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. Author manuscript; available in PMC: 2015 Oct 21.
Published in final edited form as: Curr Opin Oncol. 2012 Jan;24(1):83–89. doi: 10.1097/CCO.0b013e32834d816a

Table 1.

Pathways potentially altered by IDH1/2 mutations in glioma

Tissue studied Alteration
Methylation IDH1 mutant gliomas Hypermethylated pathways Hypomethylated pathways
Methane metabolism Protein kinase A signaling
Pregnane X receptor/retinoid X receptor activation Angiopoietin signaling
Retinol metabolism Ras-related nuclear protein signaling
Phenylalanine metabolism Retinol transport
Starch and sucrose metabolism Cell cycle regulation
Pentose and glucuronate interconversion Methylated-DNA-protein-cysteine methyltransferase (MGMT)
Androgen and estrogen metabolism Fatty acid binding
Transcription G-CIMP-positive gliomas Increased Decreased
Transcriptional regulation Polysaccharide binding
Nucleic acid synthesis Heparin binding
Metabolic processes Glucosaminoglycan binding
Cadherin based cell adhesion Collagen
Zinc finger transcription factors Thrombospondin
Cell morphogenesis
Retinoic acid signaling
Fatty acid binding
Metabolism IDH1/2 mutant cells or cells treated with d-2-HG Increased Decreased
d-2-HG NAAG
Glycerol-3-phosphate NAA
Glycerol-2-phosphate 2-Methyl butyryl carnitine
Glycine Isobutyl carnitine
Asparagine α-Aminoadipate
Glutamine Phosphocholine
Serine Propionylcarnitine
Threonine Malate
Phenylalanine Fumarate
Tyrosine Citrate
Tryptophan
Methionine

d-2-HG, d-2-hydroxyglutarate; NAA, N-acetylated aspartic acid; NAAG, N-acetyl-aspartyl glutamate. Data from [20,35,36▪,37▪▪,44▪].