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Cancer homeostasis
In reality all along cancer progression tumor and organism (WOB) maintain
an equilibrium (homeostasis), which is disrupted only at time of death. Not
only cancer, but any condition in the body maintains homeostasis.
Non-equilibrium results when organism is in a grave danger and may even die.
WOB maintains homeostasis in health and disease.
Essential hypertension
First let's turn our attention to elevated blood pressure, known as essential
hypertension. It rises extremely slowly, and many years go by until it reaches
high levels which endanger the patient. Blood pressure rises in small steps.
After each step it remains constant (invariant) for some time, and rises
again. Between two consecutive steps, blood pressure maintains equilibrium
(homeostasis). It never rises exponentially. Nor does any chronic disease
even if overwhelming the patient. It always remains under WOB control. And
so does cancer.
Chronic leukemia
WOB control is observed in chronic leukemia, which in plain English means
'White Blood'. The disease is manifested by a gradual increase of white blood
cell count (WBCC) in the blood. When accompanied by a loss of red blood cells,
blood becomes pale, or white, hence the name. A healthy person has about 10,000
WBC in a cubic millimeter of blood. As leukemia progresses, WBCC rises
in steps. From one equilibrium level to the subsequent one.
Usually, leukemia is detected accidentally. A woman applies for a job,
and her medical checkup reveals a WBCC of 80,000. She is then
told that she has chronic leukemia. Since at this stage treatment is
not required, she is invited to return for further medical checkups. WBCC
continues rising in steps, between which, count remains invariant. Generally
when it reaches 100,000, patient feels ill and is treated.
Acute leukemia
Chronic leukemia may turn unexpectedly into a dangerous acute leukemia
when patient dies within a short period of time. The higher WBCC the greater
the risk of this fateful event. Hematologists attempted therefore to reduce
cell count with chemical drugs, hoping to prevent acute leukemia. Unfortunately,
with repeated treatments, leukemia responds less and less, and the WBCC fails
to decline.
Blood irradiation
During the sixties of the previous century, scientists in Brookhaven National
Laboratory developed an x-ray machine for blood irradiation. Patients
were connected to the machine with two catheters. One drove arterial blood
from forearm into a tube that was irradiated by the machine. At the
other end the tube was connected to a second catheter through which
irradiated blood was returned to the forearm. In this manner blood
was irradiated outside the body. Since leukemic cells are more sensitive to
x-rays than other WBC, their count dropped.
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This dramatic achievement was followed by a disappointment. Within three days
WBCC returned exactly to its pre-treatment level. Neither higher nor lower.
And so was the result of repeated irradiations. Disappointed with their treatment
failure, scientists abandoned the machine and the experiment was forgotten.
However they ignored its significance. In chronic leukemia
WBCC is tightly controlled, since after irradiation WOB replenished the
exact amount of WBC which were depleted by the procedure.
WOB controls chronic leukemia
Leukemic WBC count is determined by a set point which is controlled
by WOB.. As disease advances WOB raises the set point and WBC count
rises. Irradiation depletes WBC and their count drops below the set point.
WOB then corrects the damage and replenishes the missing cells. A similar
behavior is observed also in essential hypertension. A special sensor called
baroceptor, continually monitors our blood pressure whose height is determined
by a set-point controlled by WOB. When pressure rises above this set point.
WOB lowers it and vice versa. As essential hypertension advances, WOB
raises the set point in small steps, always maintaining homeostasis.
Cancer proceeds stepwise, always maintaining homeostasis
Leukemia is a genuine cancer, and its behavior illustrates the fate of all
cancers . All proceed in small steps tightly controlled by WOB. Between consecutive
steps they maintain homeostasis. The notion that cancer rebels and evades
WOB control is a folly. WOB controls also colon cancer, which
seeds the liver with microscopic metastases early in its development.
When the tumor is detected and removed, hidden metastases in the liver grow
and become visible. Like in leukemia, the size of the colon tumor
mass is determined by a set point. When tumor is removed WOB replenishes
the missing tumor mass by growing metastases in the liver.
Uveal melanoma
A similar phenomenon was described in intra-ocular melanomas. Usually
eyes with these tumors are enucleated. Yet in 1978 Zimmerman et al,
suggested that eye removal may promote the spread of melanoma cells
to other organs and increase mortality (1).
They drew their conclusion from epidemiological analysis of patient
mortality . Similar observations were made in one mouse tumor, the Lewis lung
carcinoma. Eradication of a primary Lewis lung carcinoma by irradiation is
followed by the rapid growth of metastases that kill the animal within 18
days after the completion of radiation therapy. Metastatic seeding was inhibited
by angiostatin (2). Recently Apte et al, demonstrated
that angiostatin produced by certain primary uveal melanoma
cell lines impedes the development of liver metastasis.
They concluded :' In certain circumstances, enuclation of melanoma-cotaining
eyes may unwittingly exacerbate the metastatic potential of uveal melanomas' (3)
Putting the
tumor to sleep
Since cancer maintains an equilibrium with host (WOB), its progression can
be influenced either by treating the tumor or by lowering the set-point, which
is called here WOB boosting. In advanced cancers which spread into remote
organs, treating the tumor (metastases) generally fails. With repeated treatments,
tumors respond less and less, and resist further treatments. Here WOB
boosting is the only effective way to slow down cancer progression.
Figuratively speaking, putting the tumor to sleep remains the only option
for the patient. Here medicine has little to offer since it lacks means
to boost WOB. On the other hand, alternative medicine specializes in WOB
boosting, and ought to be recommended to the patient. It provides many
ways to prolong remission. These are applied by
Cancer-Yogis who succeed to put their tumors to sleep, and
live peacefully with cancer.
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A press that illustrates concepts like set-point, equilibrium,
and WOB boosting.
The press consists of two rods on which a blue plate is mounted. The plate shifts up and down. WOB exerts pressure on the tumor which is transmitted through a spring. The set-point indicates pressure intensity. The lower it is the greater the pressure and vice versa. Normally the plate is still. WOB and tumor are in equilibrium (homeostasis). When WOB reduces its pressure the plate moves up, set-point rises, tumor grows, and the press regains a new equilibrium which is maintained for a while.
WOB boosting strengthens WOB pressure. Set-point drops and tumor shrinks.
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References
1. Does enucleation of the eye containing a malignant
melanoma prevent or accelerate the dissemination of tumour cells.
Zimmerman LE, McLean IW, Foster WD. Br
J Ophthalmol 1978 Jun;62(6):420-5
A reappraisal of survival data
on patients with uveal melanomas has led us to these impressions: (a) that
the mortality rate before enucleation is low, estimated at 1% per year; (b)
that the mortality rate rises abruptly following enucleation, reaching
a peak of about 8% during the second year after enucleation; and (c) that
approximately two-thirds of the fatalities could be attributed to the dissemination
of tumour emboli at the time of enucleation. From these impressions we believe the following conclusions
are warranted: (a) enucleation as it has been performed in the past may have
for many patients an adverse rather than a beneficial effect with respect
to the development of metastatic disease from malignant melanoma of the choroid
and ciliary body. (b) A long-term follow-up study of untreated patients
with melanomas of the choroid and ciliary body is indicated. (c) New techniques for enucleation designed
to prevent the dissemination of tumour cells must be developed and tested
to enable the ophthalmic surgeon to remove safely the tumour-containing eye
that has developed such complications as uncontrollable glaucoma, panophthalmitis,
or proptosis from extraocular extension.
2. Camphausen K et al. Radiation therapy to a primary
tumor accelerates metastatic growth in mice. Cancer Res 2001 Mar 1;61(5):2207-11
3. Apte R.S et al. Angiostatin produced
by certain primary Uveal Melanoma cell lines impeded the development of liver
metastases. Arch Ophthalmol. 2001;119;1805-1809
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