SIMONCINI CANCER THERAPY - THE ADAPTABILITY MECHANISM OF CANCER

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SIMONCINI CANCER THERAPY - THE ADAPTABILITY MECHANISM OF CANCER

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Tumors are perceived as one phenomenon.

 

 

Tumors are one phenomenon, but there are many types. Why?

 

According to official views that see genetic alteration at the basis of

neoplastic development, it is possible that the alteration can manifest

itself in any environment with all possible typological differentiations. From

the microbiological point of view, instead, it is always Candida that invades

various anatomical parts, evoking different reactions as a function of the

organs it feeds on. These behaviors are a function of the quantity and

quality of the affected tissues. An organ whose connective tissue has been

invaded defends itself with cellular hyper-productions that attempt to encyst

the fungin colonies which are trying to completely colonize the organism.

 

It is in this way that the whole histological variety of neoplasias can be

explained. The histological variety appears not to be influential in the

determination of the cause, which is always and only Candida. It is in this

way that during a neoplastic event some genes can be hyper-expressed - that

is, amplified - in a defensive effort determined by hyper-productive needs

of the tissue. This reaction is normal and not anomalous at all.

 

Consider the following example. If we take an inert thorn, for example

that of a sea urchin, and we inoculate it first in the skin, then in the

bronchi, the bone, brain and in other body areas, we evoke an immune response of

a cellular type tending to encyst the thorn, that is, to form some kind of

a cocoon in which to enclose it.

 

By the same token, the immune system interprets fungin colonies beyond a

certain dimension as extraneous foreign bodies stimulating an encystment

reaction that is produced with the type of cells of the invaded tissue. The

thorn or the fungus can therefore cause, according to the case, an

epithelioma, an adenocarcinoma, an osteosarcoma, a gliobastoma, and so on.

 

In the first moments of the invasion, the organism is able to send mature

cells to contain the proliferating fungi: this is the phenomenon of a

differentiated tumor. As the colonies become more powerful, and tissues are

exhausted, cells become more and more immature up to anaplasia. Furthermore, the

ratio between differentiated tissues and connective tissue existing in an

organ determines the reaction capability and thus the degree of malignancy

of a neoplasia. The fewer noble cells there are, the more malignant and

invasive the tumor becomes.

 

So, on the one hand we have noble tissue which cannot be attacked (muscles

and nerves), and on the other the simple connective tissue. The glandular

tissue which is halfway between these two elements, just because it is

provided with that complex structure that confers to it a certain ability of

encysting the fungi, can oppose their invasion by producing the phenomenon of

the benign tumor. For example, if we consider the thyroid, we can see how

in this gland neo-formations can take any graduation of malignancy even when

they possess benign histological characteristics, as is the case for

capsulated follicular carcinoma, long ago called metastasizing benign adenoma.

 

This can happen because the concept of a **benign tumor** does not have an

absolute value. In this case, even if it is true that fungin cells cannot

normally go through the differentiated cells barrier, that does not mean

that under particular conditions they cannot be successful. It is for this

reason that such neo-formations are considered 'odd' in oncology. But such

oddities can be easily explained with the interpretation key of fungin

infection. When the glandular tissue is exhausted, the benign tumor becomes a

malignant one.

 

For all intents and purposes, it is always the same Candida attacking

different tissues, each time adapting itself to the type of environment it

finds. The specifications usually assigned to the various candidas (Candida

Albicans, Krusei, Parapsilosis, Glabrata, Tropicalis and others) underestimate

the fact that they all come from one single progenitor which, when it

genetically mutates to attack the host, transforms itself into this or that

stock.59

 

R.L. Hopfer for example found no less than four different Candida species

in the post-mortem cultures of a leukemia patient.

N. Aksoycan demonstrated that seven different stocks of Candida actually

have the same antigenic structure.

F.C. Odds reports how the same Candida stock can colonize different

anatomical areas at different times.

J. Hellstein has found the common clonal origin in Candida Albicans for

both commensal and pathogenic stocks.

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