In February 2007, researchers at Appalachian State University announced the results of a clinical study on the flavonoid quercetin at the Southeastern Regional Meeting of the American College of Sports Medicine, held in Charlotte, N.C. Their results showed that quercetin may help reduce illness and maintain mental performance in physcially stressed test subjects. I’ve written about the antioxidant quercetin in a previous article as an alternative to dichloroacetate (DCA), a chemotherapeutic agent that was recently shown to selectively inhibit cancer cell growth in lung, breast and brain tumor cells grown in culture and lung tumors grown in immunocompromisted rats.
Alternative to Dichloroacetate
May 4, 2007 | by
It’s been three months since an article on dichloroacetate (DCA), the chemotherapeutic agent that selectively inhibits cancer cell growth in lung, breast and brain tumor cells grown in culture and lung tumors grown in immunocompromised rats, was published on Highlight HEALTH. Since then, thousands of people have read the article. Indeed, the blogosphere has been buzzing about DCA, unfortunately focusing on a conspiracy theory accusing big pharma of suppressing a cure for cancer instead of recognizing the study for what it is — a preliminary study in cell culture and rats that cannot be translated to humans without further research and clinical trials.
Dichloroacetate Not Ready for Therapeutic Use
February 11, 2007 | by
Dichloroacetate has been in the headlines recently, reported to be a cheap, effective cancer cure. The article was published in both print and on the website NewScientist.com, and ran with the headline “Cheap, safe drug kills most cancers”, implying incorrectly that it can kill tumor cells in humans.
Researchers at the University of Alberta in Edmonton, Canada, recently reported that they found a cheap and easy drug to produce that is able to cause tumor regression in lung, breast and brain tumor cells grown in culture and lung tumors grown in immunocompromised rats. The drug, Dichloroacetate (DCA), targets mitochondria (meaning an organelle in the cell that produces energy) and induces apoptosis (meaning cell death), decreases proliferation and selectively inhibits cancer cell growth. It did not have any effects on normal, non-cancerous tissue. The findings were published in the January edition of the journal Cancer Cell.
Cancer cells don’t use mitochondria for energy, instead using glycolysis (meaning the initial process of most of carbohydrate metabolism), which is less effective and more wasteful. Researchers have long believed this occurred because mitochondria in cancer cells were damaged. However, this new data suggests that the mitochondria in cancer cells are dormant and DCA reactivates them.
