Is Cancer Actually Fungus?

[burtlancast]

If anyone's interested in the infectious theory of cancer, there's
- Virginia Livingston Wheeler
- Royal Rife
- Alan Cantwell
- John Gregory
- Thomas Glover
- Tom Deaken
- John E White
- Robert E Netterberg
- Michael J Scott
- William Mervyn Crofton
- Kiichiro Hasumi
- Antoine Bechamp
- Gaston Naessens
- Clara Fonti
- Tulio Simoncini
- Franz Gerlach

Let's add to the list William Koch, shall we:

Pg 21 of The SURVIVAL FACTOR IN NEOPLASTIC AND VIRAL DISEASES

Glover showed in 1923 that the cancer virus existed in a pleomorphic
germ that was bacillus in one phase and coccus in another, and virus in the third
phase. He also showed it could exist in a fungus or micelium phase. The latter
form has been identified lately by Irene Diller, and some others, and the whole
chain of forms was independently proved by von Brehmer, in the last few
decades as well. The work was thoroughly repeated and proved by my friend
Jacob Engel and George Clark, at the U.S. P.H.S. laboratories, bur, for reasons
we will not discuss, they were not allowed To publish their findings. The
infectious nature of natural cancer was thus proven beyond any doubt by
carefully following the four laws of Robert Koch. Doctor Clark was able to get
a paper read on this confirmation in 195 3, at Rome, Italy, at the Sixth
international Congress of Microbiology. So at last the facts are recorded in
the archives of orthodox scientific literature.

 

[Amazoniac]

...

 

[shepherdgirl]

Apologies in advance for this diversion:

Also on RP's interviews on seritonin I beleive he talked about how if he goes off of Throid supp he gets melanoma's on his skin.

Really? This bothers me... I thought lipolysis was important for cancer, and eating enough sugar would inhibit stress hormones regardless of metabolic rate. In fact, wouldn't it be easier to burn through your sugar if metabolism was higher? Would lowering thyroid somehow cause increased lactate despite an excellent diet?

 

[shepherdgirl]

Inhibiting Lipolysis May Treat / Cure Cancer

anyone?

 

[Boli]

This is interesting.

I have always enjoyed reading about Rife. Pleomorphism videos are nice to watch.

The Koch model of cancer is similar to Szent-Györgyi's. I think there is something to this.

Methylglyoxal can purportedly assume the role of O₂ (Szent-Györgyi). He speculates that life started with carbonyls being the primary reducing agent. Methylgyoxal can correct metabolism.

In cancer, the cell reverts back into an older state, the alpha state, that differentiates faster. This state evolutionarily predates the beta state, the state formed when oxygen was made available on earth.

He thinks proteins need to to lose one electron to become a p-type semiconductor radical. He says cancer is characterized by nonconductive proteins. He has a mechanism for how methylglyoxal fixes this.

Article: The living state and cancer

Royal Rife was interesting too. He has recently been validated with Raman microscopy. Yes, such things are mainstream now. Cells can emit their own radiation when exited. Here are some Raman micrographs:

The different colors are different frequencies radiating off the cell. Different molecules and functional groups resonate at different frequencies. The incident beam can be tuned to selectively view C=C bonds for instance.

Hillman would like this because this is live cell imaging.

Article: Quantitative volumetric Raman imaging of three dimensional cell cultures

And Rife's resonant frequency cancer therapy has purportedly been replicated by this guy:



I am somewhat confused. Both the Metabolic Cancer Theories and the Infectious Cancer Theories are both convincing.

My bet is the on metabolic theory. This is more fundamental and allows for the possibility for both diet, microbes, and hydrocarbons being a causative factor as long as they all can disrupt oxygen metabolism.

Both the Metabolic Cancer Theories and the Infectious Cancer Theories play a role in the development of cancer

 

[Travis]

Both the Metabolic Cancer Theories and the Infectious Cancer Theories play a role in the development of cancer

I just had discovered that certain bacteria produce polyamines, so it's a given,

I do enjoy reading about Royal Rife, since his work is so interesting. Before I start reading more about how light can effect cell replication, I'm taking the position that all carcinogenic biological signals must be small molecules—or nothing works by proximity alone. I getting the idea that many causes of cancer can be reduced to one downstream process; the growth effects of androgens appear to be polyamine‐dependent.

I can't deny the Warburg effect, but I'm starting to wonder why glycolysis (increaesed lactic acid and pH; reduced NADH) should increase cell division. Perhaps it's one of those redox‐sensitive transcription factors in the nucleus (I've read about two or them). Like glutathione, these redox‐sensitive transcription factors have thiols which form disulphide bridges only when under an oxidative environment; this intermolecular crosslinking—of course—effects the entire geometry of the protein, either facilitating transcription or impeding it. The protein p53 is one of these types.

But perhaps increased glycolylsis simply means low methylglyoxal, which does have a powerful effect of restraining division. This is Albert Szent‐Györgyi's bailiwick, and it can explain some of the lactic acid. Low methylglyoxal means more polyamines free glutathione, both necessary for cell proliferation. Could most cell growth be reduced down to just these two molecules (types)? I know that cell proliferation is basically a linear function of polyamines—predictable dose‐dependent growth effects, with no exception—and glutathione is also necessary. I feel that Koch and Szent‐Györgyi had the most powerful understanding by stressing methylglyoxal: a molecule so effective against cancer that it's tempting to define it in that framework. By cyclicizing arginine, methylglyoxal must lower polyamine production; it also spontanteously adducts with glutathione, perhaps disabling it temorarily.

What makes one bacteria pathogenic, or carcinogenic, and another safe? I already know about polyamines, but I'm sure I could find some good information on others. You might think that even bacteria have evolved chemical messengers, similar to cytokines, to communicate with eachother. Also, as serving nature's breakdown and recycling function, you might think that some could excrete proteolytic enzymes. The canonical toxins, like diptheria toxin, are globular protein toxins excreted ostensibly to disable; many other bacteria toxins are carbohydrate–lipid toxins (endotoxin), which seem to be an intergral part of the bacteria cell's membrane.

 

[Amazoniac]

I just had discovered that certain bacteria produce polyamines, so it's a given,

I do enjoy reading about Royal Rife, since his work is so interesting. Before I start reading more about how light can effect cell replication, I'm taking the position that all carcinogenic biological signals must be small molecules—or nothing works by proximity alone. I getting the idea that many causes of cancer can be reduced to one downstream process; the growth effects of androgens appear to be polyamine‐dependent.

I can't deny the Warburg effect, but I'm starting to wonder why glycolysis (increaesed lactic acid and pH; reduced NADH) should increase cell division. Perhaps it's one of those redox‐sensitive transcription factors in the nucleus (I've read about two or them). Like glutathione, these redox‐sensitive transcription factors have thiols which form disulphide bridges only when under an oxidative environment; this intermolecular crosslinking—of course—effects the entire geometry of the protein, either facilitating transcription or impeding it. The protein p53 is one of these types.

But perhaps increased glycolylsis simply means low methylglyoxal, which does have a powerful effect of restraining division. This is Albert Szent‐Györgyi's bailiwick, and it can explain some of the lactic acid. Low methylglyoxal means more polyamines free glutathione, both necessary for cell proliferation. Could most cell growth be reduced down to just these two molecules (types)? I know that cell proliferation is basically a linear function of polyamines—predictable dose‐dependent growth effects, with no exception—and glutathione is also necessary. I feel that Koch and Szent‐Györgyi had the most powerful understanding by stressing methylglyoxal: a molecule so effective against cancer that it's tempting to define it in that framework. By cyclicizing arginine, methylglyoxal must lower polyamine production; it also spontanteously adducts with glutathione, perhaps disabling it temorarily.

What makes one bacteria pathogenic, or carcinogenic, and another safe? I already know about polyamines, but I'm sure I could find some good information on others. You might think that even bacteria have evolved chemical messengers, similar to cytokines, to communicate with eachother. Also, as serving nature's breakdown and recycling function, you might think that some could excrete proteolytic enzymes. The canonical toxins, like diptheria toxin, are globular protein toxins excreted ostensibly to disable; many other bacteria toxins are carbohydrate–lipid toxins (endotoxin), which seem to be an intergral part of the bacteria cell's membrane.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2316156
/pdf/brmedj06259-0013.pdf

We also found that by the addition of lactose to the diet we could destroy all the putrefactive indole producers in two to three days, and that the disappearance of the indoxyl sulphate from the urine occurred on the same day as the disappearance of the indole producers from the faeces. Within two days of, discontinuing the lactose putrefactive organisms reappeared in the faeces and indoxyl sulphate in the urine.

Although there would still be the lactic acid to deal with.

 

[Amazoniac]

If anyone's interested in the infectious theory of cancer, there's
- Virginia Livingston Wheeler

Dear burtlan, thanks to you I was making the readings on one of her books: The Conquest of Cancer. Check this out:

"The P. [Progenitoraceae] Cryptocides is the ancestral, or primordial, hidden killer that we believe to be implicated in the cause of cancer. Initially we believe it to be a pathogen only, however! With time and further study we realized it was an essential but dormant part of all cells, only activated to repair cell damage. After the repair, it returns to a resting state in the healthy cell, where it remains dormant again. A strong immune system controls this process. However, when immunity is suppressed or weakened, it proliferates and allows cancer to gain a foothold, secreting the same choriogonadotropin hormone found in abundance in all tumors. Hence, as explained more fully later, the P. C. microbe is both a "good guy" and a "bad guy," and for this reason is called an Obligate Symbiont."​

Thank you also for your many contributions on the forum. You're a boss.

 

[Amazoniac]

"The thing that most surgeons and cancer physicians do not understand yet is that cancer is a systemic disease. The tumor is only a symptom of the disease; the disease causes the tumor, not vice versa. Frequently, after a surgeon has cut out a tumor and made a wide dissection, one hears that he "got it all." This is supposed to be good news—and indeed the surgeon announces it enthusiastically enough—but in the majority of cases nothing is subsequently done to raise the patient's immunity. There will probably be a recurrence of cancer within a few months or years."

--

"[Guineae pigs have] a natural [?] immunity and are resistant to cancer. Only 1 guineae pig in 500,000 develops cancer spontaneously."

"We were able to produce tumors in an amazing 25 percent.

It was while working with guineae pigs that my suspicions as to the method of transmissibility of tumors were confirmed. Due to an error, the infected guineae pigs were housed in cages at the top of the racks while the healthy, uninoculated controls, instead of being housed on different racks, were placed in cages underneath. To our surprise, the control animals also developed cancer. On careful inspection we found that droppings from the top cages sometimes fell into the drinking water and food of the guineae pigs below. From that time on we kept controls in separate rooms. Our animal man changed his gown, cap, mask, and gloves before going from one area to the other. The guineae pigs control thereafter stopped developing cancer. My convictions about transmissibility of cancer grew."​

 

[TreasureVibe]

"The thing that most surgeons and cancer physicians do not understand yet is that cancer is a systemic disease. The tumor is only a symptom of the disease; the disease causes the tumor, not vice versa. Frequently, after a surgeon has cut out a tumor and made a wide dissection, one hears that he "got it all." This is supposed to be good news—and indeed the surgeon announces it enthusiastically enough—but in the majority of cases nothing is subsequently done to raise the patient's immunity. There will probably be a recurrence of cancer within a few months or years."

--

"We were able to produce tumors in an amazing 25 percent.

It was while working with guineae pigs that my suspicions as to the method of transmissibility of tumors were confirmed. Due to an error, the infected guineae pigs were housed in cages at the top of the racks while the healthy, uninoculated controls, instead of being housed on different racks, were placed in cages underneath. To our surprise, the control animals also developed cancer. On careful inspection we found that droppings from the top cages sometimes fell into the drinking water and food of the guineae pigs below. From that time on we kept controls in separate rooms. Our animal man changed his gown, cap, mask, and gloves before going from one area to the other. The guineae pigs control thereafter stopped developing cancer. My convictions about transmissibility of cancer grew."​

Somatids in one body react to somatids in another body, apparently.

 

[burtlancast]

The extraordinary thing with Virginia is her very high cure rate (and i do believe it) but also the fact the patients who ceased the therapy, got a recurrence of their cancers, then promptly returned to the therapy got cured once again.

Most of the other alternative cancer therapies are nearly unable to salvage the patient once the cancer has returned following the first cure.

We saw it with Gerson, where he tried giving the wrong pituitary hormone, and almost all patients died as a result. The other herbal therapies (Hoxsey, Essiac, ...) seem to suffer from the same problem.

 

[TreasureVibe]

If cancer is a fungus...

Published october 2017
Ammonia is a ubiquitous by-product of cellular metabolism, however the biological consequences of ammonia production are not fully understood, especially in cancer. We find that ammonia is not merely a toxic waste product, but is recycled into central amino acid metabolism to maximize nitrogen utilization. Cancer cells primarily assimilated ammonia through reductive amination catalyzed by glutamate dehydrogenase (GDH), and secondary reactions enabled other amino acids, such as proline and aspartate, to directly acquire this nitrogen. Metabolic recycling of ammonia accelerated proliferation of breast cancer. In mice, ammonia accumulated in the tumor microenvironment, and was used directly to generate amino acids through GDH activity. These data show that ammonia not only is a secreted waste product, but a fundamental nitrogen source that can support tumor biomass.
Metabolic recycling of ammonia via glutamate dehydrogenase supports breast cancer biomass

Diploid S. cerevisiae strains undergo a dimorphic transition that involves changes in cell shape and the pattern of cell division and results in invasive filamentous growth in response to starvation for nitrogen. Cells become long and thin and form pseudohyphae that grow away from the colony and invade the agar medium. Pseudohyphal growth allows yeast cells to forage for nutrients. Pseudohyphal growth requires the polar budding pattern of a/alpha diploid cells; haploid axially budding cells of identical genotype cannot undergo this dimorphic transition. Constitutive activation of RAS2 or mutation of SHR3, a gene required for amino acid uptake, enhance the pseudohyphal phenotype; a dominant mutation in RSR1/BUD1 that causes random budding suppresses pseudohyphal growth.
Unipolar cell divisions in the yeast S. cerevisiae lead to filamentous growth: regulation by starvation and RAS. - PubMed - NCBI

The effect of nitrogen sources including yeast extract, peptone, soybean hydrolyzate and some inorganic nitrogen sources, as well as the nitrogen concentration on the fermentative production of pyruvate by Torulopsis glabrata WSH-IP12 was investigated. The addition of yeast extract greatly inhibited pyruvate accumulation, while peptone was shown to be the most favorable nitrogen source. In flask culture, 15 g l(-1) peptone was needed to consume 80 g l(-1) glucose with 23.4 g l(-1)of pyruvate accumulated. Pyruvate production was markedly dependent on the ratio of carbon to nitrogen (C:N), its production was improved by increasing the concentration of glucose and peptone proportionally and reduced by exclusively increasing the glucose concentration. In a glucose fed-batch culture, cell growth and pyruvate production slowed after 28 h. However, cell growth and pyruvate production recovered after further nitrogen, in the form of peptone and ammonium sulfate, was added to the culture. A final concentration of pyruvate of 54.5 g l(-1) was achieved at 64 h (yield to glucose consumed of 0.471 g g(-l)). By using aqueous ammonia instead of potassium hydroxide for pH control, 57.3 g l(-1) pyruvate with a yield of 0.498 g g(-1) was produced by 55 h. This result further indicates that nitrogen level plays an important role in the production of pyruvate.
Effect of nitrogen source and nitrogen concentration on the production of pyruvate by Torulopsis glabrata. - PubMed - NCBI

How about that?