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D-2-Hydroxyglutarate in Glioma Biology
Fu-Ju Chou1, Yang Liu1, Fengchao Lang1
1Neuro-Oncology Branch Center for Cancer Research, National Cancer Institute, National Institutes of Health, Building 37, Room 1142E, Bethesda, MD 20892, USA.
Cells
|September 28, 2021
Summary
Isocitrate dehydrogenase (IDH) mutations in glioma cause D-2-hydroxyglutarate (D-2-HG) accumulation. This oncometabolite impacts cancer biology by inhibiting key enzymes, affecting methylation and DNA repair, and presents therapeutic targets.
Area of Science:
- Oncology
- Cancer Biology
- Biochemistry
Background:
- Isocitrate dehydrogenase (IDH) mutations are prevalent in glioma.
- These mutations lead to the accumulation of D-2-hydroxyglutarate (D-2-HG), an oncometabolite.
- Elevated D-2-HG impacts cellular processes by inhibiting α-ketoglutarate (α-KG)/Fe(II)-dependent dioxgenases (α-KGDDs).
Purpose of the Study:
- To review the role of D-2-HG in the cancer biology of IDH-mutated gliomas.
- To explore emerging therapeutic strategies targeting D-2-HG pathways.
Main Methods:
- Literature review of recent studies on D-2-HG.
- Analysis of D-2-HG's effects on DNA/histone methylation, hypoxia signaling, DNA repair, and redox homeostasis.
Main Results:
- D-2-HG influences multiple oncogenic pathways in IDH-mutated cancers.
- Key affected processes include epigenetic modifications and cellular signaling.
Conclusions:
- D-2-HG plays a critical role in the pathogenesis of IDH-mutated glioma.
- Understanding D-2-HG's functions opens avenues for novel therapeutic interventions.
