DCA: Long-Awaited Cancer Killer? Not So Fast!

Most entries on this blog discuss groundbreaking research in the late stages of clinical trials or new treatments and medications just approved for use in patients. But I can't resist commenting on fascinating research still in the test tube stage that nevertheless may have implications for cancer treatment down the road-assuming enough funds are found to test it in humans.

Researchers at the University of Alberta in Edmonton, Canada, recently reported in New Scientist that the chemical dichloroacetate (DCA) killed cells from human lung, breast, and brain cancers when they were grown in test tube cultures. DCA did not harm non-cancerous human cells in culture. And adding DCA to the drinking water of laboratory rats decreased the size of the human lung cancer cells grown in the animals.

Why might DCA kill cancer cells?

DCA is an experimental drug that has been tested most often in the treatment of a condition called lactic acidosis, a dangerously high level of lactic acid in the body. Normally, the body removes excess lactic acid through organelles in cells called mitochondria, which also are involved in the conversion of glucose into energy.

We have known for more than 30 years that DCA activates a crucial enzyme within mitochondria required for the conversion of glucose into energy. The high activity of this critical enzyme produced by treatment with DCA speeds the removal of lactic acid.

About 80 years ago, the German biochemist Otto Warburg demonstrated that cancer cells derive most of their energy directly from the breakdown of glucose (a process called glycolysis) rather than the more efficient production of energy by mitochondria. Many efforts have been made to explain this metabolic feature of cancer cells, named the Warburg effect. One possible cause is poorly functioning or damaged mitochondria in cancer cells.

The Canadian researchers now suggest that DCA kills cancer cells by improving the function and even the number of mitochondria, since mitochondria also release substances that cause cells to self-destruct (apoptosis). It's not yet clear why stimulating a critical mitochondrial enzyme should overcome mitochondrial damage or stimulate the formation of more mitochondria.

Understandably, many people with cancer are excited by these findings about DCA. But caution is in order.

Killing cancer cells in test tubes and shrinking tumors in rats is a long way from proving that DCA will work the same way in humans. Clinical trials of DCA in thousands of patients must be done before it could be proven as an effective cancer treatment.

The good news is that DCA is cheap and simple to produce. Because DCA cannot be patented, however, drug companies are unlikely to spend the millions of dollars needed to carry out large clinical trials. Meanwhile, the University of Edmonton is exhorting people to donate money to start some small patient trials.

Cancer patients are warned not to treat themselves with this substance, which can be purchased from chemical companies. Though the authors of the article in New Scientist state that DCA is safe and causes few side effects, previous studies have shown that it can damage nerves and cause pain in some people.

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