Metabolic enzymes as oncogenes or tumor suppressors
Open accessAbstract
Whether mutations in metabolic pathways contribute to the pathogenesis of cancer is controversial.1,2 Cancer cells have long been noted to preferentially metabolize glucose through glycolysis, a discovery that has been translated to the clinic through positron-emission-tomography imaging of 18F-deoxyglucose uptake in tumors. Moreover, recent studies have uncovered recurrent somatic mutations in four genes involved in the metabolism of mitochondrial citrate that either cause or predispose cells to become malignant.In this issue of the Journal, Yan and colleagues3 report that 70% or more of low-grade gliomas bear mutations in one of two NADP+-dependent isocitrate dehydrogenase enzymes (IDH1 and . . .
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Cancer is associated with metabolic mutations confined to the tumor, in which metabolic enzymes behave genetically as oncogenes or tumor suppressors.
“Recently it has become apparent that cancer is also associated with metabolic mutations confined to the tumor. In these diseases, the metabolic enzymes behave genetically as oncogenes or tumor suppressors (Figure 3A) (Frezza et al., 2011a; Thompson, 2009).”
From Cellular Metabolism and Disease: What Do Metabolic Outliers Teach Us? (2012) · cites this paper as Thompson, 2009
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Puzzling Patterns of Predisposition
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Nitric oxide and tumor metabolic reprogramming
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- Authors
- Thompson, C. B.
- Affiliations
- University of Pennsylvania (US)
- Corresponding author
- Thompson, Craig B.
- ORCID
- Thompson, Craig B.
- Venue
- New England Journal of Medicine
- Publisher
- Massachusetts Medical Society
- Published
- 2009-02-19
- Volume
- 360
- Issue
- 8
- Pages
- 813-815
- ISSN
- 0028-4793 (ISSN-L)
- 1533-4406
- PMC
- PMC2848669
- OpenAlex
- W2075033593
- Cited by
- 213
- References
- 12
- Citations by year
- 2026: 2 · 2024: 12 · 2023: 4 · 2022: 15 · 2021: 8 · 2020: 7 · 2019: 10 · 2018: 11 · 2017: 9 · 2016: 10 · 2015: 11 · 2014: 14 · 2013: 18 · 2012: 16
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- New England Journal of Medicine (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Cancer Institute (P01CA104838, R01CA092660, R01CA105463)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
- Health Sciences › Medicine › Genetics › Glioma Diagnosis and Treatment
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Lipids, and Metabolism
- Keywords
- metabolic enzymes, oncogenes, tumor suppressor, isocitrate dehydrogenase, IDH1, IDH2, low-grade glioma, somatic mutations, cancer metabolism, glycolysis
- MeSH terms
- Brain Neoplasms, DNA Mutational Analysis, Fumarate Hydratase, Glioblastoma, Glioma, Humans, Isocitrate Dehydrogenase, Mutation, Succinate Dehydrogenase, Hypoxia-Inducible Factor 1
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