Kill Cancer Cells The life and death of cancer cells

PROPOSED COMMON CAUSE AND CURE FOR ALL FORMS OF CANCER: ITEMS 40-48 (SECTION 5)

Prepared for educational use by David W. Gregg, PhD.
Used with permission.

These web pages are for information only. They represent the observations, views and opinions of the author, and are not a recommendation for treatment. Anyone reading it should consult his/her physician before considering treatment.


Items 40-48 (Section 5)


40. Update (11/22/04) Mouse experiments supporting some of the key assumptions presented on this web page. AND the apparent role of lysine and predicted role argenine.
41. Update (12/1/04) Mitochondria, the gatekeeper of apoptosis
42. Update (3/20/05) Proposed Additional Cesium Cancer-Kill Mechanism - Stimulation of Immune System Attack?
43. Update (5/29/05) An Insightful Email
44. Update (6/27/05) Over 300 Alternative Cancer Treatments on Cancer Tutor
45. Update (7/12/05) Cesium Interruption of Amino Acid Transport into Cells
46. Update (11/11/05) The Cesium Puzzle
47. Update (1/06) Hydrazine Sulfate as a Treatment for Cancer
48. Update (1/07) Prostate Cancer Treatment



40. Update (11/22/04)



1) Mouse experiments supporting some of the key assumptions presented on this web page.

2) The apparent role of lysine and predicted role arginine.


Mouse Study:

I discovered (on the internet) a study presenting a systematic evaluation of the effect of a broad range of dietary nutrient variations on the development of cancer in mice. It is "Suppression of squamous cell carcinoma in hairless mice by dietary nutrient variation" by Arthur B. Robinson, Arnold Hunsberger and Fred C. Westall. The entire report can be found on the Internet by going to: www.ncahf.org/digest/01-01.html, scrolling to the title "Linus Pauling couldn't face the truth" and clicking on the link "Suppression of squamous cell carcinoma in hairless mice by dietary nutrient variation."

This is a particularly interesting study because of its magnitude (1846 mice) and the diversity of the diets tested. The primary conclusion was that good, balanced nutrition increased cancer growth rates by as much as a factor of two while severe diet restriction reduced cancer growth rates by a factor of ten. I thought it would be useful to take a close look at the data presented to see if additional useful information could be extracted in the light of the theory presented on this web page. I was surprised to discover some data that strongly supported key parts of the nutritional treatment premise/theory presented here, the significance and mechanism of which appeared to have been overlooked.

1. The role of high doses of vitamin C in oxygen transport.
The data clearly showed that low doses of vitamin C enhanced cancer growth, but at high doses its effect switched and greatly inhibited cancer growth. My premise is at low doses its effect is limited to enhancing nutrition, supporting cancer growth. However, at high doses it becomes a powerful transporter of oxygen, as discussed in this web page. The effect is to cause anaerobic cancer cells to revert to aerobic metabolism, become "normal" and exercise programmed cell death. They apparently did not recognize the oxygen transport capability of vitamin C at high doses and its potential effect on cancer. They ascribed the inhibiting effect to toxicity.

2. Synergistic effect of vitamin C and E in oxygen transport.
In another experiment they discovered a feed that contained moderately enhanced vitamin C and vitamin E had a strong inhibitory effect. They then tested each separately at the same level and found no benefit from either alone. They concluded that the benefit must have been due to something else. However, as discussed here, vitamins C and E will act as partners in the transport of oxygen potential with the vitamin C transporting it in the aqueous cell bodies and the vitamin E transporting it in the oil based membranes. This synergistic effect, explained and proposed here, was not recognized or explored further. It further supports the concept that greatly enhanced oxygen transport will inhibit cancer. It would also indicate that the high vitamin C doses that inhibited cancer could have been even more effective if combined with moderately enhanced vitamin E.

3. A number of other experiments supported the conclusion that simple enhancement of nutrition that would usually enhance general health also enhanced cancer growth rates.

4. Conclusions
They finally concluded that a strict fruit and vegetable diet had the strongest inhibitory effect. However, when they added large doses of vitamin C to the fruit and vegetable diet they found an even more inhibitory affect. The inhibitory effect went away if protein was added to the diet. It would have been interesting if they could have tested the combination of vitamins C & E with the fruit and vegetable diet. They might have done that had they recognized their synergistic effect.


The effect of lysine and arginine:
They assumed that the cancer inhibiting effect of the fruit and vegetable diet was due to it not being nutritionally balanced and was not due to any specific inhibitory effect of the fruits & vegetables. However, I noticed that they found a particularly inhibitory effect of apples and pears. They explained this as being due to their low protein content. However, I thought I would check their lysine content. Lysine is known to inhibit the herpes virus. To do this I went to www.herpes.com/Nutrition.shtml. This presents the lysine/arginine ratio for a long list of foods. Lysine inhibits herpes and arginine stimulates it. I discovered that apples and pears have the highest ratio of lysine/arginine of any fruits, and much higher than any vegetables except for beets, which has the highest of the vegetables.

The book "Cancer" by Matthias Rath
This possible lysine connection lead into another internet search where I discovered the book "Cancer" by Matthias Rath, M.D. Briefly, this scholarly book is devoted entirely to making the case for lysine inhibiting cancer.

Dr. Rath states that in order for cancer cells to spread (metastasize) they have to penetrate the walls of blood vessels, etc. In order to do this they have to dissolve collagen. The dissolving process requires special enzymes, generated/stimulated by the cancer cells, which bond to the collagen and dissolve it. Lysine stops this process by attaching to the bonding sites preventing the enzyme attack. This is an interesting theory and is fully consistent with the mice experiments. They support each other. The special effect of apples and pears may be due to the lysine content and the lysine theory of Dr. Rath may be the correct explanation.

Dr. Rath also arrives at the conclusion that it would be best to combine lysine with vitamin C even though he does not explain clearly the role of vitamin C. I fully agree with his conclusion, giving an explanation for the role of vitamin C. The combination provides a two-pronged attack by providing an oxygen transport system with vitamin C, promoting the normalization of cancer cells, while lysine blocks the cancer spread process.

The connection to lysine inhibiting herpes viruses may be that the viruses have to stimulate the same collagen dissolving process.

A new insight?: Arginine enhances cancer growth and spread?
It is well known that lysine inhibits herpes while arginine promotes it. That is why the data presented in Diet & Nutrition is presented as a ratio of lysine to arginine. This is what is important to those suffering from herpes. Could it be that arginine does this by enhancing the collagen dissolving process? If we now extend this to cancer, it would predict that a diet rich in arginine would promote the growth and spread of cancer. Supporting evidence: When we refer back to the mouse studies, they found any benefit from a fruit and vegetable diet would be totally negated by adding protein to the diet. However, the protein they added was seeds and nuts. If we refer to the table in Diet and Nutrition, we find this source of protein is very high (the highest) in arginine. If the above premise is true, it is no surprise that it counteracted the beneficial approaches. It would have been interesting if they added a different source of protein, such as cheese, which is very high in lysine. Perhaps they would have found that adding such protein had an inhibitory effect or at least no cancer enhancing effect. I predict it would have been a very different outcome.

This would also infer that any effective diet for inhibiting cancer would be very similar to one where a person wants to inhibit the spread of herpes. People with herpes are commonly familiar with this. That is the purpose of the table presented in Diet and Nutrition, which presents sufficient information for people to design their own diets intelligently.

One exception might be the consumption of some fruits such as blueberries, blackberries, grapes, elderberries, orange juice, etc. where they are known to have profound health benefits, but they also have a very low lysine/arginine ratio, similar to that of nuts. Even though the ratio is low, so too is the percentage of protein and thus total arginine content- unlike nuts. I would suspect that the low lysine content could be compensated for with lysine supplementation, improving the ratio. One could then still benefit from the rest of the highly beneficial phytochemicals in such fruits without stimulating cancer growth.


41. Update (12/1/04)


For years the function of the mitochondria was believed to be limited to aerobic metabolism. However, recent research has identified it as the gatekeeper of apoptosis (programmed cell death). A summary of the status of this research is presented in "Mitochondria at the Crossroads of Life and Death" by Amy Adams, published in "The Scientist", October 11, 2004, Vol. 18, No.19, pg 25-29.

The conclusion is that mitochondria contain the proteins that are responsible for the complex sequence of biochemistry that control the onset of apoptosis (programmed cell death). This is extremely important for cancer because cancer cells do not undergo apoptosis while normal cells do. This is why cancer cells don't die. They just continue to multiply uncontrollably. Stimulating apoptosis is the key to controlling cancer.

This is consistent with the cancer cells having anaerobic metabolism. Aerobic metabolism takes place in the mitochondria in each cell. Thus, anaerobic metabolism is the indicator that the mitochondria are shut down. One would thus conclude that functioning mitochondria are required not only aerobic metabolism, but also for programmed cell death. This is yet another piece of information that supports the primary premise presented on this web page that it is essential to turn on aerobic metabolism and thus the mitochondria to deal with cancer. The first result would be to cause the cells to revert back to the appearance of normal cells, as indicated in laboratory tests. The second would be for the mitochondria to recovery the ability to initiate programmed cell death.

It is proposed here that to do this you not only want to enhance oxygen transport to the cells (and thus the mitochondria) but you also want to provide a diversity of nutrients that support each step of aerobic metabolism which takes place in the mitochondria. This will include a large number of nutrients for steps that are known, and many that are not. Most of the well recognized vitamin and mineral supplements are known to support some steps and the demonstrated effectiveness of a diverse fruit and vegetable diet is probably due to it addressing those that are still unknown.

Suggested further enhancement of oxygen transport by breathing enriched oxygen.
The need to enhance oxygen transport to the cells by a means other than hemoglobin has been discussed. It has been suggested that large doses of vitamin C, MSM/DMSO and even alpha lipoic acid will accomplish this. These molecules circulate in the blood picking up oxygen at the lungs and transporting it to the cells. It seem reasonable to me that this step would be further enhanced by the person enhancing their oxygen intake using an oxygen bottle commonly used by many when their lungs are deficient. This would further increase the oxygen carrying capacity of these molecules.


42. Update (3/20/05)


Proposed Additional Cesium Cancer-Kill Mechanism – Stimulation of Immune System Attack?
In the prior discussion of how cesium ions accumulating in the cancer cells kill the cells, three mechanisms have been proposed:
1. It changes the osmotic pressure in the cells relative to the surrounding media, causing the cells to swell and burst.
2. It results in an opposing cesium & potassium concentration gradient that arrests the continued operation of the sodium-potassium pump, arresting the sodium-glucose co-transport system feeding glucose into the cell, thus starving the cell.
3. It results in an accumulation of negative ions inside the cell, canceling the potential gradient across the cell membrane, which is required to energize the sodium-glucose co-transport system, thus starving the cell. Mechanisms 1 and 2 are similar.

The proposed fourth mechanism:
I would like to propose a fourth kill mechanism, which may be the most likely one, at least for some cancers.

As discussed earlier in this web page, in order for cancer cells to survive and spread, they had to have the capability to defend themselves from immune system attack. It order to do this, they had to be able to display on their surface membranes a highly specific arrangement of molecules that communicated to the immune system the erroneous perception that they were normal cells, and thus would not be subjected to attack. Mutations that resulted in otherwise cancerous cells, but without this ability, would be attacked and thus would not survive to develop into cancer, the disease. The maintenance of such a normal-cell disguise would be an ongoing sophisticated cellular process. A disruption of this process would result in an attack and destruction by the immune system. This even happens in normal cells when they are damaged. Dose the disruption caused by the buildup of cesium in the cancer cells result in a breakdown of this cancer defense mechanism and in immune system attack?

In a recent phone discussion with Larry (www.essense-of-life.com), the person previously reference who sells cesium chloride, he told me that it was common for people he had sold it to related back to him that the treatment caused their tumors to become inflamed as part of the process of shrinking. I suddenly realized that this could be a key indicator of a previously unrecognized cesium kill mechanism. Inflammation is caused by immune system attack. Thus, tumor inflammation is an indication that the immune system is attacking the tumor. Is this a major kill mechanism? This would not be a surprising result because the maintenance of the normal cell disguise, deceiving the immune system, has to be a delicate balancing act, relatively easy to disrupt.

It is possible that all four cesium cancer-kill mechanisms play a role, all at the same time. The one that plays the dominant role may be different for different cases. It might be viewed that the four different kill mechanism, all of which could operate at the same time, could be providing a certain degree if redundancy, further insuring the killing of the cancer.


43. Update (5/29/05)



Another insightful email from Rich Van Konynenburg

Hi, Dave.

Hope you are doing O.K. Recently I have been doing some more digging to try to check out the mechanism for the CsCl. I want to pass on some information to you.

As you know, you suggested that one possible mechanism might be that the CsCl causes an energy crisis in the cancer cells that interferes with their ability to masquerade as normal cells to the immune system.

There are two types of cells in the immune system that are known to kill tumor cells: the natural killer (NK) cells, and the cytotoxic (or killer) T cells. The latter depend on finding non-self peptides displayed on the Class 1 MHC (major histocompatibility complex) molecules on the surfaces of cells. These are also called Class 1 HLA (human leukocyte antigen) molecules in human cells.

The NK cells, on the other hand, make their "decisions" about whether to kill cells on the basis of a combination of activator and inhibitor responses from their Class 1 HLA receptors.

Because an energy crisis would more likely result in an inability to do something that the tumor cell had been doing, I think it's more likely that the ATP shortage would cause a loss of inhibitor Class 1 HLAs. Therefore, I think it's the NK cells that are triggering the inflammation that Larry has heard about from his clients. I think the cancer cells are not able to maintain the Class 1 HLA molecules displaying normal peptides on the cell surface, and that's what causes the NK cells to go after them.

I looked into how the antigen processing and presenting machinery works for the Class 1 HLA system. It turns out that it uses the cell's normal proteasome (the complex that breaks down old proteins that have been tagged by ubiquitin) to break down cellular proteins into peptides, and then it chops them to size and hooks them onto the HLA molecules in the endoplasmic reticulum, and these then carry them to the cell surface and display them. The proteasome is an ATP-ase, and it requires quite a bit of energy to chop up the proteins. I suggest that this is where the energy crisis produced by the CsCl treatment comes into play. The proteasome can't keep up its protein processing at a normal rate, and I suspect that this makes it impossible for the Class 1 HLA system to get the peptides it needs to keep up the masquerade. When these drop off, they reduce the inhibition of the NK cells, and they attack.

I think this story makes sense.

Rich


44. Update (6/27/05)


Over 300 Alternative Cancer Treatments: I recently discovered an unusually comprehensive web site reviewing over 300 alternative cancer treatments. Webmaster: Webster Kerr.

http://www.cancertutor.com


45. Update (7/12/05)


Cesium Interruption of Amino Acid Transport into Cells:
The transport of most amino acids into cells requires a sodium co-transport system similar to glucose but involving different molecules in the membrane that are specific to different amino acids. "Medical Biochemistry" Fourth Edition pg. 333, by N.V. Bhagavan. Thus, when the cesium disrupts the sodium co-transport of glucose, discussed above, it also disrupts the transport of amino acids into the cells. This is another mechanism that would prevent the cancer cells from making more cancer cells that is in addition to the disruption of the glucose transport.


46. Update (11/11/05)


The Cesium Puzzle:
As presented here, cesium at the right dose can kill cancer cells. However there are also reports that trace amounts of cesium in the water supply of some regions are correlated with some of the longest-lived people of the world. How could this be? Cesium is not an essential mineral and does not have any known nutritional role. I would like to suggest the answer by connecting the dots, keeping the argument as brief as possible for the sake of clarity.

Cells continually divide forming a sequence of daughter cells to replace worn out cells.

Mutations occur only during cell division.

Thus, the number of cells with mutations and the number of cells with multiple mutations gradually accumulate during life.

It takes 5-10 mutations to create a cancer cell.

The aging process itself, involving gradually reduced function of cells and thus organs, is also caused by the accumulation of mutations. (Telomere shortening is also involved, but that will be ignored for this argument to keep the concept clear.)

It is has been demonstrated that calorie restriction is by far the most powerful approach for extending life from fruit flies to mammals.

It is also been demonstrated that calorie restriction inhibits the onset and progression of cancer.

Postulated conclusion: Calorie restriction slows down the metabolism of the cells and thus slows down their division rates. This slows down the accumulation of mutations and thus delays the onset of cancer, progression of cancer and the aging process itself.

Postulated cesium conclusion: Trace amounts of cesium in the water supply of said regions, consumed over a lifetime, slowed down cell division rates in the population, resulting not only in a later onset of cancer but also slowed the overall aging process. It would essentially be a substitution for calorie restriction.

This is fully consistent with the cesium-cancer treatment mechanism presented above where cesium inhibits the uptake of glucose and amino acids by cells, slowing their metabolic rate, thus slowing their division rate.

I believe this is a very significant insight related to aging and cancer. Concerning cancer, it would indicate that treatment with relatively low doses of cesium over long periods of time should slow overall cell division rates, slowing the onset of cancer (new cancers) and its progression. Even if it doesn't eradicate it, it will extend life. If it extends life long enough it effectively becomes a cure since all any cure does is delay the inevitable.


47. Update (1/06)


Hydrazine Sulfate as a Treatment for Cancer

Proposed Correct Biochemical Mechanism that Reveals its Profound Potential

The use of hydrazine sulfate to treat cancer is discussed extensively in many articles on the internet. The reports are unusually positive which drew me to try to understand its biochemical mechanism. That is the only approach I can take to convince myself as to their validity and how reproducible the results can be expected to be. Such an understanding is also essential for taking the next step, perfecting the treatment to achieve its full potential. I first concluded the conventionally accepted theory, identified in every report, was seriously flawed. Did this mean that the positive results were exaggerated? As an experiment (mental), I decided to assume that the results were valid and try to identify the correct mechanism. I believe I have done that and have concluded the treatment, properly applied, has the potential of being unusually effective. In some cases it could act as a stand-alone treatment and others as contributing to a broader treatment strategy. I suspect that the lack of understanding of its mechanism may have played a role in it becoming relatively ignored and not being perfected to its full potential.

Hydrazine sulfate was introduced in the early 1970’s and was viewed as a dramatic breakthrough in chemotherapy.  It was a relatively nontoxic therapy that fights cachexia, the severe weight loss and general wasting away of the body that is commonly seen in cancer patients, one of the primary causes of death.  Its effect on cancer was discovered in the 1960’s by Dr. Joseph Gold, then director of the Syracuse Cancer research Institute in Syracuse, New York. Dr. Gold proposed that it worked by blocking the liver from converting lactic acid to glucose. Cancer cells use glucose as their sole source of energy, deriving it by converting the glucose into lactic acid. The liver then converts the lactic acid back into glucose, providing a continued source of fuel for the cancer. Dr. Gold proposed that the hydrazine sulfate blocked this conversion, starving the cancer, arresting its progression.

This theory makes no sense to me. If the liver was prevented from converting the lactic acid back into glucose, blood glucose levels would decline and lactic acid would increase. There is no mechanism to slow down the cancer until the glucose level falls so low the cancer can no longer grow. This would also be associated with a toxic rise in the lactic acid. Glucose is the sole source of energy for the brain and brain function is very sensitive to glucose levels. There is no reason to believe that the cancer would cease to grow before the brain ceased to function. On top of this add the toxic effects of the increased levels of lactic acid. If the liver’s conversion of lactic acid back into glucose were arrested, one would expect as a minimum that the patient would feel quite ill, and possibly pass into a coma, similar to an insulin shock coma, which is caused by low blood glucose levels. Quite the opposite occurs. The patient feels far better and recovers his appetite. Gold’s proposed mechanism has to be seriously wrong.  What is the correct mechanism?

The Proposed Correct Biochemical Mechanism

The “Glutamine Shuttle”
As presented in items 18 & 19 of this web page, cancers have a voracious appetite for glutamine. ("Glutamine and Cancer" Wiley W. Souba M.D., Sc.D., Annals of Surgery, Vol. 218, No. 6, 715-728)  Briefly, glutamine is the most important "nitrogen shuttle" in the blood.  It brings the organic nitrogen to all cells, including  cancer cells, which use it to make additional amino acids and thus proteins required to make more cells.  The paper reports measurements that show as the glutamine supply in the blood (supplying a tumor) is reduced, tumor growth rate decreases, going to zero as the glutamine supply goes to zero. Muscles also need glutamine to grow. However, muscles not only consume glutamine to grow, but in times of insufficient dietary glutamine (red meats), muscles serve as a source of glutamine (for the blood) and diminish is size by doing so.  As the cancer consumes it, the muscles supply it. This, what I call, “glutamine shuttle” is responsible for cachexia, the severe weight loss and general wasting away of the body associated with cancer. (Adding red meats to the diet will reduce muscle loss while increasing tumor growth.)

Hydrazine, from Hydrazine Sulfate, Blocks the Glutamine Shuttle
Structurally Hydrazine is H2N-NH2.  It is two amino groups (-NH2) bonded together.  When present in amino acids, the -NH2 groups are bonded to a carbon atom in the amino acid and play a key role in forming the chain of amino acids that make up a protein. When hydrazine is reacted with a protein it breaks the bonds between amino acids and substitutes -NH2 groups for the adjacent amino acids. ("Medical Biochemistry" by N. V. Bhagavan, fourth edition, pg. 45)  This feature is used as an analytical tool for separating individual amino acids from a protein chain for further analysis. As an example, consider only two amino acids, R and R' bonded together (R-R').  When reacted with hydrazine, the bond between the two amino acids is broken and -NH2 is bonded in its place: R-R' + H2N-NH2 = R-NH2 + R'-NH2.  Once reacted with the –NH2 group, the amino acid is permanently altered so it can no longer participate in the formation of a protein.  Arresting protein synthesis in a tumor will stop its growth, the Glutamine Shuttle and cachexia.

When a person consumes hydrazine sulfate it enters the blood and is widely distributed. I see two possible reaction sites, either or both of them would block the Glutamine Shuttle. It could react directly with the glutamine in the blood, deactivating it. It could also enter the cancer cell where the bonding sites of individual amino acids are being prepared for reaction with other amino acids to form proteins. Such highly reactive sites would be extremely vulnerable to reacting with the hydrazine, deactivating the formation of the protein. I suspect that the dominant blockage occurs inside the cancer cells. If the dominant mechanism was to react with the glutamine in the blood, the body might see this as a loss in glutamine and still try to replace it from muscle tissue. If this happened, tumor growth might be arrested, but the cachexia process would continue. The observation is that cachexia is arrested. This leads me to believe the dominant arresting reaction happens inside the cancer cells.

Discussion
The hydrazine (hydrazine sulfate) arrests the progression of the cancer (and cachexia) but is there a mechanism that kills cancer cells? Tumor shrinkage would indicate there is. I suspect that this is caused by the accumulation of damaged protein fragments and amino acids in the cell that disrupts cell function. It could kill the cell directly or activated one of the forms of programmed cell death. If so, the treatment might be further enhanced by combining it with other treatment protocols that have programmed cell death as a strategy. This is just one suggestion. I am only one person in a world of creative people. My hope is that clarifying the mechanism will open the door for others to find innovative ways to use hydrazine sulfate, improving its protocol, or using it in combination with other treatment strategies to achieve a result that is better than what can be achieved using either alone.

Side Effects
Like all chemotherapy agents, hydrazine is toxic. Normal healthy cells are also going to be effected in a similar way. The cancer cells may be impacted preferentially at first, but continued use is also going to impact normal cells. Care would have to be taken using it. Reports on the internet could be used as a guide but always consult your physician.


48. Update (1/07)


Prostate Cancer Treatment
I received an e-mail from Jerry Nail with this information about his unusually successful approach to dealing with his prostate cancer and the detailed protocol he used to control it.



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