as the reducing power for ROS detoxification, leading collectively to low ROS levels in pancreatic pre-neoplastic cells and in cancer cells. In adult stem cells and cancer stem cells, low ROS levels have been associated with the formation of a proliferation-permissive intracellular environment and with perseverance of self-renewal capacities. Therefore, it is conceivable that low intracellular ROS levels may contribute significantly to oncogenic Kras-mediated PDAC formation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.