Minireview Dichloroacetate (DCA) as a potential metabolic-targeting therapy for cancer E D Michelakis1, L Webster1 and J R Mackey2 1Department of Medicine, University of Alberta, Edmonton, Canada 2Department of Oncology, University of Alberta, Edmonton, Canada Correspondence: Dr ED Michelakis, Department of Medicine, University of Alberta Hospital, 8440-112 Street, Edmonton, AB, Canada T6G 2B7; E-mail: evangelos.michelakis@capitalhealth.ca 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. British Journal of Cancer (2008) 99, 989–994. doi:10.1038/sj.bjc.6604554 www.bjcancer.com Published online September 2008 Remember we are NOT Doctors and have NO medical training. This site is like an Encylopedia - there are many pages, many links on many topics. Support our work with any size DONATION - see left side of any page - for how to donate. You can help raise awareness of CAM.