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Cancer Science??

I am led to believe, from experiments, that the influential orbital speed of Magee’s nuclei is a bit slower than the orbital nuclei of our body cells.

A cancer cell is a cell that has its orbiting nuclei sped up to the point where this cell is forced to divide within healthy, packed cells. I can say that using Magic Magee will stabilize and slow nuclei orbital speeds of both healthy and cancerous cells. In just a few hours the body has these treated cells back to normal body cell speed (re: Burn and Cure).

I suspect that whatever is causing this nucleus abnormality is still present so a Magic Magee treatment plan would be established.

A cancerous cell is a cell and it too requires nourishment. These fast orbit nuclei feed on faster food than that which normal cells of the body feed on.

The cause of cancer is its food; there comes a time where these dividing cancer cells run short of nourishment and desperately look for another fast food source. This source is body fat. The big problem is that the orbit speed of fat is again faster, promoting expeditious cell division. Even after death, hair continues to grow. The reason for this is that faster than normal cell orbital nuclei promotes cell division. Forces of equal evolution act upon forces of equal evolution and by administering poison (chemotherapy) the orbit nuclei speed is slowed, hampering cell division. Chemo also affects healthy cells causing nutrition to now be a predator, creating a new disease. Without forced cell division within the hair follicle the hair dies and falls out. Once a cancer cell starts feeding on body fat the orbit nuclei speed is increased enough to affect the orbital nuclei speed of a healthy cell making that healthy cell a cancer cell! At this stage the body is robbed of its fat and fat being the body’s safety from fast nutrition, fast nutrition is now predator not prey, and kills the body. For you to properly understand this paper you will need to know my science.

I think following quote also indicate about food(may be its increased speeds) to cancer cells:-

Iron Loading and Disease Surveillance
Iron is an oxidant as well as a nutrient for invading microbial and neoplastic cells. Excessive iron in specific tissues and cells (iron loading) promotes development of infection, neoplasia, cardiomyopathy, arthropathy, and various endocrine and possibly neurodegenerative disorders. To contain and detoxify the metal, hosts have evolved an iron withholding defense system, but the system can be compromised by numerous factors. An array of behavioral, medical, and immunologic methods are in place or in development to strengthen iron withholding. Routine screening for iron loading could provide valuable information in epidemiologic, diagnostic, prophylactic, and therapeutic studies of emerging infectious diseases.
http://www.cdc.gov/ncidod/eid/vol5no3/weinberg.htm

Instead of other reasons, we can first try to check how our defence system behave on getting a disease or disorder and if we can enhance our defence response, goal may also be achieved.
 
I think following quote also indicate about food(may be its increased speeds) to cancer cells:-



Instead of other reasons, we can first try to check how our defence system behave on getting a disease or disorder and if we can enhance our defence response, goal may also be achieved.

Let's all sit back and enjoy science a la Three Stooges.
 
I am led to believe, from experiments, that the influential orbital speed of Magee’s nuclei is a bit slower than the orbital nuclei of our body cells.

A cancer cell is a cell that has its orbiting nuclei sped up to the point where this cell is forced to divide within healthy, packed cells. I can say that using Magic Magee will stabilize and slow nuclei orbital speeds of both healthy and cancerous cells. In just a few hours the body has these treated cells back to normal body cell speed (re: Burn and Cure).

I suspect that whatever is causing this nucleus abnormality is still present so a Magic Magee treatment plan would be established.

A cancerous cell is a cell and it too requires nourishment. These fast orbit nuclei feed on faster food than that which normal cells of the body feed on.

The cause of cancer is its food; there comes a time where these dividing cancer cells run short of nourishment and desperately look for another fast food source. This source is body fat. The big problem is that the orbit speed of fat is again faster, promoting expeditious cell division. Even after death, hair continues to grow. The reason for this is that faster than normal cell orbital nuclei promotes cell division. Forces of equal evolution act upon forces of equal evolution and by administering poison (chemotherapy) the orbit nuclei speed is slowed, hampering cell division. Chemo also affects healthy cells causing nutrition to now be a predator, creating a new disease. Without forced cell division within the hair follicle the hair dies and falls out. Once a cancer cell starts feeding on body fat the orbit nuclei speed is increased enough to affect the orbital nuclei speed of a healthy cell making that healthy cell a cancer cell! At this stage the body is robbed of its fat and fat being the body’s safety from fast nutrition, fast nutrition is now predator not prey, and kills the body. For you to properly understand this paper you will need to know my science.
:jaw-dropp


Wow. Just wow.
 
I don't know much about cancer but I have a friend who doesn't have cancer who is drinking his own urine to build up immunity to cancer. Shouldn't there be a scientific study on this or has it already been done?
 
[stuff] Even after death, hair continues to grow. The reason for this is that faster than normal cell orbital nuclei promotes cell division. [more stuff]

This is a myth. The appearance of hair and nail growth is due to skin drying out and contracting.
 
Let us think that, inherited or acquired delicacy of cells may encourage increased mutations. In view of survival, those cells may acquire some form of compensatory hardiness and become cancerous be acquiring properties of non-responsive to body's normal signals, DNA repair and cell sucide and get enhanced survival & fast multiplications.
In the loosest sense, you are correct. Cancer is the emergent result of cells loosing the ability to be regulated by inhibitory growth queues (e.g., internal and external).
Reversing such hardiness, if possible, may cure cancer by bringing those to get normal signals--of DNA repair & cell sucide.
this has been the general goal for many different anti-cancer strategies. Including the promising vaccination approaches.
Now we have to find, what can make cells to become delicate. I suspect that, cell swelling, lactic acid(or acidosis), oxidative stress(chronic inflammation) or otherwise promoted by odd exposures can be the culprits of making cells delicate.
Again, in the most generous concepts,yes.
A few key points:
1.) oxidative stress is NOT chronic inflammation. Oxidative stress is only the condition that describes the imbalance of excess reactive oxygen/nitrogen species in comparison to the antioxidant systems. Oxidative stress DOES exist in chronic inflammation, but also occurs in a variety of other scenarios as well.
2.) Tumor bodies are typically acidodic because of poor vascularization. There's a series of drug delivery designs being studied which uses this acid domain as a trigger for drug targeting and release.
3.) treating tumors is easy compared to treating malignancies. What you are describing primarily are the approaches to dealing with tumors. How do you prevent a cell from intravasating/extravasating? How do you target circulating cells in a specific fashion such that drugs only act upon it, however not so selective as to permit the cancer cell to rapidly develop resistance to the approach.
 
In the loosest sense, you are correct. Cancer is the emergent result of cells loosing the ability to be regulated by inhibitory growth queues (e.g., internal and external). this has been the general goal for many different anti-cancer strategies. Including the promising vaccination approaches.

Thanks. This I take as, cells becoming delicate, more prone to acquire mutations, become hardy due to compensatory survival reason i.e. cancerous. If we can reverse this hardiness, probablt we may make cancer cells to behave normally. There seems to be some agents which can do that...i.e. making cells delicate. Cell swelling triggering cytolysis & apoptosis can be one mean.


Again, in the most generous concepts,yes.
A few key points:
1.) oxidative stress is NOT chronic inflammation. Oxidative stress is only the condition that describes the imbalance of excess reactive oxygen/nitrogen species in comparison to the antioxidant systems. Oxidative stress DOES exist in chronic inflammation, but also occurs in a variety of other scenarios as well.

Yes, but can't oxidative damage make cells to become delicate.

2.) Tumor bodies are typically acidodic because of poor vascularization. There's a series of drug delivery designs being studied which uses this acid domain as a trigger for drug targeting and release.

I am not sure, whether this state is harmful(due to defence response) OR beneficial(anarobic environment) to cancer cells?

3.) treating tumors is easy compared to treating malignancies. What you are describing primarily are the approaches to dealing with tumors. How do you prevent a cell from intravasating/extravasating? How do you target circulating cells in a specific fashion such that drugs only act upon it, however not so selective as to permit the cancer cell to rapidly develop resistance to the approach.

Suppose if we create an environment of hypotonicity to cancer cells, will then these become delicate & go to cytolysis or sucide?
 
Hello joobuz,

The following link is somewhat relevant to my logical thought in OP:-

Cancer cells bloat because they absorb sodium, which the diet provides mostly in the form of sodium chloride, or table salt. The more sodium they contain, the more water they absorb to dilute it. As Nobel Laureate Otto Warburg discovered, the way cancer cells get their sodium is by burning glucose without oxygen. Every time they burn one molecule of glucose this way, they have to take in two sodium ions and expel three potassium ions.
http://ezinearticles.com/?Oxygen,-Sodium,-and-Cancer&id=2867740

Burning glucose without oxygen or fermentation can mean lactic acid development and acidic condition can cause transcellular movement of Potassium.
 
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Hello joobuz,

The following link is somewhat relevant to my logical thought in OP:-



Burning glucose without oxygen or fermentation can mean lactic acid development and acidic condition can cause transcellular movement of Potassium.
What is your argument?
That a bad diet forces cells into an anerobic metabolism and that this anerobic stress causes cancer? This seems like a wag the dog scenario. It would be like saying more CO2 production causes cars to exist.
 
Thanks. This I take as, cells becoming delicate, more prone to acquire mutations, become hardy due to compensatory survival reason i.e. cancerous. If we can reverse this hardiness, probablt we may make cancer cells to behave normally. There seems to be some agents which can do that...i.e. making cells delicate. Cell swelling triggering cytolysis & apoptosis can be one mean.
Cancer cells are cancerous because they have acquired genetic mutations which make them pathologically proliferative. So reversing their compensatory mechanisms isn't an easy thing as it would require genetic approaches. As such, the typical strategy is to either circumvent or overcome their survival mechanisms.

The hallmark of a good cancer therapy is one that can induce cellular apoptosis. The question is, how do you do this selectively with cancer cells and avoid hurting healthy cells.


Yes, but can't oxidative damage make cells to become delicate.
I am having a hard time with your terminology. First let's agree that oxidative stress isn't chronic inflammation.
Next, to answer your question, Yes and no. Excessive oxidative stress can damage cells or make them more vulnerable to secondary injury. This is the current dual hit hypothesis that is running in free radical literature. If you knock out catalase (an antioxidant enyzme) from an animal, the animal will be able to function normally. if you put the animal (mouse) in a high oxygen environment, it will function normally. If you treat the animal with LPS (lipo-polysaccaride, a inflammation inducer), it will respond normally. If you do both of these things, the animal can't bounce back from it.

So that is the "yes" part of the question. The no comes in the form of the duration of the Oxidative stress. If the Oxidative stress is low and or very transiently high, cells respond by up-regulating their defense mechanisms, thereby protecting themselves to subsequent greater levels of ROS injury. This is the concept behind ischemic preconditioning and one of the reasons why cardiovascular exercise is good for you. Transiently increased blood flow causes oxidative stress in the endothelial cells This low level oxidative stress increases their protective mechanisms.

I am not sure, whether this state is harmful(due to defence response) OR beneficial(anarobic environment) to cancer cells?
I can't answer this question as I am not certain either.



Suppose if we create an environment of hypotonicity to cancer cells, will then these become delicate & go to cytolysis or sucide?
How do you propose to do this selectively to cancer cells and not healthy cells? Consider current chemotherapeutics. They offer some degree of selectivity as they are typically more toxic to proliferative cells than to non-proliferative cells. Even then, these drugs are extremely hard on the body. Now, if you presume to use a mechanism that will cause cell swelling to induce cell death, I do not see how this approach will be selective to cancer cells and not injure all cell types in the body.
 
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Cancer cells are cancerous because they have acquired genetic mutations which make them pathologically proliferative. So reversing their compensatory mechanisms isn't an easy thing as it would require genetic approaches. As such, the typical strategy is to either circumvent or overcome their survival mechanisms.

Sorry, Will it not be better if we say that they acquire mutations in genes? To me, acquiring mutations is secondary but basic question is that why they can get mutations? I assume it is due to cells become delicate due to odd exposures(I am not counting accidental mutations by chance).

The hallmark of a good cancer therapy is one that can induce cellular apoptosis. The question is, how do you do this selectively with cancer cells and avoid hurting healthy cells.

Though I may be looking this possibilty bit differently but still,Can't we make local environment hypotonic limited to or near to cancer site?

Btw, whether cancer cell can get cytolysis or sucide, if they get hypotonic environment?



I am having a hard time with your terminology. First let's agree that oxidative stress isn't chronic inflammation.

I can't say, if there can be persistent oxidative stress? If you say, it may be ok.

Next, to answer your question, Yes and no. Excessive oxidative stress can damage cells or make them more vulnerable to secondary injury. This is the current dual hit hypothesis that is running in free radical literature. If you knock out catalase (an antioxidant enyzme) from an animal, the animal will be able to function normally. if you put the animal (mouse) in a high oxygen environment, it will function normally. If you treat the animal with LPS (lipo-polysaccaride, a inflammation inducer), it will respond normally. If you do both of these things, the animal can't bounce back from it.

So that is the "yes" part of the question. The no comes in the form of the duration of the Oxidative stress. If the Oxidative stress is low and or very transiently high, cells respond by up-regulating their defense mechanisms, thereby protecting themselves to subsequent greater levels of ROS injury. This is the concept behind ischemic preconditioning and one of the reasons why cardiovascular exercise is good for you. Transiently increased blood flow causes oxidative stress in the endothelial cells This low level oxidative stress increases their protective mechanisms.

To understand it better, can you tell what can make normal cells to become so delicate that they can get mutations & increases their protective mechnisms? Whether carcinogens make cells delicate(by cell swelling, oxidative stress, inflammation--if it can also cause cell swelling or otherwise)?

I can't answer this question as I am not certain either.




How do you propose to do this selectively to cancer cells and not healthy cells? Consider current chemotherapeutics. They offer some degree of selectivity as they are typically more toxic to proliferative cells than to non-proliferative cells. Even then, these drugs are extremely hard on the body. Now, if you presume to use a mechanism that will cause cell swelling to induce cell death, I do not see how this approach will be selective to cancer cells and not injure all cell types in the body.

Though I feel I know it bit differently but still, why can't we make local environment near to cencer site(if not spread) hypotonic? I can't say, if hypotonicity to cancer cells can be selective?
 
What is your argument?
That a bad diet forces cells into an anerobic metabolism and that this anerobic stress causes cancer? This seems like a wag the dog scenario. It would be like saying more CO2 production causes cars to exist.

Abnormal Lactic acid generation can be very important in understanding this issue as acidic environment may be responsible to cell swelling--delicacy of cells, O2 concentration, gastric acidity etc.
 
Abnormal Lactic acid generation can be very important in understanding this issue as acidic environment may be responsible to cell swelling--delicacy of cells, O2 concentration, gastric acidity etc.

yes, but I have not seen anything suggesting that lactic acid generation causes cancer. It is a feature of tumors due to their hypoxic nature, but I can't imagine it being a causitive agent. If it was, you'd expect weight lifters to have increased incidence of cancer.
 

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