Too good to be true?
(A special thanks to fellow Legendaire Dwight Williams for pointing this out.) Could there be an already generic-ready drug which kills most cancers? (Click on the graphic for a larger view.)
The article is written in layman's terms and is straightforward. (I'm reprinting it below, along with the explanatory graphic I used in the header, in case New Scientist archives the piece for its paid subscription base.)
This is all extremely preliminary information, but it's too promising to simply ignore and as no one stands to make a fortune off it (and, indeed, makers of current drugs for treating cancer along with drugs for treating the side-effects of the treatments themselves stand to lose a great deal of money if any of the promise of DCA rings true) we can't trust that it will simply be followed through on because it's the right thing to do. The desperately sad fact is that quarterly reports and stock prices will feature prominently in the decisions and speed of action of some people who are in the best position to do something about it quickly. Something I'm worried about will be that there is considerable financial incentive for a drug company to isolate the critical action of DCA and try to synthesize something else that does the same thing -- something new and patentable -- and simply bury DCA.
Look around. Ask around. Mention it to people.
Odds are that your family has already been touched by one or more forms of cancer, and even if you've beaten those odds so far it's just a matter of time before they catch up with you. Treat the matter with interest and some degree of urgency now rather than cursing yourself next year for not doing so. What's the worst to come of talking and asking about it? If it simply doesn't pan out then we'll be no worse off than we are now. Proper clinical trials will take years -- a decade or more barring extreme circumstances -- so spread the word.
If you click on the University of Alberta link in the article, you can not only see more information but will find a spot to submit your email address so that they can alert you to any updates.
The article follows.
Cheap, safe drug kills most cancersTags: cancer cure?
* Updated 14:26 23 January 2007
* From New Scientist Print Edition.
* Andy Coghlan
New Scientist has received an unprecedented amount of interest in this story from readers. If you would like up-to-date information on any plans for clinical trials of DCA in patients with cancer, or would like to donate towards a fund for such trials, please visit the site set up by the University of Alberta and the Alberta Cancer Board. We will also follow events closely and will report any progress as it happens.
It sounds almost too good to be true: a cheap and simple drug that kills almost all cancers by switching off their “immortality”. The drug, dichloroacetate (DCA), has already been used for years to treat rare metabolic disorders and so is known to be relatively safe.
It also has no patent, meaning it could be manufactured for a fraction of the cost of newly developed drugs.
Evangelos Michelakis of the University of Alberta in Edmonton, Canada, and his colleagues tested DCA on human cells cultured outside the body and found that it killed lung, breast and brain cancer cells, but not healthy cells. Tumours in rats deliberately infected with human cancer also shrank drastically when they were fed DCA-laced water for several weeks.
DCA attacks a unique feature of cancer cells: the fact that they make their energy throughout the main body of the cell, rather than in distinct organelles called mitochondria. This process, called glycolysis, is inefficient and uses up vast amounts of sugar.
Until now it had been assumed that cancer cells used glycolysis because their mitochondria were irreparably damaged. However, Michelakis’s experiments prove this is not the case, because DCA reawakened the mitochondria in cancer cells. The cells then withered and died (Cancer Cell, DOI: 10.1016/j.ccr.2006.10.020).
Michelakis suggests that the switch to glycolysis as an energy source occurs when cells in the middle of an abnormal but benign lump don’t get enough oxygen for their mitochondria to work properly (see diagram). In order to survive, they switch off their mitochondria and start producing energy through glycolysis.
Crucially, though, mitochondria do another job in cells: they activate apoptosis, the process by which abnormal cells self-destruct. When cells switch mitochondria off, they become “immortal”, outliving other cells in the tumour and so becoming dominant. Once reawakened by DCA, mitochondria reactivate apoptosis and order the abnormal cells to die.
“The results are intriguing because they point to a critical role that mitochondria play:
they impart a unique trait to cancer cells that can be exploited for cancer therapy,” says Dario Altieri, director of the University of Massachusetts Cancer Center in Worcester.
The phenomenon might also explain how secondary cancers form. Glycolysis generates lactic acid, which can break down the collagen matrix holding cells together. This means abnormal cells can be released and float to other parts of the body, where they seed new tumours.
DCA can cause pain, numbness and gait disturbances in some patients, but this may be a price worth paying if it turns out to
be effective against all cancers. The next step is to run clinical trials of DCA in people with cancer. These may have to be funded by charities, universities and governments: pharmaceutical companies are unlikely to pay because they can’t make money on unpatented medicines. The pay-off is that if DCA does work, it will be easy to manufacture and dirt cheap.
Paul Clarke, a cancer cell biologist at the University of Dundee in the UK, says the findings challenge the current assumption that mutations, not metabolism, spark off cancers. “The question is: which comes first?” he says.
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