Researcher Finds Anti-Cancer Agent Is No Wonder Drug

November 22, 2010 - News Release

A University of Guelph study has found that a prescription drug thought to have anti-cancer properties when used off-label may not only be less effective than claimed but may actually protect some kinds of cancers.

"Sodium dichloroacetate is not very effective at killing some kinds of cancer cells and, in fact, it has the opposite effect and could even make things worse,” said Brenda Coomber, a professor in the Department of Biomedical Sciences in Guelph’s Ontario Veterinary College.

This research was published recently in the journal Cancer Letters.

Developed three decades ago to treat a rare serious metabolic disorder in children, sodium dichloroacetate (DCA) has been touted as a safe, inexpensive anti-cancer drug.

In patients with this metabolic disorder, DCA “resets” malfunctioning mitochondria to restore the body’s normal energy pathway. Mitochondria are cellular “power plants” that convert glucose into energy. Normally, they also generate oxygen radicals used in further metabolism but that are also toxic to cells. Mitochondria also help trigger cell death, a normal part of tissue growth and health.

Scientists believe that, when oxygen is present, DCA forces cancer cells to use the mitochondrial pathway, producing oxygen radicals that kill the cancer cells while leaving normal cells unharmed. Studies of brain tumours have found that DCA selectively kills cancer cells without damaging normal tissue.

But that’s not what Coomber found with colorectal cancer. Along with her team — research associate Siranoush Shahrzad, graduate students Kristen Lacombe and Una Adamic, and technician Kanwal Minhas — she looked at ischemic regions of tumours, or areas with low oxygen and nutrients due to abnormal blood flow. They had expected that, under fluctuating oxygen levels, DCA treatment would force cancer cells to use the mitochondrial pathway, generate oxygen radicals and die.

In normal culture, DCA killed some human colon cancer cells. But under low oxygen, the same cancer cells were more likely to survive. In mice with human colon cancer cells grown as tumours, DCA provided no therapeutic benefit; in fact, some treated tumours grew better than untreated ones. Fewer cells in ischemic regions died in DCA-treated tumours than in untreated ones.

“The bottom line is that cancer is not a single disease, so it’s unrealistic to expect a single drug to be a ‘magic bullet’ that’s effective against every type of cancer,” Coomber said, adding that many factors influence how cancer cells develop and behave.

“We are only beginning to tease these things out. DCA may well turn out to be an effective treatment in some cases, but it’s not necessarily safe in all cases. There are people out there buying this drug off the Internet and self-medicating — who knows what’s going on in their tumour? They might actually be making it worse.”

Her team now plans to study the pathways DCA uses to protect some cancer cells.

This research was funded by the Canadian Cancer Society’s Research Institute.

Prof. Brenda Coomber
Department of Biomedical Sciences
519-824-4120, Ext. 54922

For media questions, contact Communications and Public Affairs: Lori Bona Hunt, at 519-824-4120, Ext. 53338, or, or Deirdre Healey, Ext. 56982 or

University of Guelph
50 Stone Road East
Guelph, Ontario, N1G 2W1