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COPPER AND...
There are many fascinating questions about how copper reduction might be used in conjunction with other types of therapies. One that is in the early stage of consideration is coupling copper reduction with low dose chemotherapy. Some anecdotal evidence suggests that this combination may work against some cancers. The concept of low dose chemotherapy is just beginning to gain acceptance among a few oncologists. But there are many others who regard it with great suspicion. Many oncologists think in terms of the "strength" of a drug. If a chemotherapeutic drug is "strong", therefore it is good.
Many years will have to pass before oncologists think about chemo the way cardiologists think about aspirin. A standard dose of aspirin is around 325 mg, but years of clinical research have shown that around 81 mg/day of aspirin is sufficiently protective that it lower the risks for heart attack and stroke. That a combination therapy for cancer would be thought of in similar terms is new for the oncology community.
Another area is called iron loading. Some research suggests that reducing the amount of iron in the body can reduce cancer risk. Coupling this with copper reduction is claimed to help manage cancer.
Zinc supplementation has been cited as a possible adjunct in managing cancer as well. There appears to be an antagonistic to copper. They compete for some of the same binding sites in the body.
It should also be pointed out that the link between copper and cancer is controversial. The preponderance of evidence leans towards copper reduction for preventing cancer. But there are also papers suggesting that low copper might predispose one towards liver tumorigenesis. However, it is not clear if tumorigenesis automatically translates into liver cancer. Also, a paper on research into raising rats on a copper deficient diet predisposed the rats to leukemia and/or colon cancer. However, the paper failed to determine if raising rats from birth on a low copper diet is a direct cause or it because of the developmental problems it can cause. The better experiment would have various subgroups of rats put on a copper deficient diet at birth, at six months, at one year, etc., and see if the risks are the same for each group.
Also, some new evidence suggests that for breast cancer patients, zinc supplementation may be counterproductive.
This is why it is important to consult skilled, knowledgeable and experienced physicians.
OTHER THERAPIES
This section will include news and selective coverage on other cancer therapies to consider. CRT is not the whole answer, and even as CRT is being considered with various agents, new information in cancer research is developing constantly. So, it follows that there should be a section on therapies currently not related to CRT. This section will start with receptor specific anticancer agents and add more.
Receptor Specific Anti Cancer Agents
Gleevec – Produced by Novartis, it has been very successful for treating certain types of leukemia. It represents the first of a new generation of anticancer drugs that are more specific in terms of what cells they attack.
Anti-Glutamates – Certain brain tumors destroy surrounding tissue by first overstimulating the glutamate receptors on neurons. This is done by overproducing glutamate. There is some evidence that inhibiting glutamate production may inhibit brain tumor growth.
Celebrex – The evidence that CelebrexTM has an anticancer role has been building over the last two years. A surprising number of cancers have the same COX-2 mechanism as found in arthritis.
Oncolytic Viruses – There are about a dozen viruses known to attack only tumor cells. It is unknown whether this is a fortunate accident of nature or a result of some selective pressure on viruses. As a reproduction strategy for viruses it would appear to make sense to go after cells that grow rapidly. That way, a larger number of viruses could be reproduced as well. Interest is growing in conjunction with gene therapy methods.
THE COMPENSATION CONJECTURE OF CANCER
The compensation conjecture of cancer is simple. Therapeutic interventions that attack one aspect of tumor growth can stimulate activity of other aspects. The compensation theory asserts that successful therapies for more difficult cancers requires a drug combination that destroys or impairs each of several aspects. The term, aspects, describes different biological functions of cancer: Growth, mutation, proliferation, motility, and angiogenesis are common aspects. A given anticancer drug typically inhibits only one of those functions.
The idea of compensation in tumors is similar to the effects of sensory deprivation. It is often noted that a person who is blind has much more acute hearing than a normal person, or someone who is deaf may have a heightened sense of touch. Metaphorically, each biological function of cancer is like a prototypical "sense".
One piece of evidence for the compensation conjecture of cancer comes from research at Stanford Medical School. An antibody that inhibited growth of a tumor caused the tumor to proliferate instead.
Why some tumor cells would respond in this way while others do not is a mystery. Chromosomal rearrangements can confer functions found in some cells but not others. It follows though, that part of the "strategy" of a tumor cell is to keep on mutating until it gets lucky and finds a new and better way to grow.
It is argued here that many of the combination therapies tested to date have provided necessary but not sufficient degrees of coverage against the different biological functions. In developing ideas about compensation, there are questions about what is the minimum number of functions that must be inhibited. Also, a number of these functions can have redundancies. There can be several different "back up" mechanisms for angiogenesis, for example.
The other argument of the compensation conjecture is that provides a unified basis for thinking about tumors. There is some one "thing", one "organizing principle" that keeps a tumor functioning as one, let us say, "sub-organism". That organizing principle is responsible for shunting the limited resources of a tumor from an area that is blocked by a drug inhibiting, say, proliferation, to mutation or angiogenesis.
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