The contradictions of oncology
Today, after so many years of disappointed expectations in oncology, we should firmly discard the genetic matrix as cause of cancer. It is inconceivable to support this theory because the theory is anything but logical. Rather than a scientific theory, it is an issue of faith and this becomes abundantly clear when one reads the “sacred texts” available on the market. By turning the pages of any of these texts or treatises of oncology or internal medicine, in fact, one can realise that the positions, the conclusions, and the results of genetic theories are strikingly contradictory and illogical, thus not acceptable. And given their foundations, they cannot be any different.
To substantiate our conclusions, we have examined the treatises “oncological medicine” (29), already mentioned, and “internal medicine” (30) where often, at the beginning of a paragraph, a model for explanation is proposed, and that model is infallibly refuted at the end. (31)
From the treatise “Medicina Oncologica”, Bonadonna G., Robustelli G., Milan 1999.
Page 5:
The main cause of tumour consists in alteration of the genome at the level of the expression or function of genes that are act to control growth and cellular differentiation. The model that is most interesting today: cells within a clone (that is, coming from one single cell) undergo consecutive genetic variations that cause the genome to malfunction and confer to its phenotype characteristics that are favourable to proliferation.
Page 5 beginning:
The numerous changes in genes cause the cells to proliferate ever more, as in a niche in the host tissue.
Page 5 line 17:
The biochemical mechanisms of oncogens to transform cells are still little known.
It is believed that one single oncogene is not sufficient to entirely transform a cell. But a polyphasic process where more oncogens participate is necessary. The majority of tumours originate from one single cell. Cellular mutations represent a continuous cumulative process from embryo to old age; thus, the oncological risk is hereditary as well.
Current research tries to identify the altered genes.
End of page 5:
We hope that in the near future the genetic profile will be more complete.
Page 6:
The future challenge will have to move from the description of mutant genes to their use against specific targets for anti-tumoral therapies. The genetic tests that have been recently adopted and which are still in development have the potential to identify subjects at risk. The effectiveness of the possible modes of prevention of genetic tests has not yet been established.
Page 7, second indentation:
Starting from the beginning of the 1980s it has been demonstrated that specific and recurrent chromosomic rearrangements, including translocation and deletions constituted critical points in the complex event of malignant transformation.
Page 7, third indentation:
The mechanism through which chromosomic alterations occur is still unknown.
End of page 74:
The factors of growth are a not better defined group of polypeptides able to modulate the cellular function and of exerting a regulating action which is specific and potent in the growth of the target cells.
Page 77, first indentation:
The results of the most recent research clearly indicate that further future progress will occur through the unveiling of the various mechanisms through which the growth factors control the expression of the oncogenes and these in turn control the expression of the growth factors.
End of page124:
In spite of the biological interest of this class of proto-oncogenes, no growth factor has been so far demonstrated to structurally be involved in genetic lesions of human tumours.
Page 77:
…identified 20 viral oncogenes, each of them possesses a counterpart of normal cells. The expression of these genes in normal cells does not translate into the development of a neoplasia. The alteration of the proto-oncogenes can result in the development of a malignant cell.
Page 77:
In the future, dozens of genes that today are unknown will be identified. Those genes will be useful to perfect our knowledge in the intricate process of cellular regulation and differentiation.
Beginning of page124:
Multiple experimental evidence has confirmed that neoplastic transformation, as proposed by Boveri about a century ago, is caused by lesions of the cell’s DNA.
Beginning of page 7:
As Boveri foresaw at the beginning of the century, an abnormal chromosomic picture is intimately associated with the malignant phenotype of the neoplastic cell. Chromosomic aberration in fact represents an important help to find the genes that have a central role in the process of malignant transformation.
Page 7, third indentation of second column:
The concept of chromosomic anomaly, as an event that is exclusively tied to the presence of malignant cells must be revisited. There are in fact chromosomic alterations that are specific to a series of benign neoplasias such as lymphomas and fibromas of the ovaries, polymorph adenomas of salivary glands, and polyps of colon and endometrium.
Page 136:
The study of molecular lesions of human tumours had a strong impact on the management of the oncological patient. Molecular lesions, in fact, represent formidable markers of disease by far superior to the techniques used for the reading of serum markers.
Page 137:
… genetic lesions represent an important diagnostic and prognostic marker in clinical practice.
Page 137 last indentation:
In spite of the irreplaceable contribution of molecular analysis of human tumours, the impact on therapy is only in direct. A more direct use of molecular lesions in a therapeutic sense still seems uncertain today.
Although various experimental observations have demonstrated how the manipulation of the genes involved in the molecular lesions of human tumours is able to modify the biological behaviour of the tumour in vitro, the application of these results to clinical practice is problematic and it will require delicate efforts of research.
Page 138:
…virulence of cancer … which in the majority of the cases is not controllable in spite of the application of various forms of therapy.
Page 139:
The successes achieved by the vaccinations against infectious disease have raised hopes for acting in similar ways on tumours, departing form the assumption that tumoral cells have antigenic characteristics that are completely peculiar and different from those of normal cells … those characteristics would make them a possible target of specific antibodies. Scientific publications on the issue fill libraries but the results so far obtained have been disappointing.
Page 157:
We can see that we are talking about still desperate attempts in the field of anti-tumoral vaccination, in the manner of Icarus, even though they are highly technological. Nevertheless, it is still an open road that can lead to therapeutic – perhaps even prophylactic – successes.
The immunological therapy specific to human tumours which is the final goal of any immunological research is more potential than actual, although some valid theoretical basis exist as well as some possible practical application. There is no doubt that the “acceleration of science” that is taking place before our eyes will lead to successes that could be enormous, as we all hope.
Beginning of page165:
Although remarkable progress in the identification of the molecular processes responsible for change related to the specific stages of the neoplastic progression (such as mutation of dominant oncogens or reduced expression of suppressive genes) have been made, the appearance of metastatic phenotype has so far eluded any characterization at the level of molecular genetics.
End of page176:
…although the data reported for some factors such as c-erb and p53 (antioncogenes) are suggestive for a possible “identification” of the type of neoplastic agents to administer to obtain better probabilities of response, today any use of these factors is premature as predictors for response in daily clinical practice.
Page 659:
The biological response modifiers (BRM) have the property of regulating growth and differentiation of different cells and thus of modifying the function of biological systems, such as the immune system.
Numerous substances of bacterial, vegetal, viral, origin and so on have been employed to treat tumours.
Amongst the BRMs, linphokines are of particular interest. The intense work of these years has also allowed the acquisition of new biological and clinical information that only a scientifically correct study will allow to evaluate their therapeutic potential in the years to come.
Page 669:
Active immunotherapy (vaccination) and gene therapy.
Retroviral vectors transfer in normal cells or neoplastic genes, such as those of cytokines or of bacterial enzymes capable of metabolizing a propharmacon. In active immunotherapy, the transfer of genes augments the ability of the receiving cell to stimulate the immune system, while in gene therapy the transfer genes, by metabolizing the propharmacon into cytotoxic (suicidal gene), exposes the cells to the destruction of the drug itself.
(This)…is an area of scientific work that in the future could give new weapons to the doctor of oncology.
With the preparation and availability of monoclonal antibodies (MA), the attempts for the serum therapy of tumours have so far intensified with limited success.
Page 721, second line:
For many decades, there has been the strong suspicion that hormones are involved in the aetiology of breast carcinoma.
Page 721, second-last line:
In summation, epidemiological and experimental studies suggest that, at least for the most part, and especially by the duration of regular ovarian activity, the risk of contracting breast carcinoma is determined by the duration and intensity of exposure of the epithelium to extrogens and to prolactine.
Page 723, beginning of second paragraph:
The pathogenesis of human breast cancer is still little known.
Page 720, fourth paragraph, line 18:
The most solid risk factors are represented…by family history of malignant neoplasia, especially when it concerns relatives of first degree (mother, daughter, sister) …
Page 720 fourth paragraph, third last line:
Patients with a form of breast carcinoma of the familial or hereditary type (including those with bilateral neoplasia) have a global rate of survival comparable to that of other patients with breast cancer.
From the treatise “Internal Medicine”, Stein J. H., Ed. Momento Medico, Milan, 1995.
End of page1,184:
In our environment, numerous physical and biological agents of carcinogenesis have been identified. Up to a short time ago, very little about the cellular targets of those agents was known. Both the process that leads to a malignant transformation, and the genetic components of the host that are implicated in this transformation are obscure. However, in recent years the “base” research on cancer has discovered a group of cellular genes that are the probable substrata of carcinogenesis.
Although much is still to be learned we now possess a picture of the genetic events that accompany malignant transformations.
From this knowledge comes the possibility for understanding how environmental agents could interact with the elements of the host in the production of cancer. In conclusion, this work will be useful for both prevention and treatment of neoplastic diseases.
Page 1,185, second indentation:
The mechanisms at the basis of carcinogenesis from foreign bodies have not yet been clarified (asbestos, prosthetic implants, bladderinfestation by schistosoma haematobium.
Page 1,185, second paragraph:
It must be noted, furthermore, that current epidemiologists do not support the hypothesis for which the incidence of tumours is currently growing because of these environmental sources of carcinogens.
Page 1185, third paragraph:
With the exception of schistosoma haematobium, all the known biological agents that in living beings are at the basis of a neoplasia are viruses …some viruses have been strongly implicated in principle neoplastic forms.
Although many animal models of retrovirus-induced tumours are well characterized, the modalities of human leukaemia of T cells have not yet been determined.
Pages 1185-1186:
The growth and cellular differentiation are subject to regulatory influences of both positive and negative type.
The genes that have positive roles…in the process of growth are called proto-oncogenes or dominant oncogens. The genes that principally act in inhibition…are named suppressor genes. The reciprocal action of these two classes of regulatory genes in the development of tumours is being gradually clarified.
Page 1186, second paragraph:
Although we only have fragmented information about the function of proto-oncogenes, in normal cells the available data suggest that these genes undertake a role in the regulation of cellular proliferation, functioning as elements of a multi-component apparatus of signal transduction.
Page 1186-1187:
Mitogenic signals can be unleashed by the cascade transmission of (transduction) signals.
End of page1187:
Although identification and sequence of each state of signal transmission have not yet been given, we are now able to describe significant components.
Page 1188, last indentation:
The control of growth involves tumour regulatory processes concerning the transduction of signals. Those processes are not yet fully known.
Page 1188, end of first paragraph:
Although the precise roles of multifunctional proto-oncogenes have not yet been clarified, it seems possible that they work as bridges between different components of the mitogenic regulating apparatus.
Beginning of page 1192:
It is interesting to note that not even two oncogenes are sufficient to generate the complete tumoral phenotype of all the characteristics. The tumours arising from the transfer in normal cells of the common oncogenes myc and ras activated, do not invade and do not metastasize …
Page 1190, second paragraph:
One of the first observations on human tumours concerns the number and the morphology of chromosomes that can become extremely anomalous (thickening of cromatine, translocations, etc. ). This, for example, is studied in chronic mieloid leukaemia CML whose Philadelphia chromosome is a chimerical gene).
Page 1190:
…When the exact basis of this remarkable tropism is clarified, we will have acquired an exhaustive knowledge of the processes that are in control of growth and differentiation in the lymphopoietic and ematopoietic tissues.
The careful reading of the two texts highlights how obscure the description of genetics is currently: there are thousands of “ifs” which never, ever amount to a “yes”. Furthermore, there is nothing concrete in the discussions concerning possible future results.
The excerpts reported in footnote 31 are sufficiently descriptive of the smokescreen of genetics, and clarify once and for all its illusions. They demonstrate that it can be dealt with only as a debate but certainly not at a scientific level and therefore is to be discarded. It is depressing to notice, however, that all of society and worse, the individual citizen must suffer tremendously because of an endless entanglement of so many “ifs, perhaps, could, and would”.
If we refuse the validity of the current oncological perspectives, it is legitimate to ask how we are supposed to perceive the successes obtained by both official and alternative medicine. It is in fact true that almost every day, we hear from many sources that cures have taken place with this or that therapy.
At this point it is necessary to clarify that, if we admit to the possibility of improvements and cures, then logically it is not admissible to attribute them to this or that treatment that is more or less official. This is because, given that the majority of the components at play in the “object tumour” cannot be specified, then conditions that decisively establish the goodness of therapies cannot subsist. (32)
Paradoxically, the possible positive effect of any therapeutic system could stem from unknown and unforeseen elements which, in turn, could be influenced or determined somehow by any of the aforementioned therapeutic systems.
In other words, we could be in the situation where all therapies, including those of official medicine, would rightfully have the right to magnify their point of view, although the real reason for their success is unknown for any of them. In this case, even the most accurate and rigorous experimentation would take on a fictional character rather than that of true correspondence with reality. It is for this reason that, at this point, we have to accept that oncology as we know it is dead. Nothing can be done, therefore, other than looking beyond it and moving forward.