Chemotherapy, DCA and Mitochondria

It's one of the hottest areas of biology said Simon Melov, director of genomics at the Buck Institute for Age Research who reviewed recent research in the October issue of Trends in Neuroscience. Last spring, scientists in Sweden provided some of the strongest evidence yet. They shortened the life of mice and created signs of old age by injecting a small genetic defect into the mice's mitochondria.

No one single molecule is going to cure all cancers by itself. But combinations of compounds that each toxicity highly specific to cancer cells will certainly end up curing a great many cancers. Monoclonal antibodies targetted at cancers, anti-angiogenesis compounds that block blood vessel growth in cancers, gene therapies that activate in cancer cells and assorted other compounds such as dichloroacetate (DCA) are going to cure many cancers when used in combination. I think DCA can be selective for cancer because it attacks a fundamental process in cancer development that is unique to cancer cells.

Mitochondria activation reduces cancer. Cancer cells actively suppress their mitochondria, which alters their metabolism, and this appears to offer cancer cells a significant advantage in growth compared to normal cells, as well as protection from many standard chemotherapies. Because mitochondria regulate cell death - or apoptosis - cancer cells can thus achieve resistance to apoptosis, and this appears to be reversed by DCA. DCA might work well in combination with anti-angiogenesis drugs since the ability of anti-angiogenesis drugs to block blood vessel growth will decrease the amount of oxygen available to tumors and therefore make more cells in tumors susceptible to the effects of DCA.