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Cheap, safe cure for most cancers?

a_unique_person

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http://www.newscientist.com/article/dn10971-cheap-safe-drug-kills-most-cancers.html

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).

So how plausible does this sound?
 
New Scientist said:
The next step is to run clinical trials of DCA in people with cancer.

Are they really at the point where they're going to run clinical trials on humans? It will be interesting to see the results of that. It all sounds too good to be true, doesn't it?
 
They have been using the drug for years for another condition, it's not as if it's going to have any unknown side effects.

It has been used for very rare conditions. It is entirely possible it could have effects that have not been noticed yet, but would be when it is used on millions of people. Plenty of drugs have been used which only had their side-effects noticed after approved for public use, Thalidomide and Vioxx being obvious examples.

On a less pessimistic note, it does sound rather promising. Can't wait to see where this leads.
 
It's obviously not a proper cure for cancer because it's not "natural". It's made in laboratories by people in the pay of Big Pharma.

It's even got an evil three letter abbreviation! It's a CHEMICAL!!!!

;)
 
We'll see. The fact that it acts on something that's unique to cancer cells, apparently differentiating them from ordinary cells, means that it is a candidate; OTOH, we'd need to know whether there are any other cells in the human body that use this type of metabolism, and what those cells do and what might happen if they all die, to be certain of the most likely side-effect; and no telling what others might crop up. Human biochemistry is definitely not a completely enough known area to predict what might happen with any given chemical.

And on the other, other hand, if you were dying of cancer, would you try an experimental treatment? I would. If it works, I'm cured. If it doesn't, I was gonna die in incredible pain anyway. Seems like a pretty good trade-off to me.

Here's a question: anybody done a little quick research on the incidence of cancer among those patients who have been receiving this treatment compared to the general population? Seems to me like it's a quick way to gather some evidence; not conclusive, but not a bad idea either.
 
Somehow I doubt that a disease so complex and with so many diversifications like cancer will be cured by a single substance. I'd be happy to be proved wrong; I'd bet a lot of money that I won't be.
 
The complexities and diversifications are what systems in the body the cancer affects, not what the cancer essentially is; remember that all body cells have essentially the same genetic code, and the same essential structure (give or take an organelle here or there), and are therefore all essentially vulnerable to this particular type of defect, which we call cancer. If we can classify cancer cells in some manner that is the same for all such cells, and essentially different from normal body cells, and then attack the cancer cells based on that difference, that attack will not affect the body cells; and if this works, then this would be a cure for cancer.
 
It has been used for very rare conditions. It is entirely possible it could have effects that have not been noticed yet, but would be when it is used on millions of people. Plenty of drugs have been used which only had their side-effects noticed after approved for public use, Thalidomide and Vioxx being obvious examples.

Unlike Thalidomide, dichloroacetate isn't chiral.

Being an Edmontonian myself, I'll give the discoverer the benefit of the doubt and be optimistic about it.
 
I think DCA IS a carcinogen. I have a metabolic disease, so I had heard of trials. I do know DCA is considered a pollutant in rivers, caused by chlorinated water steeping vegetable matter. I'll go look.

http://cat.inist.fr/?aModele=afficheN&cpsidt=15512315

says" the suspected carcinogen 1-2 DCA is the most abundant ground water pollutant on earth". Doesn't the 1-2 DCA mean it is two DCA's linked together?

But anyhow, so tea made of chlorinated tap water prevents cancer???
 
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Are they really at the point where they're going to run clinical trials on humans? It will be interesting to see the results of that. It all sounds too good to be true, doesn't it?

I heard the guy on the local radio here in Calgary, and he made it sound that way.

I'm not positive about the whole "it's not patentable" though.. sure it's not a new drug that you can patent by itself, but using an existing compound in a new way is definitely patentable. The guy said it was possible to patent it but it would be a weak patent; too weak.

The problem I guess is if it isn't patentable and the drug will be cheap to make, everyone could do it so no one will make any money, so who would put in the hundreds of millions required to go through all the clinical trials?
 
Hi there --

I think DCA IS a carcinogen. I have a metabolic disease, so I had heard of trials. I do know DCA is considered a pollutant in rivers, caused by chlorinated water steeping vegetable matter. I'll go look.

http://cat.inist.fr/?aModele=afficheN&cpsidt=15512315

says" the suspected carcinogen 1-2 DCA is the most abundant ground water pollutant on earth". Doesn't the 1-2 DCA mean it is two DCA's linked together?

But anyhow, so tea made of chlorinated tap water prevents cancer???

I took a look at your article, and it says that "1-2 DCA" is "1,2-dichloroethane", also known as "ethylene dichloride". The news article on the hopefully cancer-killing DCA says that DCA is "dichloroacetate", aka "dichloroacetic acid". I also looked up the two on Wikipedia (I know, I know, take the stuff there with a grain of salt), but the chemical diagrams for them are completely different. Here are the links to Wikipedia:

Dichloroacetate | Ethylene Dichloride

I only took chemistry in High School (and embarassingly long time ago), so I'm not sure if these two names are synonymous, but I rather suspect that this is a case in which the same acronym is used with two different meanings (SAR = Search and Rescue? Synthetic Apeture Radar? etc.).

Hopefully someone with some Chemistry chops will come along and comment!
 
We'll see. The fact that it acts on something that's unique to cancer cells, apparently differentiating them from ordinary cells, means that it is a candidate; OTOH, we'd need to know whether there are any other cells in the human body that use this type of metabolism, and what those cells do and what might happen if they all die, to be certain of the most likely side-effect; and no telling what others might crop up. Human biochemistry is definitely not a completely enough known area to predict what might happen with any given chemical.

Does anyone know about the supposed mechanism of cancer that this is targeting? I had not heard about cancerous cells not using mitocondria, but the failures being in other areas.

So is this universal to cancers, common in cancers, or a subset of cancers? Given that cancer is a fairly diverse thing(I think, as they are any change in cells that causes them to grow out of control, why assume that they have that much in common)

As for why this isn't being used, well look at when they tried mega-dose betacaratine to prevent lung cancer, it increased the rates. so care is something that it is wise to take.
 
The problem I guess is if it isn't patentable and the drug will be cheap to make, everyone could do it so no one will make any money, so who would put in the hundreds of millions required to go through all the clinical trials?

The NIH and similar government entities overseas as well as private non-profits (e.g. American Cancer Society) would pick up the tab if they thought it was worthwhile to do so.

Here is the abstract for the research regarding this finding:

Cancer Cell. 2007 Jan;11(1):37-51
Bonnet S,
· Archer SL,
· Allalunis-Turner J,
· Haromy A,
· Beaulieu C,
· Thompson R,
· Lee CT,
· Lopaschuk GD,
· Puttagunta L,
· Bonnet S,
· Harry G,
· Hashimoto K,
· Porter CJ,
· Andrade MA,
· Thebaud B,
· Michelakis ED.
Pulmonary Hypertension Program and Vascular Biology Group, University of Alberta, Edmonton, AB T6G 2B7, Canada.


The unique metabolic profile of cancer (aerobic glycolysis) might confer apoptosis resistance and be therapeutically targeted. Compared to normal cells, several human cancers have high mitochondrial membrane potential (DeltaPsim) and low expression of the K(+) channel Kv1.5, both contributing to apoptosis resistance. Dichloroacetate (DCA) inhibits mitochondrial pyruvate dehydrogenase kinase (PDK), shifts metabolism from glycolysis to glucose oxidation, decreases DeltaPsim, increases mitochondrial H(2)O(2), and activates Kv channels in all cancer, but not normal, cells; DCA upregulates Kv1.5 by an NFAT1-dependent mechanism. DCA induces apoptosis, decreases proliferation, and inhibits tumor growth, without apparent toxicity. Molecular inhibition of PDK2 by siRNA mimics DCA. The mitochondria-NFAT-Kv axis and PDK are important therapeutic targets in cancer; the orally available DCA is a promising selective anticancer agent.

On the subject of harmful side effects with human consumption, there is this study:


J Clin Pharmacol. 2006 Dec;46(12):1449-59. Links

Human kinetics of orally and intravenously administered low-dose 1,2-(13)C-dichloroacetate.
· Jia M,
· Coats B,
· Chadha M,
· Frentzen B,
· Perez-Rodriguez J,
· Chadik PA,
· Yost RA,
· Henderson GN,
· Stacpoole PW.
General Clinical Research Center, University of Florida, 1600 Archer Road, Gainesville, Florida 32610, USA.

Dichloroacetate (DCA) is a putative environmental hazard, owing to its ubiquitous presence in the biosphere and its association with animal and human toxicity. We sought to determine the kinetics of environmentally relevant concentrations of 1,2-(13)C-DCA administered to healthy adults. Subjects received an oral or intravenous dose of 2.5 microg/kg of 1,2-(13)C-DCA. Plasma and urine concentrations of 1,2-(13)C-DCA were measured by a modified gas chromatography-tandem mass spectrometry method. 1,2-(13)C-DCA kinetics was determined by modeling using WinNonlin 4.1 software. Plasma concentrations of 1,2-(13)C-DCA peaked 10 minutes and 30 minutes after intravenous or oral administration, respectively. Plasma kinetic parameters varied as a function of dose and duration. Very little unchanged 1,2-(13)C-DCA was excreted in urine. Trace amounts of DCA alter its own kinetics after short-term exposure. These findings have important implications for interpreting the impact of this xenobiotic on human health.
PMID: 17101744 [PubMed - in process]
 
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Went to Dogpile - http://www.dogpile.com - typed in DCA cancer - got a number of hits - all of which are versions of the basic press release, some with extras like a picture version of the molecule and a schematic of how it works in cancer cell. pain and/or odd gait (I assume this means trouble walking) primary known possible side effects.
 
Does anyone know about the supposed mechanism of cancer that this is targeting? I had not heard about cancerous cells not using mitocondria, but the failures being in other areas.

So is this universal to cancers, common in cancers, or a subset of cancers? Given that cancer is a fairly diverse thing(I think, as they are any change in cells that causes them to grow out of control, why assume that they have that much in common)

To grossly oversimplify....Cancer cells tend to be immortal; they don't undergo apoptosis or controlled destruction. Mitochondria can be involved in triggering apoptosis. In cancer cells, mitochondria function abnormally and may not be able to trigger apoptosis and this may be the mechanism for cell immortality.

As for why this isn't being used, well look at when they tried mega-dose betacaratine to prevent lung cancer, it increased the rates. so care is something that it is wise to take.

It seems to me that drugs that show great promise in vitro or in early animal studies, but turn out not to work in vivo in humans, vastly outnumber those that do live up to their promise. That may be an interesting study - work out the actual ratio of hype to reality. I know that that's not fair; there's no good way to tell in advance which it will be.

Linda
 
I took a look at your article, and it says that "1-2 DCA" is "1,2-dichloroethane", also known as "ethylene dichloride". The news article on the hopefully cancer-killing DCA says that DCA is "dichloroacetate", aka "dichloroacetic acid". I also looked up the two on Wikipedia (I know, I know, take the stuff there with a grain of salt), but the chemical diagrams for them are completely different.
1,2-dichloroethane is ethane, the two-carbon alkane, with chlorine atoms replacing one hydrogen on the one carbon and one hydrogen on the two carbon.
< structural diagram removed; look in Wikipedia for it >
Actually, the chlorines can be on the ends; the real bonding pattern of carbon has each bond going to the points of a tetrahedron, so although in this structural diagram the bonds that point out toward the ends look different, they are actually identical to the ones that go vertically. It is a solvent, though not much used for that because TCE, its close chemical relative, is much more effective in that role, although now banned as an ozone-depleting chlorinated hydrocarbon, and incidentally a major groundwater pollutant. DCE is most used as a precursor to polyvinylchloride, one of the three most common plastics (the others being polyethylene and polystyrene). PVC has the characteristic of being quite inert and therefore long-lasting, because of the strong chlorine bonds it has.

DCA, OTOH, is a chlorinated version of acetic acid; which is the acid in vinegar. It is a methyl group, that is CH3, with two of the hydrogens replaced by chlorine, attached to a carbon atom double-bonded to an oxygen atom, and single-bonded to an OH radical. Like this:
< structural diagram removed >
This chemical is probably not a good solvent because of the OH radical, and the double-bonded oxygen. Its only use is as a medication; thus, despite its two chlorine atoms, it is not a measurable source of ozone depletion, nor is it a groundwater hazard, since not enough of it has been made to make it have significant environmental effects, nor is it going to be even if it is mass produced as a drug.

casebro, please don't spread FUD; this is already hard enough to fund because none of the drug companies are interested because they can't patent it, and they're making money hand over fist from other drugs they're selling to people dying in horrible agony and having hunks cut out of their bodies, which money the drug companies will no longer get if this stuff works. I know that probably wasn't your intent, but it is a potential result- and any of us could wind up doing the dying.

Jackalgirl, thanks for trying to answer that.
 
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Here is the abstract for the research regarding this finding:
This looks like a correct citation.

On the subject of harmful side effects with human consumption, there is this study:
Here, you cite a study of the wrong compound. Calling this compound, 1,2-dichloroethane, "dichloroacetate" is incomprehensible under any naming system; so, your confusion is understandable.
 

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