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Significance Mutation of isocitrate dehydrogenase 1 (IDH1 ) is believed to be the initiating event for the majority of secondary glioblastomas and lower-grade diffuse gliomas; however, the basis for tissue specificity of oncogenesis initiated byIDH1 mutation has not been apparent. We report evidence to suggest that specialization of human neocortex for glutaminergic neurotransmission provides a metabolic niche particularly suited for growth ofIDH1 R132H glioma. Our findings reveal thatIDH1 -mutant enzyme challenges growth of murine glioma progenitor cells but that these cells thrive if they are engineered to express the hominoid-specific brain enzyme GLUD2, a mitochondrial enzyme that converts glutamate to alpha-ketoglutarate in human cortex. The current findings raise the possibility that evolutionary changes contributing to human cognitive abilities may have conferred vulnerability to brain tumors driven byIDH1 mutation.

Hominoid-specific enzyme GLUD2 promotes growth of IDH1 R132H glioma

Hominoid-specific enzyme GLUD2 promotes growth of IDH1 ^R132H glioma