Cancer Theory

ricwally

The following article is an attempt to put forward an alternate hypothesis from the present
DNA model, for explaining cancer. It is regrettably long, and at times difficult to follow,
but if you manage to persevere through it, I believe you will find it intriguing, or at least
thought provoking.
A brief ‘attack’ on the present model is a necessary starting point. If it were not for the
fact that I am dissatisfied with the present hypothesis, there would be no need to propose
a new one.
The gist of this article, stems from the fact that there are two distinct methods for which a
cell can reproduce itself, yet only one of these methods is being contemplated as the root
problem in cancer.

Cancer is the disruption of the orderly and regulated cycle
of cell replication and division under the control of our genes.
This is a terse synopsis of the what is presently held as the cause of this modern pandemic.
“Control of our genes” has been attributed to our DNA. Any disruption with this process,
must therefor lie with the DNA. The ‘faulty DNA’ model is the only model put forward
to explain this disruption of the orderly regulated cycle. It has not been necessary to label
this as a theory, because no other theories have been put forward. Thus, it has been taken
as a ‘given’ that this disruption of the cell replication was the result of faulty DNA. All
efforts have thus far been concentrated on determining what it is that is causing the DNA
in some individuals to go astray. Various links to lifestyle, genetics, and environmental
contaminants (carcinogens), have all been proposed as possible explanations. Yet as the
lists of possible explanations grows larger, there appears to be no reduction in the amounts
of patients acquiring some form of cancer. A considerable amount of money has been
spent in the pursuit of finding a cure. Many new carcinogens or potential causes have been
brought to light. Many strides have been made towards extending the lives of those
afflicted with this misfortune. But much of this ‘deemed’ success could be attributed to the
‘early detection’ alone. Consider two hypothetical cases of an identical cancer that has a
duration of twelve years. The first case goes undetected until the tenth year of the ailment
before it is discovered. We then have a documented case that will be deemed as an
aggressive cancer, which took its toll within two short years. In the second case, the
patient is detected early, let’s say in the second year. So this patient will be logged as
having had a ten year survival rate, before finally succumbing to the disease. This scenario
illustrates how the move towards detecting the cancer early, in itself has led to the
appearance of great medical strides being achieved, even if this second hypothetical patient
received no medical attention after his or her early diagnosis. I do not make this point to
ridicule the medical profession. Rather, it is just one more example of one set of data
having more then one conclusion. Early detection has been attributed to being of
paramount importance in the survival rates of cancer. It could be that ‘early detection’ is
merely giving a head start to the timepiece that measures cure success.
Another critique that I have is the tendency to dilute the figures for cancer into an ever
increasing number of categories. This tendency gives the appearance that the numbers of
patients that are afflicted with a certain cancer type is on the decline. For example, in years
past, there was but one type of breast cancer. All cases of the ailment fell into this one
category. Presently there is a tendency to siphon off some of the occurrences of breast
cancer into their own categories. Inflammatory Breast Cancer, and Male Breast Cancer
are often removed from the big picture to be viewed as separate issues. The remaining
cases are divided into ductile versus lobular categories; or invasive versus in-situ. Since it
is not possible for a patient to simultaneously come down with both types, they must
therefor fall under the category of one or the other. By virtue of the numbers now being
divided, they are now being used to represent the appearance of a decline in cases of
cancer for any one category. This gives a misleading impression that the medical
community is making great strides in their efforts to combat this ‘disease’. However, it can
be observed that the overall picture is getting uglier. If we sum these categories back
together so that we can compare them with the earlier statistics of breast cancer, then we
are forced into the grim realization that there is no progress being made. This trend can
also be observed in the categorization of colon cancer patients. In earlier years, there were
no individual categories of anal cancer, prostate cancer, rectal cancer, bowel cancer, and
colon cancer. These were all under one category. As science became more knowledgeable,
it could be detected that there were differences in these types of cancer, and as a result,
new categories were required, and warranted. Since it is not possible to go back in time
and properly re-categorize the earlier statistics into the new categories, we would need to
sum these current categories together for comparison purposes, in order to see if any
progress was being made in this sector of cancer research. These figures, too are
discouraging.
The long list of potential ’links’ to cancer, does not appear to be producing any better
health. Knowing that asbestos dust, or a high fat diet, may be contributing to this
epidemic; or that a high fiber diet, or sun block lotions have been attributed to the survival
from this epidemic, does not appear to have much effect on the epidemic as a whole. It
would be expected that as our knowledge increases as to which carcinogens we need to
avoid, and which behaviors we need to adopt or promote , the resulting number of cancer
cases should be on the decline. Yet the percentage of people who can expect to have to
deal with some form of cancer in their lifetime, is on the rise. It could be argued that this is
an unavoidable byproduct of our longer life expectancy. But we can factor out this retort
by focusing on cancer statistics that are only inflicting those in the prime of their life. It
can be observed that these figures too, are still on the rise. One might conclude that this is
an overtly pessimistic interpretation of the statistics. If it does appear pessimistic, it is
only to contrast optimism, and only after 120 years of being optimistic has led nowhere. A
quick look back into old encyclopedia articles confirms that there has been little or no
progress over the years. The scientific, and medical communities are focusing exclusively
on our DNA as being the culprit. It would be expected that after more then a century of
pursuing this one angle, we could expect more progress then is presently seen.
To illustrate the claim that there has been no significant progress in the field of cancer,
here is a quotation from the American Council on Science and Health in which they defend
themselves from there critics by outlining that :
"A study published in ‘Cancer’, the journal of the American Cancer Society [1],
reports findings that confirm what the American Council on Science and Health
(ACSH) has long held: that the incidence and overall death rates from cancer have
been declining in the United States. ACSH's position on U.S. cancer rates was set
forth in detail in its 1995 booklet, "Update: Is There a Cancer Epidemic in the United
States?"
The false claim that cancer rates are rising is a favorite of quackery promoters who
want to undermine public trust in food companies, drug companies, chemical
manufacturers, and the medical profession. ACSH's 1995 report concluded that, with
a few exceptions -- primarily lung cancer (caused by cigarette smoking), melanoma (a
skin cancer related to overexposure to sunlight), and AIDS-related cancers -- there
had been little overall increase over the previous 40 years in either the number of new
cases reported or the number of cancer deaths."(end of quotation)
This claim, in my opinion does not represent progress. It would be equivalent to claim that
the fleet gas mileage of domestic passenger vehicles was on the rise, so long as we exclude
the SUV’s and pick-up trucks. When we start to pick and choose the statistics that we are
going to include,(or in this case exclude) we are manipulating the data to say anything that
we want it too. There is a self evident ‘fallacy’ with this practice. For this reason, I try to
limit my use of numbers and percentages, since there are so many of them to choose from,
and it is human nature to use the figures that support your claim, and dismiss those that do
not.
My quest into the subject of cancer begins before the industrial revolution, when cancer
was an exceptionally unusual disease. I will start with a passage taken from an
Encyclopedia Britannica article from 1949, in which the German pathologist Rudolf
‘Virchow laid great stress upon the importance of chronic irritation in the causation
of new growth ...The rival theory put forward by Cohnheim about 1880 that new growth
arises from embryological remnants included within the tissue owing to some slight error
in development.’
Here we learn that the first views on cancer (prior to 1880) were thought to be caused by
the body repairing cells that were subjected to “chronic irritation”.
Evidently, this original theory fell out of favor to the ‘new’ rival theory ( the Cohnheim
theory which has evolved into the present day DNA theory) but I can only speculate as to
why.
I will begin by re-examining the original explanation that was held back in 1860 in which;
“chronic irritation” is the cause of the growth (cancer)(*1). This chronic irritation would
imply the breakdown or continuous damage inflicted on one group of cells, or one tissue
type. It had long been observed that betel-nut chewing had been linked to oral cancer. This
phenomena was originally accounted for with the claim that the abrasive quality of these
nuts caused an irritation in the cheek tissue of the mouth. When the new theory came
along, this phenomena was attributed to arecoline, one of the properties that could now be
scientifically identified to this plant, as being responsible for the oral cancer. Similarly,
connections were made between scrotum cancer and soot by observing the high
percentage of chimney sweeps who came down with this ailment. As time progressed, it
could be isolated that it was benzopyrene, an ingredient in coal tar that was causing the
irritation. This new ability to isolate the specific element that were responsible for this
cause-effect relationship, coincided with the new proposed theory from Cohnheim (which
held that the cancerous growth was caused from “embryological remnants included within
the tissue owing to some slight error in development” . The newly discovered technique of
microscopical staining, lent itself remarkably well to the belief that there was something
going on inside the individual cell that was causing it to lawlessly reproduce itself, and had
just become available in 1872. I can well imagine how this new ability to examine
carcinogens at the molecular level, helped this new ‘molecular theory’ win favor over the
older chronic irritation theory. Nevertheless this does not invalidate the original theory.
The original theory was never revoked, or flat out rejected, but rather it was passed over
when these new scientific tools came on line. It would have been preferable for the
supporters of the original theory to concede that it was not the soot that was causing the
irritation,( or more specifically the benzopyrene in the soot,) as opposed to overturning
the theory altogether. It should have been conceded that it was not the abrasive irritant of
the betel nuts that was ‘physically’ weakening the tissue, but rather something in the nut
that was ‘chemically’ weakening the tissue at this location. Then the cronic irritation
principal would still remain applicable as a possible cause for cancer. This adaptation
would have allowed the ‘chronic irritation’ theory to co-exist with the ‘embryological
remnant’ theory until more was known about the disease of cancer, and the cells that it
attacks. If we concede that it is a ‘chemically’ weakened tissue, as opposed to a
‘physically’ weakened tissue, what then is the difference between the chronic irritant
theory( read: chemically weakened tissue that begins this uncontrolled growth,) and the
Cohnheim theory for cancer, which holds that the growth stems from a flaw within the
tissue owing to some internal flaw? (Although the model for DNA was only discovered
fifty years ago, it had previously been understood that there must have existed some form
of ‘gene’ that was responsible for passing along the genetic information from parent to
offspring.)
The major distinction between these two theories is in the role of the immune system. The
immune system plays no role in the Cohnheim theory ( which places the blame solely on
the DNA of the affected tissue cells.). If we re-investigate the chronic irritation theory
now, with our new found knowledge of the roles of the immune system, we might
conclude that the original theory should not have been so quickly overlooked. Recognize
that the immune system has three main components;
i) to ‘identify’ foreign antigens that are deemed to be ‘enemies of the body’
ii) to ‘destroy’ these enemies of the body; and
iii) to ‘repair’ any damage that may have occurred during this onslaught.
This theory will be re-examining the chronic irritation theory by focusing on this ‘repair’
aspect of the immune system, which expressed simply, is the bodies ability to promote
rapid cell division (the formation of scar tissue) to quickly heal over breaks, wounds or
openings in the skin. The mechanism that starts this process is triggered when the body
experiences some form of trauma. A mechanism must also be 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 the rapid formation of scar tissue is no longer required. If this process of
repairing a wound is set in motion, there must also be some form of mechanism to inform
the immune system as to when to cease this activity. It doesn’t require too much
imagination to realize that the inability to shut off this repair process, would obviously
result in a similar situation to that which we presently attribute to cancer. Similarly, if this
healing process were to begin without there first being a requirement for it, then this too
would result in an activity that could only be described as cancerous. Since there are two
distinct ways in which a cell can be reproduced, we should be considering both of these
scenarios as possible explanations that might be the cause when something goes wrong.
Thus far, only the DNA model has been investigated as being the cause of this affliction.
This article will now examine scar tissue as a possible cause of this non-requested cell
replacement that we call ‘cancer’.
The immune system has in its arsenal, the ability to inflame an area with increased blood
flow, and stimulate the neighboring cells into rapidly reproducing themselves, in order to
quickly seal over an opening in the skin, which stops blood loss and prevent foreign
antigens from entering the body by way of this new opening. This process is set in motion
when the body experiences some form of trauma. When we analyze this activity more
closely, we notice that there are similarities between cancerous activity; and the
inflammation and formation of scare tissue. When we can readily observe scar tissue, as in
the case of skin surface scars, it can be detected that this is an altered form from that of
the surrounding tissue. Because it was manufactured rapidly, and by a different process
than that of normal tissue replacement (normal cell division, as outlined in that cell’s
DNA), it has different characteristics. For example, 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. A clinical
definition is as follows:

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.
www.google.com final report on Grant GR/K71394
Mathematical Model of Scar Tissue
This excerpt acknowledges that there are indeed two distinct ways that a cell can be
reproduced. Firstly, by the well understood way of the cell’s natural means of replicating
itself as outlined in the cell’s DNA code, which is referred to as ‘normal’ cell replacement,
and secondly, by a less obvious, and less understood process whereas the bodies immune
system triggers the cells into this slightly altered scar tissue. Note that this second means
of cell replacement (scar tissue) is described as “functionally and cosmetically inferior”.
The primary means of cell replacement does not have attributed these inferior qualities that
the immune system replacement method has. The purpose of a ‘Burn Unit’ is to hinder the
bodies tendency to rapidly heal over the burned area with scar tissue, when the trauma of
a burn has set off this immune response, and allow the slower process (but cosmetically
superior) of natural cell replacement to have enough time to heal the area. The rapid
growth, and the inferior quality of tissues are two attributes shared by both the tissues
manufactured by the immune system, and the tissues manufactured by cancer cells.
The easiest cancers to observe are the surface cancers. Notice that Basil Cell Carcinoma
has all of the characteristics of scar tissue (smother, denser, waxy.). This common skin
cancer could conversely be described as a slow formation of scar tissue that is both
unnecessary, and unyielding. This cancer is not considered to be a dangerous cancer
because it is slow growing and easily removed surgically. With this new model, we could
regard this cancer to be different in that; although it has the cell division element,( cells
being divided by either faulty DNA, or a faulty immune system) it does not have the
accompanying blood supply (inflammation) which is necessary to support the existence of
these newly formed cells. Note that the shape of the basil cell carcinoma would indicate
that it can only grow to a size that can be supported by the existing blood supply, and as it
grows, the center cells cannot receive oxygen or nutrients, and as a result, these center
cells die off, leaving a hollow in the middle. If this tumor were to have its own blood
supply, it would become considerably more dangerous.
Both the original ‘chronic irritation theory’, and the ‘embryological remnant theory’
are able to adequately account for the cancer cells having shared characteristics from the
‘host’ cells, however the latter theory becomes much more complex by virtue of the fact
that it must also account for the modification of

vcavanagh

Hello Ricwally, Thank you for your thoughts. You have clearly studied long and hard. I have to say that while I read your message O.K. and found it easy to understand as I went along, it was difficult to crystallise what you were trying to express. Could you give us an abbreviated version which might make it easier to grasp the thrust of the message. All thoughts should have a fair hearing. Best Wishes,
V.C.

ricwally

vcavanagh said:

Hello Ricwally, Thank you for your thoughts. You have clearly studied long and hard. I have to say that while I read your message O.K. and found it easy to understand as I went along, it was difficult to crystallise what you were trying to express. Could you give us an abbreviated version which might make it easier to grasp the thrust of the message. All thoughts should have a fair hearing. Best Wishes,
V.C.

The best answer can be taken from the opening paragraph "The gist of this article, stems from the fact that there are two distinct methods for which a cell can reproduce itself, yet only one of these methods is being contemplated as the rootproblem in cancer".