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Fig. 2 | Radiation Oncology

Fig. 2

From: Oncometabolites and the response to radiotherapy

Fig. 2

Schematic representation of how oncometabolites can modulate radiosensitivity. The indicated oncometabolites (orange) can accumulate as a consequence of mutations of TCA cycle enzymes or environmental cues, such as hypoxia and even without oncogenic mutations e.g. by pharmacologic inhibition of SLC25A1. 2-HG, succinate and fumarate induce metabolic reprogramming and a “pseudo-hypoxic phenotype” via stabilisation of HIF1α. Moreover, indicated oncometabolites are competitive inhibitors of the αKG-dependent KDM and TET families of epigenetic enzymes, thereby modulating DNA repair and pathway choice and offer novel therapeutic opportunities with IR. αKG = α-Ketoglutarate, C = cytosine, K = Lysin, L/D-2-HG = L/D-2-hydroxyglutarate, mt = mutant, Orange colour represents increased metabolite levels

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