How to Cure Cancer - Cure Medical Research
Cancer is not a medical problem; it is a human problem. Ever since the war on cancer was unleashed in 1971, very little progress has been made in the fight because the research system is itself suffering from cancer.
There are several agents which I’ve been made aware of which have not been given the due attention by the medical research establishment. For example, 3-Bromopyruvate, discovered at John Hopkins has completely eradicated liver cancer in murine trials. This discovery was made in 2004 with very little follow up research conducted.
In 2007, Dr. Evangelos Michelakis at the University of Alberta tried Dichloroacetate (DCA) on rats with giant tumors. Three short weeks later the tumors had dramatically reduced in size. He had a ‘eureka’ moment because DCA, if it worked in humans, would be the holy grail of cancer treatment: one that did not harm regular cells and it worked against a broad spectrum of human cancers.
Dr. Michelakis published his paper waiting to receive his laurels. His paper was met largely by silence. The problem is that DCA is an old, simple chemical which has successfully been used in humans for years in an unrelated condition: Congenital Lactic Acidosis. As such, the chemical is not eligible for a patent and the mainstream pharmacy companies are therefore not interested.
What all oncology researchers acknowledge is that Dr. Michelakis has revealed an entirely new course of attack against cancer: a metabolic approach. It was and is still commonly held that the mitochondria in cancer cells are damaged beyond repair. This causes the cancer cells to use the less efficient, more primitive, glycolysis as a fuel source. Since cancer cells are, individually, less efficient than the rest of the body’s cells, the common approach is chemotherapy based upon this differential survivability.
The chemotherapy approach, trying to ‘outgun’ the cancer cells, represents a fundamental misunderstanding of the underlying symbiosis that exists everyday in our cells. 2.5 Million years ago, Eukaryotic cells first appeared. Lynn Margulis (“Symbiosis in Cell Evolution”, 1981) suggests that mitochondria and cholorplasts were once separate organisms which were ingested and entered into symbiosis with the host cells. (See figure 1) Both mitochondria and choloroplasts use a proton gradient developed across an internal membrane to perform their benefits to the cell. The choloroplasts build sugar from CO2 and the mitochondria produce ATP from sugar in a far more efficient manner than glycolysis.
During this symbiosis and co-evolution some mitochondrial functions, indeed mitochondrial DNA, has migrated into the nucleus. Most notably, aptopsis has not migrated into the nucleus. Aptopsis is still a mitochondrial function. Thus if the mitochondria are deactivated or incapacitated by a lack of oxygen or other environmental insult, the cells revert to anaerobic metabolism and moreover, are effectively immortal. This corroborates the Warburg Hypothesis of the early 20th century which is summarized by his own quote: “Deprive a cell 35% of its oxygen for 48 hours and it may become cancerous.”
Figure 1: Serial Endosymbiosis Theory
Enter into the equation DCA. Generally speaking, DCA reactivates the mitochondria which were merely (it turns out) dormant, not damaged beyond recovery. In a cancerous cell, ‘Myc’ an oncoprotein stimulates PDK which goes on to antagonize PDK preventing Pyruvate’s transformation to Acetyl Co-A. This in effect halts the Citric Acid Cycle, stalling aerobic respiration and rendering the mitochondria dormant. DCA antagonizes the activity of PDK which in turn prevents the antagonizing of PDH. Pyruvate is now able to transform to Acetyl Co-A and aerobic respiration resumes. (see centre of figure 2) Critically, the mitochondria, now restarted is able to detect the cell is in an abnormal state and immediately effects aptopsis. DCA is capable of restoring successful symbiosis. Further, cancer should no longer be thought of as a simple malfunction, but rather a cellular dysbiosis.
In May 2010 Dr Michelakis was published the results of a Phase I trial of DCA in glioblastoma patients. The study included 5 patients and confirmed that the metabolic action of DCA in humans was the same as that in rats. Dr. Michelakis was able to secure funding for the trial via private investment and some government assistance. As I’m sure you’re aware, Phase II and Phase III trials are hugely more expensive and cumbersome. It’s unlikely that these trials will ever take place.
Just the same, a legal loophole exists which allows doctors to prescribe DCA this very instant. Since the drug has been previously approved for use in human trials, doctors are free to prescribe it ‘off label’ for treatment of cancer. Indeed Drs Akbar and Humaira Khan prescribe it ‘off label’ from their Toronto practice. I’ve interviewed them on my internet program. (see www.martincwiner.com/
Figure 2: Cellular Action of DCA
Empirical evidence shows that DCA is not only applicable to a wide type of cancers but that it can be effective against typically chemo resistant tumors. In the case of chemo resistant tumors DCA is often best when concerted with other therapies. In one case (here in Toronto) a patient with non small cell lung cancer (a typically resistant cancer) was given a very poor prognosis. In this case a Chemo Fit Assay was performed which revealed that the combination of Tarceva (a milder approved chemo therapy) and DCA produced a 97% response. This patient is alive to this day and doing well. Parenthetically, the use of Chemo Fit Assays is also not considered a mainstream approach. The mainstream approach is to look up a table of cancer type to an established protocol unleashing a torrent of toxic chemicals into the patient without much further thought. (see figure 3 for the Chemo Fit Assay)
Figure 3: Chemo Fit Assay
Cancer has long been thought of as a complex and intractable disease. It turns out only our research establishment embodies those characteristics.
Full Article: http://www.martincwiner.com/