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Cancer researcher Evangelos Michelakis and his team at University of Alberta in Canada created a sensation in 2007 when they published a research paper claiming that a common chemical dichloroacetate (DCA) (see Figure 1) specifically killed cancer cells in culture without affecting normal cells, and inhibited the growth of human cancerous tumours that developed in rats . (NB: it is the sodium salt of DCA that is used in cancer therapy, and not the acid.)
Figure 1 Sodium dichloroacetate
Unfortunately, there was no support forthcoming from pharmaceutical companies for clinical trials because DCA is a widely available chemical and cannot be patented. Nevertheless, it had been in use for more than 30 years with a good safety record, and there was a strong case for testing the drug in human cancer patients.
Results of first clinical trial promising
With funding from private foundations and public donations as well as the Canadian National Institutes of Health, the team carried out the first clinical trial on five patients with glioblastoma (a fast-growing malignant brain tumour nearly always fatal), and the results were published in 2010 . Of the five patients treated, one of the three with terminal cancer died after 3 months on DCA, but the rest were clinically stable at month 15 of DCA therapy, and still alive at month 18. Three of the patients showed some evidence of the tumour shrinking on magnetic resonance imaging. The results were promising.
One noted side effect of higher doses of DCA was peripheral neuropathy, which was reversed when the dosage was lowered. The team concluded: “Indications of clinical efficacy were present at a dose that did not cause peripheral neuropathy and at serum concentrations of DCA sufficient to inhibit the target enzyme of DCA, pyruvate dehydrogenase kinase II, which was highly expressed in all glioblastomas. Metabolic modulation may be a viable therapeutic approach in the treatment of glioblastomas.”
But Michelakis rightly stressed it is too soon to say whether DCA will provide an effective treatment against cancer in humans, and proper placebo-controlled trials were needed . The trial was complicated by the fact that each patient received different treatments and was also simultaneously on other anti-cancer drugs.
What prompted Michelakis and colleagues to use DCA in treating cancer?
Cancer cells have abnormal energy metabolism
The inspiration to use DCA for cancer therapy came from observations made since the 1920s by German physiologist Otto Heinrich Warburg on the energy metabolism of cancer cells compared with normal cells. Normal cells obtain energy by breaking down the 6-carbon molecule glucose to two 3-carbon pyruvate molecules in a series of reactions in the cytoplasm called glycolysis that does not require oxygen, followed by oxidation reactions in the mitochondria (special ‘power houses’ inside cells) in which oxygen is needed.
Cancer cells, however, depend heavily on glycolysis to obtain energy, and were thought incapable of oxidative metabolism even though sufficient oxygen is present. This phenomenon – aerobic glycolysis subsequently referred to as the Warburg effect – prompted Warburg to propose that mitochondrial malfunction was the primary cause of cancer .
As glycolysis is a much less efficient way of extracting energy from glucose, cancer cells are extra hungry for glucose. Actually, it was later found that not all cancer cells are unable to carry out oxidative metabolisms (see  Cancer a Redox Disease? SiS 54). Some cancer cells appear to have working mitochondria, and in the presence of an adequate oxygen supply, they carry out both glycolysis and oxidative phosphorylation simultaneously, and still generate a lot of lactic acid, the end product of pyruvate that does not get oxidized in the mitochondria.
Warburg’s idea fell into disfavour as the view of cancer as a metabolic disease was gradually displaced with one of cancer as a genetic disease caused by mutations in specific cancer related genes, or oncogenes .
In recent years, positron emission tomography (PET) imaging has confirmed that most malignant tumours have increased glucose uptake and metabolism. But still, this was thought to be an effect of cancer rather than its cause.
The ability of DCA to inhibit cancer and tumour growth is just short of miraculous, and deserves our full attention. It is a cheap, commonly available chemical that selectively kill malignant cells, without hurting normal cells, and with the minimum of side-effects. But its