About the Latest Cancer Cure

by Bill Sardi by Bill Sardi

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My email box fills with reports of a newly found cancer cure. No, not another herb touted by a poneytailed herbalist who just returned from Katmandu, but from the University of Alberta. OK, it deserves attention.

God knows, humanity needs a treatment for cancer that works and doesn’t kill the patients before it cures. Take Tamoxifen for example. The most recent study found, after 12 months, 22% of women being treated for breast cancer had ceased using the drug. At 24 months 28% had stopped Tamoxifen, and at 3.5 years 35% had stopped the treatment. [Cancer, Online: January 22, 2007 Print Issue Date: March 1, 2007]

Tamoxifen’s side effects are horrendous, and the drug only marginally effective. In one Tamoxifen study, among 6600 healthy women who took Tamoxifen, there were 69 fewer tumors compared to 6000 other women who took a dummy pill. In other words, Tamoxifen benefited only about 1 in 100 high-risk women as a preventive measure. Yet it was widely hailed as a breakthrough! [Associated Press Oct. 30, 1998] Ninety-nine women would have to take Tamoxifen and be subject to its side effects for one woman to escape breast cancer.

Among the serious and life-threatening events associated with Tamoxifen are uterine malignancies (yep, cancer!), stroke, and pulmonary embolism (life-threatening blood clot in the lungs), not to mention blinding cataracts, aged skin, hair loss. A "Tamoxifened" woman looks terrible.

Back to our report about the new cancer wonder drug. So the University of Alberta press release says a "small molecule offers big hope against cancer." So far, sounds attractive, since small molecules are avidly being investigated for cancer treatment as they can enter the cell nucleus and switch cancer promoting/inhibiting genes on or off.

The surprising molecule that does this is dichloroacetate (DCA), an odorless, colorless, inexpensive, and "relatively non-toxic" drug that has already been used in humans to treat a condition called lactic acidosis.

OK, lactic acidosis is the common state of metabolism in cancer cells. Cancer cells, lacking the ability to produce energy from within their own cellular machinery (mitochondria), revert to producing sugar for cell energy, which produces lactic acid as a by-product. The lactic acid dumps outside the cell, repelling anti-cancer agents and making the cancer cell immortal. Dammit, these tumor cells won’t die off like normal cells.

So the researchers found that dichloroacetate (DCA) revives the energy-producing compartments (mitochondria) within cancer cells, eventually resulting in cancer cell death (what researchers called apoptosis). DCA did no harm to surrounding healthy cells, so it might be non-toxic.

Modern medicine is desperately searching for anti-cancer molecules that kill cancer cells and leave healthy cells alone. Unfortunately, chemotherapy today is very toxic to tumor and healthy cells alike, and the patient often succumbs to the treatment rather than their disease. Furthermore, cells don’t like the toxic drugs; they develop a resistance to them, so chemotherapy usually only works for a short time.

The University of Alberta researchers note that DCA has already been used in humans to treat mitochondrial disease with "relative" non-toxicity. But they lament that DCA is unpatentable so it is not likely to receive any attention, or research funding, from a pharmaceutical company.

Now there is the rub. The admission there may be a cure for cancer out there, but it’s gotta make a big profit for a drug company or they won’t pay attention to it. This is commercially understandable. However, this serves to say, simpler remedies may exist, but patients are going to have to go on a scavenger hunt to find them on their own.

The university-based researchers sought widespread publicity for DCA hoping a private source would provide research funds. [Small molecule offers big hope against cancer, University of Alberta press release, Jan. 17, 2007]

But treating mice in the laboratory is a long way from proving a cancer drug not only kills cancer cells, but actually improves survival. There are a lot of drugs that shrink tumors, but don’t improve survival. When DCA was used in humans in 1983, it effectively reduced lactic acidosis and normalized blood pressure. The drug itself produced no known toxicity, but 12 of 13 DCA-treated patients still died. [New England Journal Medicine 309: 390—96, 1983]

In animals, DCA induces liver toxicity and neoplasia (yep, cancer!). DCA is actually a by-product of water chlorination, chlorine being one of the most toxic molecules on the planet. [Environmental Health Perspectives 106 (Suppl 4): 989—994, 1998]

Of interest, the toxic side effects of DCA may emanate from inducement of a vitamin B 1 (thiamine) deficiency. The chronic use of dichloroacetate (DCA) for diabetes has been compromised by nerve and other forms of toxicity. DCA is metabolized to glyoxylate, which is converted to oxalate and, in the presence of adequate thiamine levels, to other metabolites. Nerve toxicity from DCA administration appears to result from depletion of body thiamine stores and abnormal metabolism of oxalate, a known nerve toxin. The co-administration of vitamin B1 with DCA reduces urinary oxalate levels from 86% above normal to only 28% above normal. [Toxicological Sciences 14: 327—37, 1990] Maybe this tips off how DCA actually works, by depriving cells of an essential nutrient.

Anyway, you’ve learned more about DCA than you care to, or need to, know. That’s because there is another small molecule that deserves more attention. Like DCA, it is a small molecule that can enter the cell nucleus and switch genes on or off. It is perceived by the body as a toxin, but actually is non-toxic, and it is very stealth, it can penetrate any resistant cancer cell. It works in a similar manner to DCA by inducing cancer cell death (apoptosis). The molecule is resveratrol, known as a red wine molecule. Resveratrol appears to kill off cancer cells by depolarizing (demagnetizing) mitochondrial bodies within tumor cells.

Resveratrol is 100 anti-cancer drugs in one. Resveratrol works in so many ways to block cancer, researchers can’t find a cancer-promotion pathway it doesn’t inhibit. It is virtually non-toxic since, after oral ingestion, it is quickly metabolized by the liver, attached to a detoxification molecule called glucuronate, which renders it harmless, though biologically inactive, at least for a time.

At the site of tumors cells there is an unzipping enzyme (glucuronidase) that uncouples resveratrol from glucuronate. This is nature’s "drug delivery system," releasing resveratrol at the right time and place. This explains resveratrol’s stealthiness. [Cancer Letters 231: 113—22, 2006; Oncogene 23: 6702—11, 2004; Toxicology Letters 161: 1—9, 2006; World Journal Gastroenterology 12: 5628—34, 2006; Investigative Ophthalmology Visual Science 47: 3708—16, 2006; Cancer Detection Prevention 30: 217-23, 2006; Molecular Cancer Therapy 4: 554—61, 2005; Journal Biological Chemistry 278: 41482—90, 2003]

There are currently two human resveratrol/cancer trials underway, one for cancer prevention at the University of Leicester, and one for colon cancer at the University of California, Irvine. Both trials have passed the safety arm, meaning no overt toxicity. Cancer patients await the completion of these studies.