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Registered Member #1792
Joined: Fri Oct 31 2008, 08:12PM
Location: University of California
Posts: 527
There's no such thing as a cure for cancer:
wrote ... Canadian scientists tested this dichloroacetate (DCA) on human’s cells; it killed lung, breast and brain cancer cells and left the healthy cells alone. It was tested on Rats inflicted with severe tumors; their cells shrank when they were fed with water supplemented with DCA. The drug is widely available and the technique is easy to use, why the major drug companies are not involved? Or the Media interested in this find?
From this it sounds like they have done preliminary studies and are hyping it up in the media, playing the david vs. goliath angle, to get more funding. Or the media is hyping it up because that's what the media does. It doesn't mean that this drug isn't worthwhile, but it's not some miracle cure that greedy phamaceuticals are ignoring to protect their profits. On the contrary, if there were a single cure for cancer (extraordinarily unlikely) then the pharmaceuticals would be fighting to be the company to sell it.
Registered Member #30
Joined: Fri Feb 03 2006, 10:52AM
Location: Glasgow, Scotland
Posts: 6706
There are dozens of candidate "cures for cancer" working their way through clinical trials right now. The ones I'm aware of are based on viruses genetically engineered to infect only the particular kind of cancer cell in question.
DCA sounds like a fairly simple poison that does what fluorouracil does to skin cancers. It also sounds like a generic chemical that can't be patented, which is the kiss of death for drug company involvement.
Registered Member #1321
Joined: Sat Feb 16 2008, 03:22AM
Location:
Posts: 843
Oncogene. 2011 Apr 18. Role of SLC5A8, a plasma membrane transporter and a tumor suppressor, in the antitumor activity of dichloroacetate. Babu E, Ramachandran S, Coothankandaswamy V, Elangovan S, Prasad PD, Ganapathy V, Thangaraju M. SourceDepartment of Biochemistry and Molecular Biology, Medical College of Georgia, Georgia Health Sciences University, Augusta, GA, USA.
Abstract There has been growing interest among the public and scientists in dichloroacetate (DCA) as a potential anticancer drug. Credible evidence exists for the antitumor activity of this compound, but high concentrations are needed for significant therapeutic effect. Unfortunately, these high concentrations produce detrimental side effects involving the nervous system, thereby precluding its use for cancer treatment. The mechanistic basis of the compound's antitumor activity is its ability to activate the pyruvate dehydrogenase complex through inhibition of pyruvate dehydrogenase kinase. As the compound inhibits the kinase at micromolar concentrations, it is not known why therapeutically prohibitive high doses are needed for suppression of tumor growth. We hypothesized that lack of effective mechanisms for the entry of DCA into tumor cells may underlie this phenomenon. Here we show that SLC5A8 transports DCA very effectively with high affinity. This transporter is expressed in normal cells, but expression is silenced in tumor cells by epigenetic mechanisms. The lack of the transporter makes tumor cells resistant to the antitumor activity of DCA. However, if the transporter is expressed in tumor cells ectopically, the cells become sensitive to the drug at low concentrations. This is evident in breast cancer cells, colon cancer cells and prostate cancer cells. Normal cells, which constitutively express the transporter, are however not affected by the compound, indicating tumor cell-selective therapeutic activity. The mechanism of the compound's antitumor activity still remains its ability to inhibit pyruvate dehydrogenase kinase and force mitochondrial oxidation of pyruvate. As silencing of SLC5A8 in tumors involves DNA methylation and its expression can be induced by treatment with DNA methylation inhibitors, our findings suggest that combining DCA with a DNA methylation inhibitor would offer a means to reduce the doses of DCA to avoid detrimental effects associated with high doses but without compromising antitumor activity.Oncogene advance online publication, 18 April 2011; doi:10.1038/onc.2011.113.
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