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• W2018971639 abstract "The unique metabolism of most solid tumours (aerobic glycolysis, i.e., Warburg effect) is not only the basis of diagnosing cancer with metabolic imaging but might also be associated with the resistance to apoptosis that characterises cancer. The glycolytic phenotype in cancer appears to be the common denominator of diverse molecular abnormalities in cancer and may be associated with a (potentially reversible) suppression of mitochondrial function. The generic drug dichloroacetate is an orally available small molecule that, by inhibiting the pyruvate dehydrogenase kinase, increases the flux of pyruvate into the mitochondria, promoting glucose oxidation over glycolysis. This reverses the suppressed mitochondrial apoptosis in cancer and results in suppression of tumour growth in vitro and in vivo. Here, we review the scientific and clinical rationale supporting the rapid translation of this promising metabolic modulator in early-phase cancer clinical trials." @default.
• W2018971639 created "2016-06-24" @default.
• W2018971639 creator A5021152638 @default.
• W2018971639 creator A5032920417 @default.
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• W2018971639 date "2008-09-02" @default.
• W2018971639 modified "2023-10-14" @default.
• W2018971639 title "Dichloroacetate (DCA) as a potential metabolic-targeting therapy for cancer" @default.
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• W2018971639 doi "https://doi.org/10.1038/sj.bjc.6604554" @default.
• W2018971639 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2567082" @default.
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• W2018971639 hasPublicationYear "2008" @default.
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