Scientists Cure Cancer, But No One Takes Notice (continued)
Scientists used to think that these mitochondria cells were damaged and thus ineffective against cancer.
So they used to focus on glycolysis, which is less effective in curing cancer and more wasteful. The drug manufacturers focused on this glycolysis method to fight cancer.
This DCA on the other hand doesn't rely on glycolysis instead on mitochondria; it triggers the mitochondria which in turn fights the cancer cells.
The side effect of this is it also reactivates a process called apoptosis. You see, mitochondria contain an all-too-important self-destruct button that can't be pressed in cancer cells. Without it, tumors grow larger as cells refuse to be extinguished. Fully functioning mitochondria, thanks to DCA, can once again die.
With glycolysis turned off, the body produces less lactic acid, so the bad tissue around cancer cells doesn't break down and seed new tumors.
Pharmaceutical companies are not investing in this research because DCA method cannot be patented, without a patent they can't make money, like they are doing now with their AIDS Patent.
Since the pharmaceutical companies won't develop this, the article says other independent laboratories should start producing this drug and do more research to confirm all the above findings and produce drugs.
All the groundwork can be done in collaboration with the Universities, who will be glad to assist in such research and can develop an effective drug for curing cancer.
This article wants to raise awareness for this study, hope some independent companies and small startup will pick up this idea and produce these drugs, because the big companies won't touch it for a long time.
RESEARCH PUBLISHED HERE
Metabolic Modulation of Glioblastoma with Dichloroacetate
1. E. D. Michelakis1,*,
2. G. Sutendra1,
3. P. Dromparis1,
4. L. Webster1,
5. A. Haromy1,
6. E. Niven2,
7. C. Maguire2,
8. T.-L. Gammer1,
9. J. R. Mackey3,
10. D. Fulton3,
11. B. Abdulkarim3,
12. M. S. McMurtry1 and
13. K. C. Petruk4
+ Author Affiliations
1Department of Medicine, University of Alberta, Edmonton, Alberta, Canada T6G 2B7.
2Department of Biomedical Engineering and Diagnostic Imaging, University of Alberta, Edmonton, Alberta, Canada T6G 2B7.
3Department of Oncology, University of Alberta, Edmonton, Alberta, Canada T6G 2B7.
4Department of Neurosurgery, University of Alberta, Edmonton, Alberta, Canada T6G 2B7.
1. *To whom correspondence should be addressed. E-mail: firstname.lastname@example.org
AbstractBack to Top
Solid tumors, including the aggressive primary brain cancer glioblastoma multiforme, develop resistance to cell death, in part as a result of a switch from mitochondrial oxidative phosphorylation to cytoplasmic glycolysis. This metabolic remodeling is accompanied by mitochondrial hyperpolarization. We tested whether the small-molecule and orphan drug dichloroacetate (DCA) can reverse this cancer-specific metabolic and mitochondrial remodeling in glioblastoma. Freshly isolated glioblastomas from 49 patients showed mitochondrial hyperpolarization, which was rapidly reversed by DCA. In a separate experiment with five patients who had glioblastoma, we prospectively secured baseline and serial tumor tissue, developed patient-specific cell lines of glioblastoma and putative glioblastoma stem cells (CD133+, nestin+ cells), and treated each patient with oral DCA for up to 15 months. DCA depolarized mitochondria, increased mitochondrial reactive oxygen species, and induced apoptosis in GBM cells, as well as in putative GBM stem cells, both in vitro and in vivo. DCA therapy also inhibited the hypoxia-inducible factor1α, promoted p53 activation, and suppressed angiogenesis both in vivo and in vitro. The dose-limiting toxicity was a dose-dependent, reversible peripheral neuropathy, and there was no hematologic, hepatic, renal, or cardiac toxicity. Indications of clinical efficacy were present at a dose that did not cause peripheral neuropathy and at serum concentrations of DCA sufficient to inhibit the target enzyme of DCA, pyruvate dehydrogenase kinase II, which was highly expressed in all glioblastomas. Metabolic modulation may be a viable therapeutic approach in the treatment of glioblastoma.
FootnotesBack to Top
Citation: E. D. Michelakis, G. Sutendra, P. Dromparis, L. Webster, A. Haromy, E. Niven, C. Maguire, T.-L. Gammer, J. R. Mackey, D. Fulton, B. Abdulkarim, M. S. McMurtry, K. C. Petruk, Metabolic modulation of glioblastoma with dichloroacetate. Sci. Transl. Med. 2, 31ra34 (2010).
* Copyright © 2010, American Association for the Advancement of Science
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