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Updated: May 7, 2026

Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer
Published on: July 21, 2018
Twenty-fifth annual Pezcoller Symposium: Metabolism and tumorigenesis
William Kaelin1, David Livingston, Massimo Loda
1Authors' Affiliations: Dana Farber Cancer Institute; Harvard Medical School, Boston, Massachusetts; and The Beatson Institute for Cancer Research, Glasgow, Scotland.
Abstract:
Choking cancer via inhibition of metabolic enzymes essential for tumor but dispensable in normal tissues was discussed as was the altered metabolism in cancer cells related to: tumor suppressor protein (pVHL) function, the histone acetylation dependence upon glucose, the epigenomic reprogramming of acetyl CoA synthesis, the plasticity of aging mechanisms, and the metabolism orchestration in macrophage polarization. The p53 and p73 pathways role in metabolic adaptation, the effects on growth of AMP-dependent kinase, the growth regulation by the mTOR pathways, and the bioenergetics requirements of cancer cells were also discussed. A novel computational model of personalized metabolic changes in cancer was outlined with applications in patients with breast cancer. Imaging metabolic characteristics of tumors by MRI and (13)C-nuclear magnetic resonance was described. The cancer metabolism regulation related to O-linked β-N-acetylglucosame was described. DNA hypermethylation and impaired hematopoietic differentiation in AML after isocitrate dehydrogenase 1/2 mutation and 2-hydroxyglutarate increases were outlined.
Insights
Targeting cancer
Area of Science:
- Oncology and Metabolism Research
- Cancer Cell Biology
- Biochemistry and Molecular Biology
Background:
- Altered cellular metabolism is a hallmark of cancer, involving key enzymes and pathways.
- Dysregulation of tumor suppressor proteins like pVHL and signaling pathways (p53, p73, AMPK, mTOR) impacts cancer metabolism.
- Epigenetic modifications, including histone acetylation and acetyl-CoA synthesis, are crucial in cancer development.
Framework:
- Discusses targeting metabolic enzymes essential for tumors but not normal tissues.
- Explores the role of O-linked β-N-acetylglucosamine in cancer metabolism regulation.
- Highlights the interplay between aging, macrophage polarization, and cancer metabolism.
Implementation:
- Introduces a novel computational model for personalized cancer metabolic profiling.
- Details imaging techniques like MRI and (13)C-NMR for visualizing tumor metabolic characteristics.
- Examines metabolic alterations in AML associated with IDH1/2 mutations and 2-hydroxyglutarate accumulation.
Implications:
- Provides insights into novel therapeutic strategies by targeting cancer-specific metabolic vulnerabilities.
- Enables personalized medicine approaches through computational modeling and advanced imaging.
- Advances understanding of metabolic reprogramming in cancer and its clinical relevance.
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