Simoncini Cancer Therapy

Dr. Simoncini writes...
dr tullio simoncini

The adaptability mechanism of candida

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.

  • 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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