Oncometabolites: unconventional triggers of oncogenic signalling cascades
Free Radical Biology & Medicine
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Sciacovelli, M., & Frezza, C. (2016). Oncometabolites: unconventional triggers of oncogenic signalling cascades. Free Radical Biology & Medicine, 100 (18), 175-181. https://doi.org/10.1016/j.freeradbiomed.2016.04.025
Cancer is a complex and heterogeneous disease thought to be caused by multiple genetic lesions. The recent finding that enzymes of the tricarboxylic acid (TCA) cycle are mutated in cancer rekindled the hypothesis that altered metabolism might also have a role in cellular transformation. Attempts to link mitochondrial dysfunction to cancer uncovered the unexpected role of small molecule metabolites, now known as oncometabolites, in tumorigenesis. In this review, we describe how oncometabolites can contribute to tumorigenesis. We propose that lesions of oncogenes and tumour suppressors are only one of the possible routes to tumorigenesis, which include accumulation of oncometabolites triggered by environmental cues.
mitochondria, cancer, oncometabolites, FH, SDH, IDH, fumarate, succinate, 2-hydroxyglutarate
MS and CF are funded by an MRC Core Funding to the MRC Cancer Unit.
MRC (MC_UU_12022/1_do not transfer?)
Medical Research Council (MC_UU_12022/6)
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External DOI: https://doi.org/10.1016/j.freeradbiomed.2016.04.025
This record's URL: https://www.repository.cam.ac.uk/handle/1810/255829
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