The audacity of questioning the root cause of cancer.

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The audacity of questioning the root cause of cancer.


Gilbert K Chesterton once referred to a paradox as “truth standing on her head to get attention”. A prim example to illustrate this is with our solar system. Prior to Nicolaus Copernicus (1473- 1543), everyone in the world held the belief that the earth was in the centre of the universe. It was presumed that the sun, moon, planets and stars all orbited around the earth. The bulk of the observed evidence tended to support this first model of the world. But there was this one perplexing abnormality that persisted throughout the ages. The truth standing on her head was the fact that some of the planets appeared to move backwards during part of their orbit. This was the anomaly that caused Copernicus to first question the validity of the earth-centred model. He went on to design a new model for explaining the workings of the solar system, which placed the sun at the centre of the universe. This new model did account for the anomalies that had existed with the Earth-Centred model, yet nearly a century passed before this idea was taken seriously, and was not accepted until after Galileo (1564-1642) started observing the night sky with a telescope, which had just become available, and could for the first time see moons orbiting other planets. The ‘truth’ it appears, does not care if we believe it or not. The earth circled the sun even when everyone on it thought otherwise.

 

The word 'anomaly' is a prelude for us that points out that the current explanation is lacking or incomplete and inevitably a superior explanation will one day come along to explain/account for the shortcomings that the current beliefs do not address.

 

In the field of cancer, there remain a number of anomalies with the present DNA model. Why was it relatively scarce prior to the industrial revolution? Why is it less prevalent in developing (third world) countries? Why is it not contagious? Why can we not derive a vaccination for it, or ‘shared immunity’ from someone who does not develop cancer , yet has been exposed to all the same antigens as the cancer patient? Why do some treatments work well for some patients, and not at all for others? Why does the list of childhood cancers differ from that of adults, when our DNA does not change? And of primary concern; why does our immune system not respond to it? Just as in the case with our solar system model, it is possible that each paradox and each anomaly can be understood if we adopt an alternate framework for viewing cancer.

No one has ever questioned the premise that cancer is caused from a fault in the cell’s DNA. There has never been a challenge brought forward or an opposing hypothesis suggested. It has always been taken as a ‘given’ that cancer was caused from a defect in our DNA. This premise would appear to be the central point from which all studies into the disease stem from. But what if this is wrong? What if we made a mistake right out of the gate? The last 125 years have been spent looking exclusively at our DNA as the culprit for this unwanted tissue growth, with questionable progress and frustrating statistics. Yet there are two distinct methods from which a living cell can be generated. Since the procedures that are capable of creating a living cell are limited to just two methods, then a flaw in the generation of unwanted cells should therefore be limited to one of these two methods. That is to say that cancer, which is defined as the growth of unwanted tissues, must either be the result of a defect in our DNA, or a defect in the repair process of our immune system ( the only other way in which a cell can come into being). A third scenario does not exist that is capable of creating a living cell, therefore a third scenario should not exist that could be a possible explanation for when something goes wrong. Thus far only one of the two methods of cell production has been considered as the culprit for when something goes wrong with the orderly generation of cells. Only the DNA method (the much studied process in which the cell’s DNA instructs the cell to divide as outlined in the internal code of the cell) has been considered as the root cause of cancer. 
Because the DNA method of cell regeneration has never been challenged or called into question, it has avoided the need of a label. For the purposes of this dissertation, I will be using the term ‘DNA model’ to refer to a sporadic mutation flaw which is currently believed to be the root cause of cancer. Cancer has only been considered as a defect at the cellular level and as a result, a solution to the problem of cancer has only been looked at from the cellular level. One cell generating method has been studied ad nauseam, and one cell generating method has been overlooked. Perhaps now it will be possible to turn the page and look at our immune system, the only remaining viable explanation that is capable of generating living tissue cells and therefore could also account for this unwanted cell activity.

This 'second method' (and only other process that exists) that is capable of generating a living cell will also require a label. I will refer to this as the scar tissue model, a much less studied, and less understood method whereby the body’s own immune system is sent to a region immediately following some form of trauma; initially to stimulate the neighbouring cells into rapidly reproducing themselves in an endeavour to seal over a wound to hinder or prohibit any blood loss, as well as prohibiting the entrance into the body of foreign contaminants, and then the mending process of repairing the wound that set the activity in motion. We refer to this process as the formation of scar tissue, and it is a function of our immune system.
The immune system is complex and much remains unknown about it. A similar situation exists now with our understanding of the immune system as it did with our DNA before the double helix sequencing chromosome model was first proposed in 1953. It could be observed and was understood that genetic traits were being passed down from generation to generation, however it was not known how that this information was being passed down After 1953 we were in a better position to understand some of the intricacies with which the system of information sharing actually worked. Similarly we presently live in a time where it is understood that the immune system is being sent to accomplish the tasks it was designed for, however we just don't yet know the intricacies which set the process in motion. Within our existing heading of the 'immune system' there are actually three distinct systems with three distinct functions. We don't yet have names for these divisions of the immune system so presently they are lumped together and collectively referred to as our immune system. For the purposes of this dissertation it will be necessary to divide the immune system into its three components. I will label the 3 divisions of the immune system simply as identify, destroy, and repair which are all completely different functions and require completely different sets of tools. First of all within our immune system there exists a complex system tasked with the responsibility of identifying foreign antigens that are deemed to be enemies of the body. There are instances when this system fails to properly identify or distinguish between foreign antigens and the bodies own cells and the classification of autoimmune diseases is the result. In addition to identifying these enemies , the immune system also has the task of setting up a strategy to destroy any and all identified threats. The immune system has control of an arsenal of specialized cells for the purpose of carrying out these missions, and a complete lymphatic system is at its disposal to deliver these specialized cells to the targeted areas. And on top of all that, and of principal interest to this alternate approach to cancer, the immune system has the responsibility of repairing any damaged cells that may have occurred during this onslaught. This new approach to understanding the root cause of cancer will be specifically concerned with this third branch of the immune system, namely the repair function.
Without fully understanding the process we can acknowledge that there is indeed a start code that sets everything in motion. Clearly once this process has been set in motion, there needs to be a corresponding mechanism in place to inform the body of when the healing process has been completed. That is to say, the body must be made to know when to start this healing process, and then when to stop this rapid formation of scar tissue, so that the immune system may end this elevated activity, and restore itself to the level of activity that existed prior to the trauma that set the event in motion. It doesn't require too much imagination to realize that the inability to shut off this ‘repair process’ would result in a situation indistinguishable from what we presently call ‘cancer’.

 

 

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We generally tend to think of scar tissue as principally associated with our skin tissue. However any cell in the body is capable of being stimulated by the immune system into generating scar tissue. Broken bones or torn cartilage are repaired with the controlled formation of scar tissue. In fact there are over 200 different types of cells in the body, and not by coincidence there are now over 200 types of identified cancers. A defect in the ’start mechanism’ would set the immune system into motion as if it had experienced some form of trauma, and the body would begin doing repairs to tissues without first being given a need too. Similarly, a defect in the ‘stop mechanism’ would result in the inability for this repair process once it had been started, to know when to shut off this process. Either one of these two scenarios would result in the manufacturing of unwanted tissues. Instead of viewing cancer as a defect in the p53 tumor suppressor gene, we could view it as a defect in our immune system which is carrying out repairs on tissues that do not first need repairing, and/or repairing cells and then not receiving the signal to stop. There must be a stop code.


All of what we presently know about cancer can be viewed from, and accounted for using this model for cancer. When further examined, all of the anomalies that currently surround cancer can be explained away. All of which has a tendency to add support to this new framework for understanding the disease, and simultaneously call into question the original premise of the DNA model.
 
The cancer cell is distinguishable from the normal cell because it was manufactured by a different process than normal cell replacement. But the DNA method of cell regeneration is not different and not distinguishable from the original. No explanation has been put forward to offer as to why this underlying characteristic would change just because the controlled order of cell replacement went astray. If the DNA model were to be true, then tumors should be clusters of cells indistinguishable from the host cells around them. A defect in the P53 gene should result in the formation of a wart, or a small polyp that could only grow to a size that could be supported by the existing blood supply. But we are still faced with the fact that the cancerous tumors are distinguishable from the surrounding tissue, and often accompanied by their own modified blood supply.
A close examination of tumor tissues reveals that there are similarities between the formation of scar tissue (with its accompanying inflammation that is necessary to support and maintain the existence of this newly generated cell) and cancerous activity. This relationship is most easily observed by comparing skin surface scars with skin cancer. Because scar tissue was manufactured rapidly, and by a different process from normal tissue replacement (normal cell division as outlined in the cell DNA), it has different characteristics. Scar tissue made from skin cells has a distinct appearance with a smoother surface, firmer density, (described as a waxy appearance) and a different pigment from that of the surrounding tissue. The following quote can be found at the final report on Grant GR/K71394 Mathematical Model of Scar Tissue
“Scar tissue formation is a ubiquitous feature of adult wound healing, with the resulting repair both functionally and cosmetically inferior to normal skin. At microscopic level, the main difference between scar and normal tissue is in the alignment pattern of the collagen fibers of which they are composed.”
 

‘Functionally and cosmetically inferior’ are characteristics shared by cells thought to be manufactured by cancer cells, and cells known to be manufactured by our immune system. And yet ‘functionally and cosmetically inferior’ characteristics are not attributed to cells known to be manufactured by the normal DNA method in cases other than cancer.

If cancer was a disease of the cell losing the ability to replicate itself in a controlled manor, then we could expect to see uniformity between the cancer tumor and the parent cell that had lost this ability to replicate itself in a controlled manner. However; there would be no reason to expect to see uniformity between the various cancers themselves (if this uniformity did not first exist between the parenting cells). But the Nobel laureate Otto Warburg, while studying the metabolism of tumors, noted that "cancers of various species and tissue origins reveal a high uniformity from tumor to tumor." Warburg, O.: Stoffwechsel d. Tumore, Springer, Berlin, 1926. Engl. edn., The Metabolism of Tumors, tr. F. Dickens, London, 1930.
In fact there have been numerous studies all of which point to a number of parallelisms between cancer tumors of all types. There are a series of ‘common denominators’ that are shared between all cancerous tissues that do not have this shared characteristic with the host cells, which becomes an anomaly under the present DNA model for explaining cancer. The following 4 quotes with references point this relationship out.

i) "Correlatively, the Coris find the lactic acid and sugar content of the various exhibitions of cancer to be highly uniform. Williams and his co-workers report a pronounced degree of uniformity in the concentration of eight B vitamins in a great variety of animal and human tumours, regardless of the tissue of origin or the manner of their induction." Cori, C.F., and Cori, C.J.:J. Biol. Chem., 64:11, 1925

ii) "Shack describes an almost complete uniformity in cytochrome oxidase content in a number of mouse tumors.” Shack, J.: J. Natl. Cancer Inst. 3:389, 1943
 

iii) "Maver and Barrett describe substantial evidence for an immunological uniformity among malignant tumors. Greenstein reports an impressive degree of uniformity in enzyme concentration among malignant tissues, regardless of their means of induction, tissue of origin or species of origin." Greenstein, J.P.: Symposium on Cancer, A.A.A.S. Research Conference on Cancer, ed. F.R.Moulton, Am. Assoc. Advancement of Science, Washington, D.C., 1945, p. 192
 

iv) "The uniformity of various exhibitions of cancer in respiratory properties, lactic acid production, vitamin content, enzyme content, action on a given substrate, effect on liver catalase, cytochrome oxidase content immunological properties, and many other characteristics is correlative to an uniformity of malignant tumors in the ability to metastasize, in their amenability to heterotransplantability, and in their autonomy, invasiveness and erosiveness. Indeed, there is no known basic property unique to any single exhibition of cancer---the only variation being a morphological one partially conditioned by admixed benign or somatic components." Cancer and the Immune System The Vital Connection

After considering all the above quotations, a fair question to be asked would be; why is there such uniformity between cancer tissues from tumor to tumor? If a fault in the DNA is causing this tissue growth, why then is the daughter cell even distinguishable from the normal cell? If we grant that a flaw in the p52 gene is allowing for the orderly manufacture of cells to going astray, this by itself does not give licence to allow for the cells that are spontaneously being generated to be any different from the host cell. All of this uniformity seems to point to the possibility that there is one common theme in all cancers, which implies a single source of manufacture. It is impossible for the present DNA model to account for this anomaly of uniformity when such shared characteristics were not first present in the host/parent cells. Yet ‘uniformity’ is an obvious inference if the cancers were all being formed from a single source (i.e. the ‘repair’ arm of our immune system). A pattern of uniformity would be necessary if the immune system were responsible for the manufacture of all of these tissues and a pattern of uniformity is what is being observed. This uniformity then becomes a truth standing on her head to get attention. To account for this uniformity under the present definition of the DNA model of cancer, it is said that the original cancer has metastasized to another part of the body. The word ‘metastasized’ imparts the belief that the new cancer has similar characteristics to the original cancer. The patient is never considered to have come down with two bouts of cancer, but rather one which has managed to have cells ’break away’ and commence their havoc at a new site. The model for explaining how cancer can ‘spread’ like this under the DNA framework is troubling. The belief is that some cancer cells have broken away from the original site, and migrate to a new location and began work there (metastasized). But the original cancer is thought to have been caused by some antigen entering the body and attacking the DNA gene that is responsible for the orderly generation of cell replacement. The secondary site is never thought to be caused from a new antigen that has managed to enter this same patient, and started a new defect in the patients DNA. This ‘metastasize’ model allows for the similarities in the various cancer tumors to be understood and accounted for within the dogmatic framework of the current DNA model. The new cancer is described as a continuation of the original cancer at a new location. But the DNA model requires a host of special abilities being granted to these ‘cancer cells’ in order for them to be able to pull this off. They are given the ability to recruit allies, and ‘cloak’ themselves in the endeavour to explain how they can travel undetected and unharmed by the immune system as they journey to this new site.

Since there are only two ways in which a cell can be manufactured, and only one of the two methods can account for this ‘uniformity’, and in conjunction, account for why the new cell is distinguishable from the parent cell, and in turn account for why the cells can travel undetected in the body, then it would be prudent to entertain the possibility that the ‘repair’ aspect of our immune system (the only other way in which a living cell can come into existence) could be responsible for this non requested cell growth we refer to as ‘cancer‘.
 


There still remain many mysteries surrounding the immune system, and much is remaining to be learned. At present, the term ‘immune system’ is used to describe a complex series of body functions that more accurately could be described as three distinct systems with three distinct responsibilities. The term ‘immune system’ is currently used to describe all three of these functions; it is the responsibility of the immune system to
i) Identify foreign antigens that are deemed to be enemies of the body.
 
ii) Destroy these enemies of the body; and
 
iii) Repair any damage that may have occurred during this onslaught.
 
( Enveloped within the repair aspect, is the immune system’s ability to ‘inflame’ the site with increased blood flow, a natural and vital component necessary to sustain the life of these newly generated cells by supplying oxygen and nutrients, as well as waste removal. The DNA model can account for the generation of new tissues, but not the accompanying modifications to the blood supply. An entirely distinct explanation must be employed that is thought to be happening simultaneously to account for the accompanying blood supply necessary to maintain the existence of these newly generated cells from the framework of the DNA model).
 

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Re: The audacity of questioning the root cause of cancer.

I've tried to have this exact conversation with people but unable to put the words together this well

May I forward this to a few friends ?

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Re: The audacity of questioning the root cause of cancer.

It’s public so you don’t need my permission but it’s nice of you to ask. I was cutting and pasting this into sections that were small enough to fit into the 20,000 character limit and was cut off before I finished. I thought there may have been a 3 post limit per day. If that is the case I will resume pasting sections again today if I have 2 left. If you pm me your e-mail I could send the essay to you whole so you don’t have to wait.  

 

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The cancer cell is distinguishable from the normal cell because it was manufactured by a different process than normal cell replacement. But the DNA method of cell regeneration is not different and not distinguishable from the original. No explanation has been put forward to offer as to why this underlying characteristic would change just because the controlled order of cell replacement went astray. If the DNA model were to be true, then tumors should be clusters of cells indistinguishable from the host cells around them. A defect in the P53 gene should result in the formation of a wart, or a small polyp that could only grow to a size that could be supported by the existing blood supply. But we are still faced with the fact that the cancerous tumors are distinguishable from the surrounding tissue, and often accompanied by their own modified blood supply.
A close examination of tumor tissues reveals that there are similarities between the formation of scar tissue (with its accompanying inflammation that is necessary to support and maintain the existence of this newly generated cell) and cancerous activity. This relationship is most easily observed by comparing skin surface scars with skin cancer. Because scar tissue was manufactured rapidly, and by a different process from normal tissue replacement (normal cell division as outlined in the cell DNA), it has different characteristics. Scar tissue made from skin cells has a distinct appearance with a smoother surface, firmer density, (described as a waxy appearance) and a different pigment from that of the surrounding tissue. The following quote can be found at the final report on Grant GR/K71394 Mathematical Model of Scar Tissue
“Scar tissue formation is a ubiquitous feature of adult wound healing, with the resulting repair both functionally and cosmetically inferior to normal skin. At microscopic level, the main difference between scar and normal tissue is in the alignment pattern of the collagen fibers of which they are composed.” 

‘Functionally and cosmetically inferior’ are characteristics shared by cells thought to be manufactured by cancer cells, and cells known to be manufactured by our immune system. And yet ‘functionally and cosmetically inferior’ characteristics are not attributed to cells known to be manufactured by the normal DNA method in cases other than cancer.

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If cancer was a disease of the cell losing the ability to replicate itself in a controlled manor, then we could expect to see uniformity between the cancer tumor and the parent cell that had lost this ability to replicate itself in a controlled manner. However; there would be no reason to expect to see uniformity between the various cancers themselves (if this uniformity did not first exist between the parenting cells). But the Nobel laureate Otto Warburg, while studying the metabolism of tumors, noted that "cancers of various species and tissue origins reveal a high uniformity from tumor to tumor." Warburg, O.: Stoffwechsel d. Tumore, Springer, Berlin, 1926. Engl. edn., The Metabolism of Tumors, tr. F. Dickens, London, 1930.
In fact there have been numerous studies all of which point to a number of parallelisms between cancer tumors of all types. There are a series of ‘common denominators’ that are shared between all cancerous tissues that do not have this shared characteristic with the host cells, which becomes an anomaly under the present DNA model for explaining cancer. The following 4 quotes with references point this relationship out.

i) "Correlatively, the Coris find the lactic acid and sugar content of the various exhibitions of cancer to be highly uniform. Williams and his co-workers report a pronounced degree of uniformity in the concentration of eight B vitamins in a great variety of animal and human tumours, regardless of the tissue of origin or the manner of their induction." Cori, C.F., and Cori, C.J.:J. Biol. Chem., 64:11, 1925

ii) "Shack describes an almost complete uniformity in cytochrome oxidase content in a number of mouse tumors.” Shack, J.: J. Natl. Cancer Inst. 3:389, 1943
 

iii) "Maver and Barrett describe substantial evidence for an immunological uniformity among malignant tumors. Greenstein reports an impressive degree of uniformity in enzyme concentration among malignant tissues, regardless of their means of induction, tissue of origin or species of origin." Greenstein, J.P.: Symposium on Cancer, A.A.A.S. Research Conference on Cancer, ed. F.R.Moulton, Am. Assoc. Advancement of Science, Washington, D.C., 1945, p. 192
 

iv) "The uniformity of various exhibitions of cancer in respiratory properties, lactic acid production, vitamin content, enzyme content, action on a given substrate, effect on liver catalase, cytochrome oxidase content immunological properties, and many other characteristics is correlative to an uniformity of malignant tumors in the ability to metastasize, in their amenability to heterotransplantability, and in their autonomy, invasiveness and erosiveness. Indeed, there is no known basic property unique to any single exhibition of cancer---the only variation being a morphological one partially conditioned by admixed benign or somatic components." Cancer and the Immune System The Vital Connection

After considering all the above quotations, a fair question to be asked would be; why is there such uniformity between cancer tissues from tumor to tumor? If a fault in the DNA is causing this tissue growth, why then is the daughter cell even distinguishable from the normal cell? If we grant that a flaw in the p52 gene is allowing for the orderly manufacture of cells to going astray, this by itself does not give licence to allow for the cells that are spontaneously being generated to be any different from the host cell. All of this uniformity seems to point to the possibility that there is one common theme in all cancers, which implies a single source of manufacture. It is impossible for the present DNA model to account for this anomaly of uniformity when such shared characteristics were not first present in the host/parent cells. Yet ‘uniformity’ is an obvious inference if the cancers were all being formed from a single source (i.e. the ‘repair’ arm of our immune system). A pattern of uniformity would be necessary if the immune system were responsible for the manufacture of all of these tissues and a pattern of uniformity is what is being observed. This uniformity then becomes a truth standing on her head to get attention. To account for this uniformity under the present definition of the DNA model of cancer, it is said that the original cancer has metastasized to another part of the body. The word ‘metastasized’ imparts the belief that the new cancer has similar characteristics to the original cancer. The patient is never considered to have come down with two bouts of cancer, but rather one which has managed to have cells ’break away’ and commence their havoc at a new site. The model for explaining how cancer can ‘spread’ like this under the DNA framework is troubling. The belief is that some cancer cells have broken away from the original site, and migrate to a new location and began work there (metastasized). But the original cancer is thought to have been caused by some antigen entering the body and attacking the DNA gene that is responsible for the orderly generation of cell replacement. The secondary site is never thought to be caused from a new antigen that has managed to enter this same patient, and started a new defect in the patients DNA. This ‘metastasize’ model allows for the similarities in the various cancer tumors to be understood and accounted for within the dogmatic framework of the current DNA model. The new cancer is described as a continuation of the original cancer at a new location. But the DNA model requires a host of special abilities being granted to these ‘cancer cells’ in order for them to be able to pull this off. They are given the ability to recruit allies, and ‘cloak’ themselves in the endeavour to explain how they can travel undetected and unharmed by the immune system as they journey to this new site.

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Alexanderwallen1@gmail.com
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Since there are only two ways in which a cell can be manufactured, and only one of the two methods can account for this ‘uniformity’, and in conjunction, account for why the new cell is distinguishable from the parent cell, and in turn account for why the cells can travel undetected in the body, then it would be prudent to entertain the possibility that the ‘repair’ aspect of our immune system (the only other way in which a living cell can come into existence) could be responsible for this non requested cell growth we refer to as ‘cancer‘.


There still remain many mysteries surrounding the immune system, and much is remaining to be learned. At present, the term ‘immune system’ is used to describe a complex series of body functions that more accurately could be described as three distinct systems with three distinct responsibilities. The term ‘immune system’ is currently used to describe all three of these functions; it is the responsibility of the immune system to
i) Identify foreign antigens that are deemed to be enemies of the body.
ii) Destroy these enemies of the body; and
 
iii) Repair any damage that may have occurred during this onslaught.
( Enveloped within the repair aspect, is the immune system’s ability to ‘inflame’ the site with increased blood flow, a natural and vital component necessary to sustain the life of these newly generated cells by supplying oxygen and nutrients, as well as waste removal. The DNA model can account for the generation of new tissues, but not the accompanying modifications to the blood supply. An entirely distinct explanation must be employed that is thought to be happening simultaneously to account for the accompanying blood supply necessary to maintain the existence of these newly generated cells from the framework of the DNA model).

It has been observed and acknowledged that there is a corresponding activity in the lymphatic system in episodes of cancer. Often it is observed that the cancer has spread to the adjacent lymph nodes, and a study of the individual’s lymph nodes is used to determine if the cancer has spread (metastasized). Yet the purpose of the lymph nodes is to serve as the center for production of phagocytes, which engulf bacteria and poisonous substances. Lymph nodes are a vital component of the immune system, and are always associated with immune system activity. In other words, with every non-cancerous situation, the enlarged lymph nodes indicates that the immune system is active and fulfilling its function. However; we are told in episodes of cancer, although it is acknowledged that the lymph nodes are active, the immune system is thought to remain inactive, and they are not fulfilling their function. Under the DNA model, it is not yet understood why the immune system would sit idle while events that it is designed to avert, takes place. No explanation is provided to account for how or even why the cancer employs the lymph nodes in the spread of the disease. From the framework of the scar tissue model, the lymph nodes would obviously be enlarged as the immune system was carrying out this work. But the present definition of cancer is thought to be having this activity take place without arousing an immune system response. If the cancer is to be defined as a defect at the cellular level as outlined in the DNA model, it is a necessary maxim to hold that the immune system is permitting the existence of these newly generated cells because it is unaware of their existence. From the framework of the DNA model the evidence that supports this observation is the fact that the immune system does not make any attempt to prevent this cancerous activity from taking place. The explanation for how these cancer cells do this requires that the cancer cells are bestowed a number of special abilities that are unique only to the cancer cells, all of which exceeds my level of gullibility. These special abilities are attributed to the cancer cells to help explain away why this event is being observed. This anomaly has never been adequately addressed and remains as a major conundrum of the present DNA model of cancer. It defies reason to accept that the immune system is doing nothing, and simultaneously accept that the lymph nodes are enlarged, but for a reason other than an immune system activity. A more credible explanation for this phenomenon is that the immune system is doing everything. If cancer were found to be a function of a defective immune system then this conundrum becomes a logical inference. The immune system will not attack the cancer because the immune system sent the cancer. The term ‘cancer’ should refer to a maverick arm of the immune system, i.e. the patient has a defective ‘repair arm’ of his or her immune system which has lost the ability to know when not to commence work on damaged tissues, and/or lacks the ability to know when to shut off this work once it has commenced.

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All of the anomalies that surround this disease would suddenly vanish if cancer were to be viewed as a product of a defective immune system. We would not have to address how the cancer causing antigens enter the bodies of some individuals, and not others. These ‘antigens’ are the genesis point and mark the birth of cancer from the DNA model yet still remains to be unobserved at the cancer site. We would not have to address how cancer can move undetected throughout the body and take up residence at a new location without being detected, or encountering any form of resistance along the way. The study of cancer would then become an analysis of the way in which various cultures treat their immune systems, which then paves the way for this malfunction to take hold. Cancer becomes much less mysterious if we simply take the point of view that the immune system is causing the lawless proliferation of growth, (since it is its job to do so,) and the immune system is also supplying the essential blood supply to support this newly generated growth, by way of inflammation (again, because it is its job to do so). To read the present accounting of how the cancer cells manage to build the infrastructure of a blood supply system to support the existence of these newly generated cells requires an unrealistic level of trust. The cancer cells are attributed with a host of special abilities unique to them alone, all of which are necessary to account for this event taking place within the confines of the DNA model. Yet at the same time, the philosophy in treating cancer patients with radiation and chemotherapy is from the belief that these are the weakest cells and will be the first ones to die. Why would these cancer cells which are deemed invincible, immortal, perpetual cells be expected to be the first ones to die?
Mark Twain is quoted as having said “What gets us into trouble is not what we don't know… It's what we know for sure, that just ain't so.”


Cancer should be viewed as the fulfillment of a two part equation. First, the individual must be in possession of a faulty immune system that is capable of generating cells without there being a need, and/or generating cells and not receiving the stop code. Secondly, this individual must then have their defective immune system directed toward and perform this non requested work on a specific group of tissues.
Statistical connections have been difficult to extract using the DNA framework because the scientific community is only looking at half the equation, i.e. why the cancer cells are attacking a specific tissue. Currently, scientists are only looking at the hierarchy of cell types to come under attack, which produces only ‘links’ to lifestyle choices or environmental exposures, etc.. If we factor into this how an individual treats their immune system, then perhaps some concrete relationships could be observed, and the global mapping of cancers would have significance. From the framework of this new model for cancer, the global mappings can be understood, and they do tend to have significance.
Immunosuppressant medications were developed to intentionally decrease the effect of the immune system in organ transplant patents, for the purpose of preventing the body’s defence mechanism from attacking (rejecting) the foreign tissues of the transplant operation. If the patient survives the operation, and overcomes the rejection, they will live longer lives then they would have, had they not had the operation. Unfortunately, the statistical evidence shows that the transplant patient will ultimately succumb to a bout with cancer. This phenomenon has scientists struggling for an explanation:
“Scientists believe transplant recipients were already at risk
for cancer because their weakened immune system could not
keep healthy cells from becoming malignant”.
“The use of immunosuppressants(cyclosporine) increases the
chance cancer cells will divide and invade surrounding tissue.
However it is not clear if cyclosporine can change normal cells
into cancer cells researchers say”
web search for ‘organ transplants’
Organ Transplant Drug Increases Cancer Risk
Friday, Feb.12, 1999\
By using this new model for explaining cancer, we would predict that by creating a defective immune system, we increase the likelihood that some form of cancer will result. We would then have satisfied the first part of the two part equation. We have an individual with a weakened immune system that is capable of generating non requested tissues. All the other ‘links’ and ‘markers’ merely help to ascertain which of the numerous types of cancer the patient is apt to acquire. That is to say, the numerous lifestyle links, dietary links, and environmental links (physical carcinogens, chemical carcinogens and biological carcinogens.), all have a tendency to either promote any given tissue in the body towards cancerous activity, or to demote specific tissues away from being the likely candidate for cancerous activity. If the immune system is the root cause of cancer, then obviously it will be difficult to discover a cure so long as our efforts are focused on employing the immune system to attack itself. The immune system is designed to recognize and not attack itself. Perhaps this helps to explain why there are presently only treatments for cancer, and not yet any cures.

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Re: The audacity of questioning the root cause of cancer.

If a weakened immune system has been shown to causes cancer, as in the cases of patients taking immunosuppressants, would it not therefore follow that a strengthened immune system, should overcome, or at least prevent cancer? There is a disturbing pattern with immunosuppressant medications which clearly establishes that there is a cause-effect relationship between cancer and a weakened immune system. It would be anticipated that a concrete cause/effect relationship between cancer and a substance would be the Holy Grail in the cancer research world. This is the one thing that I would expect everyone would have been searching for. But no one seems to be able to recognise this because it doesn’t fit with the DNA model. The DNA model is focused exclusively on the inner workings of the cell for the answer as to why it is reproducing itself relentlessly. When the malfunctioning immune system generates this relentless cell production from outside the cell itself, it is dismissed as an unexplained anomaly because it cannot be accounted for within the confines of the dogmatic view that cancer is happening at the cellular level.

Cold-Hot; Inactive-active; benign-malignant. These are the differences between non life threatening benign tumours, and life threatening malignant tumours, specifically one is active (cancerous) and one is benign (scar tissue). It may turn out that the fundamental difference between a benign tumor and a cancerous tumor is in the timing of when they are being observed. If you discover a benign tumor (or perhaps we could call it a tumor ‘‘after-the-fact’’), the body has stopped, and there is a mass of fibrous scar tissue that is currently not undergoing any development. If however, you were to stumble upon this very same tumor as it was being manufactured, it would be deemed to be a cancerous tumor. If your body is capable of producing a benign tumor, it is capable of producing a cancerous tumor. In the benign tumor, the immune system began a repair process that may or may not have been required, but evidently it did in due course receive the ‘stop code’. In a cancerous tumor, either the cells do not receive the ‘stop code’, or it is being observed before it has received the ‘stop code’. I have never heard of an Oncologist saying to a patient “You’ve got some sort of tumor being produced, but let’s leave it be, and see if it doesn’t stop and become benign on its own”. If that same tissue were to be observed when it was inactive, it would simply be dismissed as a benign tumor that had previously been produced at some time in the past. It is dismissed as scarring, and is of no immediate concern, because it poses no danger to the patient. Everyone freely accepts that the inactive scar tissue was manufactured by the repair arm of the immune system. It should therefore be an easy inference to accept that cancer, or active scar tissue, or perhaps ‘runaway scar tissue’, is currently being manufactured by this same arm of the immune system, though be it a defective one.

When medical professionals discover an active tumor being produced, they may opt to surgically remove the tumor and the offending cancer cells that made it (excision biopsy). As this radical surgery has not yielded the desired success rates, the medical profession has expanded the scope of the surgery to include the surrounding tissues (margin), believing that these tissues might also contain some of the stray cancer cells. They then close up the wound and hope that they have managed to remove all of the cancerous tissue. Now they must wait until the immune system has had time to heal up the surgical wound before testing the area, because the activity of the inflammatory nature of the healing process will read as ‘hot’. We then have the defective immune system, which may turn out to have caused the tumor to begin with, being invited back to the site, and being expected to heal up this surgical cut. Healing is what the immune system does. Therefore, this is an exercise for it. Often, the immune system heals over the surgery and then stops. The surgery was a success. Sometimes, however; the immune system doesn’t stop. The immune system continues to produce scar tissue, and rapidly divide the adjoining tissues without receiving the message that the task has been completed. The poor surgeon is mystified that he or she could have missed some of the cancer cells, and now they appear to have merely taken up where they left off. If the DNA model were to be true, that some carcinogen ventured to the site and caused a defect in the cell DNA, then this patient, now rid of the offending tissues, should mathematically be given the same bill of health as a non patient (i.e. someone who has never had cancer). But the statistics do not support this optimistic expectation. Quite often, the cancer patients who undergo surgery have recurrences at the original site. If the cancer returns but at another location, then the surgery would be statistically labelled as a success. Even with this clemency being granted, the statistics for the surgery are not too favourable. The apparent failure of the surgery has given birth to the suspicions that exposing the cancerous tissue to the air helps it to spread. Or exposing the cancer to the light of the Operating Room, perhaps, is what causes it to flourish. Exposing the cancer to the light and air is merely a necessary by-product of the fact that these cells have been operated on, and as a result, the immune system is re-invited back to the region to repair the surgical wound. The suppositions that the light or air has anything to do with any re-occurrence can be dismissed because surgeries that are preformed on patients, who have not been diagnosed with cancer, are not subject to similar incidences of tumors, despite also being subjected to the light and air. These patients do not have the first prerequisite, namely the faulty immune system that is incapable of generating the “stop code“. Even the supporters of the DNA model, acknowledge that cancer cells are in all of us (because the ‘spontaneous existence of matter’ is a hard concept to ‘sell’ and an absurd proposition). If we were to attribute this reaction to the light and/or air as yet another mystical feature enjoyed only by cancer cells, we would still need to account for why every surgery was not subject to the same level of re-occurrence. From the point of view of this new model, this anomaly would be addressed as follows; the non cancerous patient has a properly functioning immune system which still has the ability of knowing when to stop the healing process. In cancer patients, the immune system has already shown to be defective, therefore it should not be surprising to find out that sometimes it does turn out to be relentlessly continuing the healing process and in so doing, inflict the area with a new cluster of cancerous activity, despite how diligent and careful the surgeon had preformed.

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