Dr. Rife and the Death of the Cancer Industry By Gary Wade

[Guest guest]

http://educate-yourself.org/gw/rifedeathofcancerindustry%20.shtml

 

 

 

 

Dr. Rife and the Death of the Cancer Industry

 

By Gary Wade

http://educate-yourself.org/gw/rifedeathofcancerindustry .shtml

 

The Possible Genetic Cause of the Great Majority of Cancer Cases

that are Microbe Induced

 

In 1931, after seven years of attempting to isolate a microbe

cause of cancer from over 20.000 cancer tissue samples, Dr. Royal

Raymond Rife did just that. Rife's 1931 discovery of a cancer microbe

finally reached general public notice in 1944. That year a article

entitled The New Microscopes was published both in the February issue

of The Journal of the Franklin Institute and in the 1944 Annual Report

of the Board of Directors of the Smithsonian Institution.

 

Rife's work was not then and has not yet been appreciated by

microbiology. because microbiology has a large blind spot, both in its

physical visual view of the living microworld and in its conceptual

view of the structure and life cycles of the living microworld. If you

wish to look at living cells, the best research optical microscopes

generally available throughout the world only reach about three

thousand power. These microscopes in general cannot detect viruses,

unless a fluorescence technique like Rife's fluorescence technique is

used. These microscopes give very limited structural detail about

living cell organelles. If the biologist wants detailed structural

information about some cell structure, they use an electron

microscope. However, the electron microscope picture is the picture of

a dead, often highly degraded and distorted structure. This is because

the sample preparation process, which produces a sample that can

withstand the conditions of high vacuum and bombardment by a high

energy electron beam has degraded and distorted the original living

structure. So at best you end up with a distorted snap shot of a non

living structure.

 

I do not mean to denigrate the great and marvelous contributions

made by the electron microscope. I have considerable personal

experience with the use and operation of scanning electron microscopes

and I hold them and transmission electron microscopes with high

regard. I particularly appreciate the immense contributions made to

the understanding of micro cell structure by the massive ultra high

resolution transmission electron microscopes such as can be found at

the University of Colorado at IBoulder,CO. . However, all this not

withstanding. I also know the electron microscopes' limitations, both

physically and in its actual use by researchers. If you have a

interest in understanding biological microstructure, go to the trouble

of going to a good research library and look up the Feb. 1944 issue of

The Journal of the Franklin Institute or the 1944 Annual Report of the

Board of Directors of the Smithsonian Institution. In the RE. Seidel

and M. Elizabeth Winter article, The New Microscopes, look at the

photographic plates. Note the high quality resolution comparable to

that of current electron microscope photographs. The photograph of the

typhoid bacillus was taken with the Rife Universal Microscope at

23,000 power and then photographically enlarged to 300,000 power.

 

Note that this photograph has the resolution commonly found in

todays high resolution electron microscope pictures of bacteria.

Further note that the resolution in this print is not as good as the

resolution on the negative it came from do to the limitations in

printing pictures in 1944 and even today. As was explained in

technical detail in Appendix A, Rife had discovered an optical

assembly configuration that effectively suppressed all Fraunhofer

diffraction phenomenon. while at the same time he made the organism

light itself by a natural fluorescence phenomenon. This fluorescence

phenomenon was achieved by illuminating the specimen with an intense

narrow wavelength band of light. The particular band of light was

unique to each microbe. Also note that this is a photograph of an

intact living bacterium. If you are familiar with current

microbiology. you know that little if any time is spent by the great

majority of researchers watching and studying live microbes. Except

for spot optical microscope checks to make sure live cultures are as

they should be or are as assumed they should be. research is carried

out by biochemical techniques the results of which are interpreted in

the light of past perceived research results. In short actually very

little live observation on microbe life cycles are carried out by

researchers anywhere on the entire planet.

 

This brings us to the other blind spot in biology. Its name is

pleomorphism or the ability of a microbe to change its physical form.

During the later half of the 19th century and into the early part of

this century, a sharply fought battle over whether or not some

microbes could change their physical form was waged. Those infavor of

monomorphism won out and it became " heresy " to advocate pleomorphism.

After two years of reviewing the research for and against

pleomorphism, it is clear that the monomorphists were wrong. The

monomorphists won the argument because they had political prestige and

economic positions of leverage. The monomorphists used optical

microscopes and lab techniques not adequate to determine the issue due

to inadequate magnification power, lack of non-lethal staining

methods, sheer ignorance, and sloppy to lazy research work. If you go

to the trouble of looking up the Feb. 1944 issue of the Franklin

Journal, note that the Rife microscope photograph of the typhoid

bacillus clearly shows the formation of a filter passing form (the

original operational meaning of the word virus) of the typhoid

bacillus, in the top end of the bacillus. Rife found that when this

bacillus virus was released by the bacillus, it had a bacterium

flagella and was motile. Now all of this is just plain crazy, if you

are a currently trained microbiologist. However, no currently trained

microbiologist owns or uses a Rife type optical microscope which could

easily view this and the similar BX cancer virus, which is also a

motile virus (ovoid body with bacterium flagella). The ovoid body

dimensions of the BX cancer virus are 750 angstroms long by 500

angstroms thick. It is propelled by a proton transport flagella the

same as the parent bacterium. This " virus " will easily fit inside the

so called AIDS virus (HIV) outer capsid and is comparable in size to

the inner (HIV) capsid. I now ask you microbiologists reading this:

Will this BX cancer " virus " be recognized in a high power electron

microscope photograph for what it is or will it just be considered

another piece of degraded cellular debris in the prepared cancer cell

section sample? Much of what you see is what you are trained to see.

How are microbiologists trained to see?

 

Rife, using his Rife type microscope, had for seven years been

able to observe and isolate a microbe from carcinoma cancer tissue.

However, upon injection of concentrations of this microbe into test

animals, no cancer was produced. In 1931, Rife got the idea to expose

a sample of card normal breast cancer tissue to 24 hours of broad band

violet to ultraviolet light exposure from a argon gas discharge tube

(see Journal of the Franklin Institute article). A one half centimeter

on a side cube of carcinoma breast cancer tissue was placed into a

test tube containing Kendall medium and incubated at 37 degrees

centigrade. The test tube was then exposed to 24 hours of argon gas

discharge light. The test tube growth medium was then examined under

the Rife Universal microscope. at a magnification of 10.000 diameters.

The medium was found to be teeming with animated ovoid microbes 1/15

microns long and 1/20 microns thick. which Rife eventually named the

BX cancer virus. This BX cancer virus was then carried through

fourteen transplants from Kendall Medium to Kendall Medium. The

animated BX cancer virus multiplied and remained of constant form. The

fact that the BX cancer virus could multiply on a sterile non-living

growth medium indicated that Rife's BX cancer " virus " was a living

microorganism unlike the currently accepted understanding of a virus

as a biological structure dependent on cellular metabolism to

regenerate (multiply) and propagate its existence. From current

knowledge, we must assume that Rife's BX cancer virus contains within

its structure, a gnome, DNA decoding enzymes, protein digestive

enzymes, transfer RNA, ribosomes, and associated proteins.

 

When concentrations of this BX cancer virus were injected into 426

albino rats, all rats developed cancer tumors at the injection release

site in the animal tissue. Further experiments with the BX cancer

virus demonstrated that it can be easily changed from one microbe form

to another by means of altering the media upon which it is grown. Rife

found more than six forms, which the BX cancer virus could be

transformed into. These included: 1) BY cancer virus, which caused

sarcoma cancer tumors. 2) Cryptomyces plemorphia fungi, which Rife

found implicated in rheumatoid arthritis. 3) Progenitor cryptocides.

4) Bacillus coli. 5) Bacillus typhosus, and 6) Virus of the bacillus

typhosus, which can be clearly seen in the photograph of the typhoid

bacillus appearing in the article The New Microscopes of Feb.1944.

 

Rife was not the only researcher to find a microbial cause for

cancer. Many others have also. Nor was Rife the only one to build an

optical microscope that could see the BX cancer virus. Currently in

Canada the biologist Gaston Naessens uses an ultraviolet microscope

which can easily view the BX cancer virus in living blood from cancer

patients. Naessens' microscope uses an ultraviolet light source which

is first polarized. then focused down and sent through a frequency

doubler crystal and finally sent into a special condenser section for

dark field microscopy. Looking at live blood from cancer patients,

Naessens has found and made videos of at least sixteen different forms

the BX cancer virus can be transformed into. I have viewed some of

these videos and the anti mated (motile) BX and BY cancer virues are

clearly visible and look just as Rife described them.

 

As for the other researchers who have found the same microbial

cause for cancer as Rife, they have all been persecuted, while their

work has been maimed and discredited by the corrupt higher ruling

circles of what currently passes for legitimate medicine and

microbiology. Perhaps a brief review of the work of one victim is in

order.

 

Dr. Virginia Livingston-Wheeler in 1947, while studying tumors,

found the same organism in all of them. Her findings were published in

August 1948 by the New York Microscopical Society Bulletin. Later in

Dec. 1950, Wheeler had an article published in the American Journal of

Medical Sciences on microbes cultures taken from both human and animal

tumors. On Sept. 10, 1953 The Washington Post reported the discoveries

of Dr. Wheeler and her team from Rutgers-Presbyterian Hospital

Laboratory which were disclosed at the 6 th International Congress of

Microbiology in Rome. They had found conducive proof of a microbial

cause for cancer. When Dr. Wheeler and her group returned from Rome to

Rutgers-Presbyterian Hospital they found that the funds for their

laboratory were being cut off. The laboratory was closed. This was the

behind-the-scenes work and doings of Dr. Corneluis P. Rhoads, the head

of Memorial Sloan-Kettering Cancer Center. The fear of the cancer

industry elite is and was immense. If the truth about the true cause

of cancer becomes known, a cheap cure will be found shortly

thereafter. This will kill the cancer goose which lays tens of

billions of dollars worth of eggs a year. Is there nothing these scum

will not do for their god money? No!

 

The San Diego Union of July 31st, 1949 reported on the work of Dr.

Gruner of Mill University, Montreal, Canada and Dr. J.E. Heft of

Windsor, Canada. They were in agreement with and had experimental

proof that Dr.Royal Raymond Rife's discovery that cancer was caused by

a microbe was correct.

 

In 1950 Dr. James Hillman of RCA Labs in Princeton, N.J. found the

BX cancer virus using an electron microscope.

 

For an in-depth documented overview of the massive suppression by

allopathic medicine of real cancer treatment breakthroughs that

worked, I recommend you read: 1) The Cancer Cure That Worked, by Barry

Lynes, and 2) The Healing of Cancer, by Barry Lynes. Both books are

available through Marcus Books, P.O. Box 327, Queensville, Ontario,

Canada LOG 1 RO. (41 6)-478-2201.

 

I will now share with you some observations about cancer cells and

a classic experiment in which they are compared to normal cells, which

suggests a simple answer to how cells infected with the BX cancer

virus become cancerous. It has long been noted that cancer cells act

and appear somewhat like undifferentiated embryonic cells.

Furthermore, cancer cells apparently have mostly an anaerobic (without

oxygen) metabolism. Note that the only time in the normal life cycle

of mammalian cells in which they are of a undifferentiated embryonic

nature and also have an apparent appreciable anaerobic metabolism is

the period between the time the female egg, the ovum, has been

fertilized in the fallopian tube and just before a viable placenta has

developed in the uterus. Geneticists and embryologists have shown that

the entire development of the fetus from just-fertilized ovum to the

fully developed fetus is governed completely by sequentially read and

expressed genetic information. There is an exceedingly complex genetic

interchange and feedback control system in operation. Some of this

genetic code is used only for a short period of time and is then

sealed away not to be read or opened up again in the individuals

existence, except during chromosome copying prior to cell division.

Cancer cells act as though they have had some set of embryonic gene

sequences reactivated. However, in the now mature differentiated

mammalian cells from which this cancer cell has been derived, the

control system that normally would have deactivated this embryonic

gene sequence(s) is itself long since deactivated. The cancer cell is

in a run away catch 22 situation.

 

It has been found that many genes occur in sequenced sets in which

none of the genes in the sequence can be read and expressed unless the

first gene in the sequence has been opened to be read. Just in front

of that first gene there is a DNA code sequence which has to have a

promoter protein bound to it so that the DNA code sequence reading

enzyme can temporarily attach to this promoter protein and then begin

reading/translating the DNA code of the gene sequences into messenger

RNA for protein synthesis by ribosomes. For this promoter protein to

attach to its DNA coupling sequence at the beginning of the gene

sequence, this sequence must be in the normal B-DNA right handed

double helix form (see Figures 1 and 3). If the coupling site code

sequence or the DNA code sequence immediately in front of it has a

blocking protein attached or is in the form of the left handed Z-DNA

double helix (see Figure 2), the promoter protein can not bind/couple

with its DNA code sequence and therefore the entire sequence of genes

will not be read and expressed. The Z-DNA double helix form is a very

compact form of the double helix.

 

It has no major grove structure like the B-DNA double helix which

allows a promoter protein to physically match up with a specific DNA

code sequence which will manifest itself in the unique molecular

structure of the surface of the major grove for that unique DNA code

sequence. The Z-DNA double helix structure gives very little

information about what the DNA code sequence is in its core. For a

left handed Z-DNA double helix associated with a specific DNA code

sequence to convert itself into a right handed B-DNA double helix, so

that the promoter protein can attach, the concentrations of various

ions in the cell nucleus must be in certain specific ranges for that

specific Z-DNA sequence. The specific concentrations and ratios of

ions in the nucleus is determined by the actions of ion gates and

pumps in the cell outer membrane. These ion gates and pumps are

controlled by messenger proteins and compounds from both inside and

outside the cell membrane. What this means is that the cell genetic

expression can be greatly influenced and controlled by the genetic

expression of other cells and cell sets (organs). And of coarse during

embryonic development this external cell influence is in dominant

control of the whole cell system of membrane ion gates and pumps.

 

Now that some of the basic genetic control process has been

stated, several questions need to be asked. Can one or more microbe

proteins or chemical compounds be generated and released inside a

mammalian cell by a parasitic microbe? Can these proteins or compounds

act as a messenger to open up or close down cell membrane ion gates or

pumps? Can this opening or dosing of ion gates and or pumps cause a

gene sequence which is normally only open during early embryonic

development to open up again and thereby cause the cell to go

cancerous? I believe the answer to all these questions is yes. Of

course there are many other possibilities i.e. some of these protein

fragments may act as promoter proteins or combine with and remove

blocker proteins, thereby allowing a promoter protein to attach to a

DNA sequence and thereby initiate DNA transcription.

 

Dr. Robert 0. Becker, M.D. has written a book The Body Electric in

which he goes into great detail about tissue regeneration processes

and their electrical and ionic connection to genetic expression. I

will now use information distilled from Becker's book which supports

my above suppositions. In 1948 Dr. Meryl S. Rose performed a mile

stone experiment on salamanders. Rose transplanted frog kidney cancer

tumor tissue onto a salamander's hind limb. These frog tumors were

virus induced. The results of his experiment, however are the same

even if the tumor is carcinogen induced, which was done later. The

transplanted tumors would grow and spread, leading to the salamander's

death, if no intervention was taken. However, if Rose amputated the

limb below or through the middle of the tumor, the salamander would

regrow the limb and in the process the tumor(s) would disappear, even

if the tumor had already spread to other body locations. Tissue

biopsies of the wound region during regeneration showed that both

salamander cells as well as cancerous frog kidney cells

dedifferentiated into embryonic cell forms during the blastema

formation process as the wound healed.

 

Even more amazing, as the blastema propagated forward,

regenerating the limb, both embryonic frog and embryonic salamander

cells of the blastema multiplied (devided). They differentiated into

the cell types needed to form the new limb tissue, i.e. muscle cells,

cartilage cells, capillary cells, etc. In later years researchers such

as Becker demonstrated that it was the near unique ability of the

salamander's nervous system to drastically change the ionic

environment around blastema cells, along with hormone secretions from

nerve dendrites, which allowed blastema cells to dedifferentiate into

embryonic cells and then to red differentiate into the new cell types

of the regenerating limb. Becker and other researchers were able to

get rats to regrow most of, or all of a amputated limb. They implanted

a negative current source that produced a negative electric potential

distribution inside the limb directly behind the amputation site. This

closely mimicked what a salamander would have at that site if it were

scaled up to the rats size. To understand what is happening here, you

need to know that in a rat just as in a salamander the myelin sheath

cells coating the motor nerve fibers carry an electron current through

collagen fibers which are N-type semi-conductors.

 

This current is deposited mostly into the body's electrolytic

solution surrounding the cells near where the nerve fiber ends. The

myelin sheath cells coating the sensor nerve fibers carry an electron

current on their collagen fibers away from where the sensor nerve

fiber ends. The motor nerve fibers are essentially all in the body

interior and the sensor nerve fibers are essentially all on the body

surface. As a amputation wound heals over with skin, surface sensor

nerve fibers cover over what is normally a motor nerve fiber region.

In a short period of time the cells under the new forming skin layer

can be converted into dedifferentiated embryonic cells under the

influence or control of the external cell membrane ionic environment

at the wound site as determined by the electric currentipotential of

the combined sensor and motor nerve sheaths activity in the wound area

( blastema formation zone). I can not here go into all of the

wonderful detail of Becker's book. However, I hope I have given the

reader at least an understanding of how cancer can possibly come about

by a simple change in the ion environment in the cell nucleus. If you

are interested in tissue regeneration or are aserious biologist. I can

not recommend Becker's book enough. Particularly the last chapter,

Postcript: Political Science. This chapter with great clarity and

skill, clearly shows why we as a nation need to dismantle all

centralized cesspools of corruption as exemplified by the National

Institutes Of Health. The NIH needs to be replaced by regional

institutes which are government funded, but ran and controlled by

democratically elected administrators elected by the research community.

 

Before ending this appendix, a warning and an explanation of why

X-ray radiation should never be used to treat cancer. Rife was able to

isolate the BX cancer virus from cancer tumor tissue samples. He then

exposed these viruses to 24 hours of ultra violet light exposure. This

virus obtained in this manner was 100% effective in inducing cancer in

lab animals. His form of the BX cancer virus was exceedingly virulent.

Other researchers who apparently isolated the same BX cancer virus, or

a form of it, and inoculated test animals by similar methods only had

approximately 25% cancer induction rates. A possible simple answer for

the discrepancy is that the ultraviolet light from the argon discharge

caused some of the adjacent thimine DNA base codes to dimerize

(chemically bond together). When the DNA reader enzyme which

translates the DNA base code into messenger RNA for protein synthesis

comes across a dimerized thimine base code pair, it stops RNA

synthesis. The reader enzyme then breaks into two fragments.

 

One fragment stays at the dimerization site to mark it and the

other fragment initiates a complex set of enzyme reactions to remove

the dimerized pair and replace them with a new undimerized pair.

During this repair process the messenger RNA generated fragment is

released. If this messenger RNA fragment contains the genetic RNA base

code sequence for ribosome attachment, it will be read by the

ribosomes and a protein fragment will be generated and released. In

particular, if the RNA fragment is fed into a cluster of ribosomes

(polyribosomes) which are located on or associated with the

intercellular matrix web intersections, we can expect many copies of

the coded protein fragment to be generated and released Furthermore,

since the RNA fragment does not contain the normal stop synthesis code

and message RNA end sequence base code, the RNA fragment is not likely

to be immediately dismantled after polyribosome reading and protein

synthesis like regular messenger RNA is. This fragment is likely to be

read over again and again. Now. if the generated protein fragment

happens to be an activator or suppressor of a cell membrane ion

channel or ion pump you have the potential beginnings of a cancer

producing situation as discussed above.

 

This protein fragment(s) might also act as a promoter protein that

enables the DNA reader enzyme to attach to and read a gene sequence.

Or this protein fragment may combine with a blocker protein on a

repressor gene at the front of a DNA gene sequence and remove it,

thereby allowing a promoter protein to combine with a DNA sequence and

then facilitating attachment of the DNA reader enzyme (RNA

polymerase). All of this is not the normal " plan " of the normal cell

metabolism. An excellent example of this sort of defective protein

production and its cancerous consequences is the genetic disease

xeroderma pigmentosum. In it the individual has an inherited defect in

their ability to repair the aforementioned DNA base code dimerization

damage. They are hypersensitive to sun light exposure and develop

pre-cancerous and cancerous skin conditions. They usually die of skin

cancer before their twentieth birthday. Now what does this have to do

with massive cellular tissue damage suffered by cancer patients while

under going standard allopathic medical X-ray treatment for cancer? As

stated in Appendix B. Rife's normal treatment for cancer patients was

three minutes of exposure once every three days to his frequency

instrument.

 

This frequency instrument, when treating cancer, probably produced

repeating packets of 11,780,000 or 23.560,000 light pulses per second.

These light pulses in turn produced ultra low intensity ultra sound in

the patient's body of a frequency of 11.780.000 or 23.560.000 cycles

per second, which is the approximate mechanical structural resonance

frequency of the BX cancer viruses. The Bx viruses disintegrated. In

the normal carcinoma cancer cell, there are thousands of BX cancer

viruses. When these BX cancer viruses all disintegrate together at the

same time, they release their gnome, digestive enzymes, ribosomes,

assorted proteinslenzymes, etc. into the cell. The cancer cell is

overwhelmed, dies, and promptly disintegrates. When using Rife's

cancer treatment method on a cancer patient that has undergone

extensive allopathic medical X-ray damage, there is the high

possibility of an encounter with a new kind of cancer cell which

Rife's treatment method won't work on.

 

Allopathic medical X-ray treatment causes significant ultraviolet

light, ionization, and free radical production both in tumor tissue

and adjacent normal tissue. With this ultraviolet light, ionization

and free radical production, there is the associated dimerization of

adjacent DNA base code molecular pairs. Both cancer cells and adjacent

non cancer cells suffer significant cell membrane integrity damage

from the X-ray radiation. All of this culminates in the possibility of

a heavily radiation damaged BX cancer virus penetrating the cell

membrane of a non cancerous cell and instigating production of cancer

causing protein fragments as discussed above. But its own gnome so

badly damaged that it can not propagate itself. If this were to occur,

then a cancer cell could be created which was not infested with the BX

cancer virus and therefore not treatable by Rife's frequency

instrument or ultra sound of 11.789,000 or 23.560.000 cycles per

second. Of coarse the X-ray radiation alone could generate a cancer

cell that the original Rife's treatment method would not cure.

 

Well we have skimmed over a lot of technical data in this

appendix. however, I hope the reader now has a conceptual frame work

in which to begin questioning the current allopathic medicine approach

to cancer causes, treatments, and cures. Only by honest researchers

going back and looking at the suppressed results of past honest cancer

researchers can we hope to find honest valid answers about cancer

causes and cures.

 

Gary Wade

 

" An important scientific innovation rarely makes its way by

gradually winning over and converting its opponents: it rarely happens

that Saul becomes Paul. What does happen is that its opponents

gradually die out and that the growing generation is familiarized with

the idea from the beginning. "

 

Max Planck

 

Taken from: DR. RIFE AND THE DEATH OF THE CANCER INDUSTRY. a paper

by physicist Gary Wade.

 

P.S. - It is now empirically known that many types of cancer can

be easily and quickly killed by exposure to pressure square waves of a

frequency of approximately 2127 cycles per second. It appears that one

or more of the higher frequency hidden fourier sine wave components.

i.e. 3 x 2127Hz = 6381Hz; 5 x 2127Hz = 10,635Hz; 7 x 2127Hz = 14,

889Hz; 9 x 2127Hz = 19,143 Hz, etc. , etc. opens up ion gates on the

cancer cells' membrane and radically changes the ionic conditions

inside the cancer cell such that it drops the bi-lipid layer potential

difference below some critical value below which the cancer cell can

not recover and it dies.