Specificity of Serine enzymes to Cancer glyco-proteins
R.Cathey, 1997, RCRS

In cancer chemotherapy, selective destruction is the ideal. But no
artificial formulations of cytotoxins or anti-metabolites fits this
description. All are general poisons, and the normal as well as the cancer
cells are affected. In some cases the somatic components are alone
affected in the tumor, giving the false impression that some good effect
has been rendered, when in fact the ratio of the malignant component has
merely increased due to ablation of the somatic elements.  Tumor-size
reduction is not a good measurement of tumorostatics or tumor destruction.
The only reliable and consistent measurement of cancer activity is the
sensitized hCG test; and ultimately patient life-extension.  Even
site-specific delivery of cytotoxins or antimetabolites, or radiation are
not, in their effects, limited to the cancer. There is always a
generalized somatic response when these compounds leach away from the
lesion, or by the inherent limitations in site-specific methods developed
thus far.  Again all such toxic agents are inhibitors of important enzyme
systems of the host.

Fortunately there are endogenous counterparts to our pathetically limited
ability to create artificially such a selective program: the selectively,
antithetical-to-cancer serine enzymes along with the cytotoxins of the
lymphocytes; and exogenous, dietarily derived nitrilosides.

The rationales for the complete resolution of the cancer problem have been
known and relatively well understood in the greater part for almost 100
years (John Beard, 1902, Lancet).  A dietetic or exogenous component
forming a part of this triply-redundant protection against the asexual
generation of the life-cycle was discovered and applied rationally more
recently: since the 1950s, namely Laetrile or nitrilosides.

Cancer is trophoblast. Period. We challenge anyone to refute the
trophoblastic nature of cancer using the same criteria of corrosive
scientific critical thought and investigational methods that provided the
evidences and proofs of this contention. These scientific proofs were for
the most part supplied by researchers without the least knowledge of a
trophoblastic or Beardian basis of cancer. Thus it is independently
supported.

These facts have been broadcast repeatedly over the past 95 years with
little effect on the standard or generalized methods of practice.  The
trophoblastic fact of cancer was only most recently re-broadcast world
wide in none other than the official organ of the American Cancer Society
in 1995: Cancer, Volume 76, Number 8, pages 1467-75, by Dr. Hernan
Acevedo, M.D. But even here, the realizations of the significance of these
findings has been missed, and have spurred little more than interest in
possible immunological adaptations of the cancer hormone.

Cancer cells form a specifically appropriate substrate in their substance
for the serine pancreatic enzymes; normal cells for the most-part do not.
Where-ever normal tissues might be affected by these enzymes there are
appropriate levels of enzyme inhibitors which are highly localized and
the inhibition reversible.

The trophoblast of pregnancy, too, form a likewise appropriate substrate
for these serine enzymes, and which enzymes play the role of transforming
cytotrophoblast (the malignant, erosional, metastasizing trophoblast cell)
into the steroid-producing, non-dividing (relatively "benign")
syncytial-trophoblast, and finally these too are completely destroyed or
digested by these enzymes: principally carboxypeptidase, trypsin,
chymotrypsin and amylase. Upon the complete ablation of these "pregnancy
trophoblast" cells, which Hertig called nature's first cancer and nature's
first cure, birth commences.

Cancer being trophoblast, these same enzymes must perform the same
functions here as well, as a matter of invariant natural law.  It is not
theory, these are commonplace facts to the experimental biologist and
these established facts can all be freely examined by anyone with the
willingness to examine the literature as well as the clinical record where
these facts are put to practice.

After the action of these pancrearic enzymes have sufficiently breached
the pericellular sialomucinous coatings of the cancer/trophoblast cells
the phagocytes and cytotoxic bodies of the immune system may move in and
further kill and remove these completely along with the further digestion
by the serine enzymes which work conjunctively and form part of the immune
system.  The sialomucin coating renders cancer cells immunologically inert
or repulsive to the immune bodies such as the lymphocytes because they
share the same electrochemical charge (negative).  Just so, the conceptus
is a successful "graft" by the same means.

In addition, the diet provides a nutritionally essential co-factor:
hydrogen cyanide from the dietary nitrilosides.  Because the steroid
producing phase of trophoblast elicits from the hostal tissues enzymes
which degrade and serve to conjugate these cancer steroids into inert
forms (namely by beta-glucuronidase:BG) therefore the dietary nitrilosides
(which are glucosides that can be oxidized and conjugated to glucuronic
acid to form glucuronides) are also activated or "unlocked" by BG in the
environment of the cancer or trophoblast. Thus HCN is released which is a
well known accelerator of proteolysis,  thus aiding the pancreatic
enzymes. But HCN also has the capacity to poison the cancer cell, which is
specifically deficient in mechanisms or enzymes capable of detoxifying the
cyanide radical.  Normal tissues do possess this required means of
detoxification: rhodanese, or thiosulfate transulferase, also found in
foods. The synthetic nitriloside, Laetrile, is composed of a moiety of HCN
and Benzaldehyde. Acting together they are more than 100 times more
cytotoxic to the cancer cell than each is alone.  Benzaldehyde is oxidized
in the somatic environment, while the cancer cell is less capable of this,
so Benzaldehyde lags in the cancer environs and kills it.

In dietary nitrilosides we find one of the most potent means not only of
selectively destroying the cancer cell, and preventing cancer, but of
reactivation of inhibited proteolytic enzymes.  That cancer cells as well
as normal trophoblast secrete trypsin- and plant-derived
proteolytic-enzyme-inhibitors (serpins) is a commonplace in the universe
of the relevant expert in cancer research. The biochemist or enzymologist
also knows that HCN is a reactivator of these important enzymes, along
with glutathione and other reactivators.

Furthermore, this essential factor..nitriloside..provides a means for the
normalization of hypertension through its metabolite thiocyanate; which
also plays a role in prevention of the crisis of sickle cell anemia; the
nitrile contributes to the formation of vitamin B-12 from pro-vitamin
B-12, another cyanide bearing vitamin: cyanocobalamin; Through these
metabolites the nitrilosides play an important role in hemopoiesis. They
are antiparasitic, bacteriostatic; through the metabolization of the
nitriloside amygdalin (L-mandelonitrile-beta-diglucoside), found in
apricot seeds, benzaldehyde is released, which upon oxidation yields
benzoic acid, a known antirheumatic, and antiseptic.

The potentiated serine enzymes due to the assistance of nitrilosides (and
biologically active tri-valent chromium is important here as well) are
effective against malaria, tuberculosis (against which anti-biotics are
losing ground rapidly) "sticky blood" (polycythemia vera), inflammations,
and a host of other chronic, metabolic disorders attributed to old-age, or
as para-neoplastic syndromes.

This factor meets all the criteria for a vitamin itself.  In animals and
man, when deprived of this factor, cancer is a commonplace; in less severe
expressions of deficiency, there are still widespread susceptibility to
infectious disease, pancreatic insufficiency, high blood pressure, etc. It
well deserves the status of a vitamin that Dr. Krebs gave it: vitamin
B-17, and the common therapeutic form Laetrile
(laevo-mandelonitrile-beta-glucuronoside) is nothing more than a synthetic
form of the common nitriloside amygdalin.


Roger Scott Cathey
Robert Cathey Research Source
E-mail: rsc@europa.com
http://www.europa.com/~rsc/