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Dichloroacetate (DCA) inhibits pyruvate dehydrogenase kinase (PDK), helping shift cancer cells away from the “Warburg effect” (their tendency to rely heavily on glycolysis and produce excess lactate). Earlier preclinical studies provided evidence that DCA may alter GBM metabolism and potentially make tumor cells more vulnerable to cell death.
A new study has now provided additional evidence that DCA reaches recurrent GBMs and produces the intended metabolic changes. In 37 patients undergoing surgery for recurrent GBM, patients received either one week of DCA or no DCA prior to surgery. The resected enhancing and non-enhancing tumor tissue, and serial plasma DNA and lactate levels were analyzed. Patients who received the DCA had reduced markers of PDK activity and tumor-cell proliferation and significantly lowered blood lactate levels. DCA was well tolerated, but the study did not show that DCA improved progression-free survival. The researchers conclude that, although the study did not show a clinical benefit, the metabolic effects warrant further investigation, particularly in combination with other treatments.