Journal of Cancer Therapy, 2013, 4, 1362-1365 Published Online October 2013 (
Cancer as a Therapeutic Agent?*
Mario Gosalvez
Laboratorío y Servicío de Bioquímica Experimental (1970-2010), Clínica and Hospital Universitario Puerta de Hierro Madrid and
Majadahonda, Comunidad de Madrid, Spain.
Received September 6th, 2013; revised October 4th, 2013; accepted October 12th, 2013
Copyright © 2013 Mario Gosalvez. This is an open access article distributed under the Creative Commons Attribution License,
which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
The author, concisely and generically, proposes experimental testing on suitable laboratory animals, in state-of-the-art
international centers endo wed with cancer reversal experimental techniques. Using mild carcinogens to induce more or
less benign growths can be reversed back to a normal state by single or dual strategy: in spinal paralysis by medullar
contusion in young rabbits; for blindness caused by the severing of the optic nerve in sheep; for neural deafness caused
by severing the acoustic nerve in rabbits. If these techniques could be shown to be feasible and successful for higher
order primates and if having then already cured for life a sufficient number of malignant cancers by cancer reversal by
dual strategy in human beings, of course these methods could be then considered for patients.
Keywords: Mild Carcinogenesis and Cancer Reversal; Animal Recoveries from Spinal Paralysis; Blindness and
Deafness; Mitochondrial Filamentation
1. Introduction
I should like to draw your atten tion to some initial possi-
bilities on the use of cancer as a therap eutic agent. Some
years ago, there is going a process which might lead to
the understanding of a defect in mitochondrial filamenta-
tion in the tumoral cell as a basis for a better comprehen-
sion of its nature, cause, diagnosis and treatment [1-10].
My first contribution to these discoveries has simply
been assisted with some pilot experiments and first clini-
cal studies in animal and human malignant tumors [11-
21]. It is only now that the field of mitochondrial fila-
mentation might begin to go forward, hand in hand, at
least, with the most proficient experimental and clinical
cancer research [4-6,9].
This field of mitochondrial filamentation augurs well
for a good harvest in several applications: from the ex-
tension of metabolic life in cases of transitory physio-
logical death [6,22] to an increase of sporting prowess
[3], including degenerative illnesses and aging [6,7,10]
schizophrenia or obesity [6,7], for example. I have re-
cently published my proposal to explain the in timate me-
chanism of the aerobic glycolisis of tumoral cells [8],
based in our studies on th is last in cognita of the n ature of
cancer [1,3,16].
I only have but a few years left in an advisory capacity
on mitochondrial filamentation, and its future applica-
tions before being overtaken by the new generation of
experts. The ball therefore is now in the court of the in-
terested youth. I should now like to explain to your read-
ers, concisely and directly, the possibility of applying
cancer to animal experimental treatments for spinal pa-
ralysis, blindness and neural deafness. There are three
species of creature on which, in my judgment, trials
could be started now by experts: the young rabbit for
spinal paralysis; the young sheep for blindness and the
adult rabbit for deafness. Matters would be ready, possi-
bly, to begin immediately on animals in some centers of
clinical and surgical excellence in the USA, Europe and
2. Spinal Paralysis
Up until now, this problem—the interruption of the spi-
nal cord—has been attempted on rats using neural graft-
ing and stem cells, more or less first-order ones. Among
the issues encountered are the impermanence of the solu-
tion and the cancerification of the implant. We firmly
believe that the exquisite embr yonic cell concatenatio n in
time and space for the differentiation continues in the
adult organism on account of the suitable molecular cor-
relations for dedifferentiati on and re di f ferentiat i on.
In such a way, in our opinion, that besides those useful
*An experimental proposal for low order laboratory mammals.
Copyright © 2013 SciRes. JCT
Cancer as a Therapeutic Agent ? 1363
bone marrow transplants in human leukemia, there will
probably be only two ways to replace damaged cells in
the spinal cord of superior mammals:
1) Cancerify cells locally to cells of low malignancy
and subsequently apply reversal techniques back to nor-
mality when the problem has been resolved.
2) Locally inducing the dedifferentiation to stem cells
so as to redifferentiate them subsequently to normal cells.
In respect of the second way, I believe that decades of
study are needed. The first one, I consider, is feasible
now in some very capable centers.
Spinal paralysis should be induced in the recently
weaned bunny rabbit by spinal cord contusion. As soon
as it has been filmed, and its number of movements per
hour determined, following the consolidation of the le-
sion, the pre-carcinogen cocktail-to be metabo lized to the
final medullar carcinogen suitable for the rabbit, should
be injected in few microliters in the neurons immed iately
in front of and behind the spinal cord hiatus.
Naturally, at the moment there are several possibilities
for those local initiators of benign spinal tumor. Only by
trial and error on dozens of rabbits will the best ones
manifest themselves. The cocktails that may work best in
filamented mitochondria and in primary neural cultures,
in addition to adult rabbits, will allow us to experiment
on the miniature pig with chances of a good success rate.
It is considered important, in my opinion, to repeat these
experiments on as many different species as possible.
As soon as a success rate of more than 70 percent is
guaranteed for the generation of a spinal cord tumor,
especially in pigs, reversal back to the normality of a
benign tumor could be started, as soon as the slightest
reactive movement has been observed in the tails of the
stimulated animals.
At that point, very possibly, the comparison of move-
ments per hour would show a marked increase and the
detection by PET-SCAN of the spinal cord tumor would
have yielded some indication of its malignancy. There-
fore, very shortly afterwards, the beginning of the tumor
reversal with techniques solely directed at benign tumor
cells, or by dual strategy, (including therefore cytotoxics
for tumor reducts) could be shown [13-16,20,21].
Following the complete recovery of movement, with-
out any other added toxicity, an observation period of at
least eight weeks will be set up, to ensure that there is no
tumor reappearance and then to progress to the ape and
When sufficient monkeys may have been cured com-
pletely the therapy could be considered in volunteers.
Especially in those young tetraplegics previously well-
prepared in suitable centers if these persons could blink
their approval. Having tak en the due assessorial informa-
tion, family advice and insurances, of course, these pro-
cedures could be followed, only if a sufficient number of
human malignant cancers had then cured for life duration
3. Neural Blindness
A young sheep would be the animal of choice. All the
optic nerves would have to be cut very cleanly at the best
height of their length, leaving it without sight in one eye.
Neural atrophy would be expected, taking due ophthal-
mologic measures at regular intervals for both eyes, the
sightless and the healthy one.
From that moment, the retinal hyperplasic cocktail
suitable for sheep, a specialization directed at the cells
with aerobic glycolysis, would begin to be administered.
The observation of pre-carcinogenic hyperplasia in the
cells of the retina of both eyes would need to be done
daily at the back of both eyes. The intestinal crypts
would also have to be checked.
In the healthy eye the reversal treatment would be per-
formed locally. For the sightless eye only a local reversal
treatment would be done for the benign cancerification.
When the photon charge tests were almost identical for
both eyes using intracerebral electrophysiological Regis-
ter, the process would be stopped until co mplete cure had
been instated and registered by complete vision returning
to the eye that was sightless, with the healthy eye cov-
Naturally, the adaptation of the hyperplasic cocktails
and the local benign cancer which function best on sheep,
in order to progress to the ape and monkey and then on to
the human being, would need to be proven with primary
cultures and filamented mitochondria of retinas of the
species in question.
4. Neural Deafness
The cochlea contains neurons that charge metals very
The cocktails of benign cancerification of this organ
must be manufactured as metal complexes suitable to be
digested intracellularly in their target cells. In such a way
as to be able to distinguish similarities between the ear
whose nerve has been cut and the healthy one by in-
tracerebral sound charge resister. Reversal, whether by
single or dual technique, should begin as soon as the deaf
ear can hear. The treatment of the healthy ear must be
local and start from the beginning. At the final stage of
recovery the procedure would be the same as for neural
5. Important Considerations
The accumulated research on agents acting on cell hy-
perplasia is very extensive. The collection of agents, hy-
poplasic, hyperplasic, pre-carcinogens and soft carcino-
Copyright © 2013 SciRes. JCT
Cancer as a Therapeutic Agent ?
gens, is very large. The primary culture techniques, of
cells, tissue and organs, is well embedded. Trials on fila-
mented mitochondria [6-10,21] are easy to perform and
will represent a very rapid screen ing of hundred s of co m-
pounds per month capable of returning more or less neo-
plastic cells to their state of normality.
It is recommended that the proposed studies be per-
formed, in a calm and serene manner, with the collabora-
tion of all, especially doctors and chemists of different
specializations, to achieve this possible step forwards. If
at some future point these studies were successful on
apes, the techniques could be considered for patients. Of
course, only when the complete cure of cancer diseases
had been obtained in humans [4-6,9].
6. Discussion
A new adventure of ideas that surpasses the avenues of
habitual thinking may be taken as too daring by those
experts who have the right equilibrium between the past
and the path to the fu ture. Our prop ositio n, first of all, fo r
animal experimentation, comes after having observed not
too much progress with the stem cell approach in the last
decade, with science still not counting on localized tech-
niques of adequate stem cell formation to resolve clearly
these problems.
We have recently published on-line a concise account
of our methodological expertise in the isolation and assay
of filamented mitochondria and some proposals for pos-
sible future applications of this now emerging field [1,2,
4-10,21,22]. A search for private national and interna-
tional financing for this and other future possible appli-
cations in this area of molecular physiology and medi-
cine has already been started.
7. Conclusions
The due opportunity for this proposal in laboratory ani-
mals is timidly requested to the scientific community. It
would be almost ready for the task with the security that
if it should result in another failure, at least we would
have clarified possible new ways. This proposal brings
out a humble request for a combination of neurologists
and oncologists of various types working closely together
for some years on several animal species.
I considered that this, perhaps too daring an idea,
could be contemplated with attention by the Journal of
Cancer Therapy. Other journals declined previously rap-
idly and kindly to publish this paper. Most surely based
on the lack of expertise on one or another of the two as-
pects considered in the proposal: Cancer and Neurolog y.
8. Acknowledgements
The author is grateful to Mr. Andrew Guy for his review
of the English text and for his inestimable help in the
initial submission process.
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Cancer as a Therapeutic Agent ?
Copyright © 2013 SciRes. JCT
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toxics and Minor Tranquilizers,” Aminoacids Chemistry,
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Proceedings of the 36th ISOTT Meeting, Sapporo, 3-7
August 2008, p. 52.