[Note: In the following, footnotes are represented as letters within
brackets, and endnotes as numbers within brackets.]
Abstract: Cancer has long been recognized to share histological and
behavioral characteristics with pregnancy trophoblasts. Modern methods have
proven biochemical and genetic characteristics are shared between cancer and
pregnancy trophoblasts. Cellular or cytotrophoblasts are the source cells
for the entire placenta and are the first differentiated tissue that forms
after sperm and egg unite to form the zygote. Cellular trophoblasts are
invasive, eroding, and metastasizing cells, which mediate the parasitization
of the mother's uterus with a new life form which grows concomittantly and
distinctly alongside the placental process. The relationship between
placenta and fetus represents a unique process in terms of tissue and organ
development: an extra-somatic tissue, an organ, is developed with transient
functions that forms no part of the somatic complement of tissues and
organs, and whose growth and development is unrestricted by intrinsic
factors, that is, factors within the trophoblasts themselves. It is proposed
that factors extrinsic to the trophoblasts themselves eventually cause these
trophoblasts to surrender their grasp on the uterine tissues, and the fetus
itself. Furthermore, that these extrinsic factors are principally
hydrolytic enzymes secreted by the maternal and fetal systems, and
secondarily immunological factors. This degradation and cellular
destruction of the trophoblasts that comprise the interface between placenta
and uterus initiates a sequence of events which eventually culminate in the
birth of the baby. It is believed that these same mechanisms may be
pertinent to the regression or destruction of cancer cells as well, since
there is a fundamental genetic identity between cancers of all types and
from all origins and pregnancy trophoblasts. Thus the cause of birth and
the control of wandering trophoblasts in pregnancy may provide insight to
the control and possible rational therapeusis of cancer.
Key words: trophoblast, hCG, biomarkers, enzymes, hydrolysis, immune
augmentation, hybridization, catalysis, degradation, inhibitors,
proto-oncogenes, tumor-necrosis-factor (A glossary is appended).
Introduction:
Early histologists and embryologists conceived of trophoblasts primarily as
a mediating tissue responsible for passing nutrients to the fetus. This is
the basis of the name given these cells by Ambrosius Arnold Willem Hubrecht
in 1888: from trophe: nourishment, and blastos: germ[1]. The first
embryologist to strongly suggest that cancer and trophoblast may be one and
the same was John Beard [2] in 1902. However, it was beyond the experimental
and analytical techniques of his time to isolate any genetic proof of an
identity between placental trophoblast and cancers. The Krebses [3] compiled
an extensive list of hundreds of functions and products expressed or shared
exclusively between cancer and trophoblast but not by body or somatic
tissues [a]. In the 1940s Howard Beard [b] and others developed more
sensitive techniques similar to those used for detecting pregnancy, focusing
on hCG, which they found in all cancer sera [c] to varying degrees.
Anti-body, sedimentation and agglutinization tests also were developed that
could work in cancer serum analyses, such as those developed by Navarro [4].
HH Beard also found that the glycoprotein hCG was an effective enzyme
inhibitor [5].
In 1995, a crucial work by Acevedo et al.[6] provided the first quantitative
genetic analysis that proved that hCG-holo (see glossary), or it's subunits
were always found as a perfusing and/or membrane bound expressions in all
cancers, regardless of type or origin. They also demonstrated that the
transcriptional RNA resulting in this glycoprotein could be detected upon
analysis. Numerous other researchers have confirmed these findings by
performing corroborative genetic and biochemical analyses of cancers of all
types and from all sources (pathological samples or clonal cultures).
Furthermore, yet other studies have demonstrated expression by cancer cells
of other hormones of pregnancy trophoblasts, trophoblastic or placental
enzymes, and other products or gene activity [7,8,9,10,11,12], none of which
are expressed by somatic cells. A simple search of Medline with just two
terms: trophoblast and cancer will return some 50 pages of 20 citations per
page, and the number of studies and observations is always increasing. Not
by any means focusing exclusively on gestational cancers. Collectively,
these studies and especially because of the genetic motifs they have
revealed compel the conclusion that cancers of all types, regardless of
origin are trophoblastic.
Amongst the immediate questions that arise are: 1) what causes the
spontaneous degradation of the placental trophoblasts which represents, in
its culmination, the commencement of birth of the fetus? and, 2) are the
same mechanisms applicable towards the regression and control and remission
of various cancers?
This paper examines these questions and proposes that the cause of birth and
the regression of cancer may be
A) mediated not by intrinsic genetic programs (within the trophoblast), but
by extrinsic, "epigenetic" factors akin to an immunologic processes.
B) that these anti-malignant processes consist primarily in enzymatic
digestion after enzyme inhibition is overcome.
C) that the enzyme expression effecting these changes is primarily a
combined assault from the pancreases of both mother and fetus, therefore
making the pancreas a component of the immune system, and
D) that the normal cellular immune components of the maternal system are
potentiated by this prior maternal-fetal pancreatic enzymatic attack.
Identity of Trophoblast and Cancer systems, Shared transcription products of
Trophoblast and Cancer
Amongst a much longer list of biochemical properties shared by both cancer
and trophoblast may be listed these: hCG: human chorionic gonadotropin with
2 subunits: alpha and beta. hC-GnRH: human chorionic gonadotrophin
releasing hormone. hPL: human placental lactogen, or human chorionic
somatomammotrophin (hCS). hCT: Human chorionic thryotrophin. hCCT: human
chorionic corticotrophin. hC-TRH: human chorionic thryotrophin releasing
hormone. Enzymes shared by Trophoblast and Cancer: CAP: Cystine
aminopeptidase (oxytocinase). HSAP: Heat-stable alkaline phosphatase. DO:
Diamine oxidase (histaminase).
Proteins whose function is unknown, and all of which appear to be
expressions of the syncytio-trophoblasts and cancers: SP1 or PSBetaG:
Pregnancy Specific Beta1-Glycoprotein, a syncytio-trophoblast transcript
product (Schwangershafts protein 1) (Bischoff, 1980) PAPP-A and B: Pregnancy
Associated Plasma Proteins A, B, etc. PP5: Placental protein 5.
These are all products not found in the non-pregnant adult except in
association with cancer, and thereby may be used as "biomarkers" for the
detection of cancers of various types. While not all cancers have the same
degree of expression of any of these products into the plasma (or sera) at
detectable levels, and there is currently no single infallible test for all
cancers, hCG has by far the widest and most persistent occurrence, and most
easily detected. A new test for detecting the antigenic proteins, the
Anti-Malignin Antibody Serum test (AMAS)[13] may enable easy early
recognition of the malignant horizon as it detects the underlying
trophoblastic proteins. As will become evident further on, enzymatic
therapy will potentiate this test. By combining various pregnancy-standardized
analyses, we believe a positive diagnosis can be
arrived at long in advance of current techniques that do not take into
account the trophoblast/cancer motif. These have the advantage of being
non-invasive and non-toxic.
Immune avoidance or invisibility is a defining characteristic of both cancer
and the placenta. In pregnancy the trophoblast expresses proteins and
enzymes that are antithetic to those hormones and enzymes that mediate the
monthly cycle. This causes a preservation of the swollen tissues of the
uterus. Digestion and sloughing off of these tissues is mediated by
proteolytic enzymes, thus those protein products whose function is unknown
from trophoblast may act as proteolytic enzyme inhibitors.
On the basis of immunologic invisibility and ultimate rejection of
trophoblast (the placenta)--and by default the fetus to which it is mutually
associated--pregnancy has been termed both an allograft and homograft[d]
(Hertig, 1964)[14]. It is a temporary graft and in its duration there is
continuous immune suppression [15], just as there must be in any
successful allograft [16]. At some point, however, the rejection process
is successful. Thus the birth of the individual and the associated processes
of the placenta represent, essentially, an immunological rejection of the
blood dependent phase of the fetal "parasite" [e]. The immuno-privilege
of trophoblasts has been postulated on various foundations [17], but the
exact cause of birth has never been established to everyone's satisfaction.
Joseph Needham developed an exhaustive bibliography and data base on
pregnancy, the placenta, and the various theories on development as well as
the cause of birth, including John Beard's[18]. Beard's contention devolved
upon the commencement of the function of the fetal pancreas whose enzymes
could freely circulate into the placenta and therefore act as a principal
cause of birth by means of digestion of the placental trophoblast. Beard
based his inference on the coincidence of 1) the completion of the formation
of the fetal digestive tract, 2) onset of fetal pancreatic function and 3)
the sudden onset of morning sickness by the mother as well as the first
signs of the degradation of the placental trophoblasts. He inferred
therefore that pancreatic proteinases represented the antithetic principles
causing the loss of interface with the uterine tissues. Beard later defined
this as the ultimate biochemical test for malignancy: reactivity to
pancreatic trypsin and amylase (Beard, 1907).
The majority of opinion states that the basis of immuno-privilege of
trohoblast depends on the membrane bound glycoproteins or hCG[19]. The
membrane coat of the cancer cell is characterized as a glyco-protein. This
means it is composed of a protein part and a carbohydrate part. The
carbohydrate is composed of a variety of different sugars. To the main
sugars are appended side-chain sugars consisting of a particular type that
can carry an electrochemical charge. These are the sialic acid side chains.
For this reason the coating is sometimes referred to as a sialomucinous
coat. These sialic acids render the coating electronegative in charge,
which also happens to be the same charge as that on the white blood cells.
Furthermore, these sugars and their sialic acid side chains, cover and mask
the protein part which is embedded in the cell surface. Since antibodies
are specific to proteins, the cancer cell escapes detection and resists
attack [f]. This hormone is also a powerful enzyme inhibitor, and is found
throughout the blood-stream. Therefore, for there to be antigenicity, this
coat and the diffusing hormone that acts as the "mote" around the tumor or
placenta must be overcome. This is a problem, since there is often a limit
to the ability of the body to produce enzymes in sufficient quantity.
A review of the literature shows that much of the speculation on the topic
of the expulsion of the fetus and his or her associated processes consisting
of the chorion and amnion or the placenta has focused primarily, and we
think correctly, on immunologic principles. However, the concept of
immunologic function can be restated to accommodate a Beardian[g]
perspective that is closer to the Metalnikov-Metchnikovh definitions. This
in turn will provide a basis of understanding the role of enzyme digestion
as another way of viewing the term: "antibiotic."
Proteo- and glyco-lysis as the basis of General Immunity
When a foreign, or antigenic protein or non-genome-translated product enters
the blood stream by some means, the first action taken by the body is
enzymatic attack or activation of hydrolytic enzymes...enzymes of
digestion[20]. These enzymes are, principally amylase, lysozyme, chymase and
other proteases. Since these are acting outside the digestive tract,
Metchnikov described the process as 'parenteral digestion', that is, along
side the digestive tract.
It was Flemming who first delineated the cellular enzyme lysozyme, when
after dropping some effluvia from his nose on a petri dish, it was later
observed to have digested the cultures growing thereon. The principle
modality of protection of the germs and molds was described by Metchnikov
and Metalnikov as a special carbohydrate coating, a mucin or waxy coat that
prevented both dehydration and repulsed the like-charged white blood cells
of the contact or cellular immune system.
This modality of resistance by means of a carbohydrate coating is also
common to cancer cells[21]. The membrane bound glycoprotein hCG consists,
as noted above, of two parts: a protein part (moiety) and a carbohydrate
(glyco-) part. Since white blood cells are designed to recognize foreign
proteins, and the proteins of the trophoblast are masked, or covered by the
carbohydrate moiety, it is evident that this coating must be stripped away.
Amylase is a pancreatic enzyme that is found in the plasma of normal adults
and especially high in pregnancy. It is secreted in the mouth, by the
pancreas and liver, and a similar form is found in the white blood cells.
It digests carbohydrates and glycogen. It is believed that through action
of this carbohydrate digesting enzyme (or similar ones) the antigenic
proteins that have been expressed by the maternal-paternal hybrid tissue of
the placenta are unmasked. This constitutes potentiation of the immune
system against it. (See for a graphic depiction
of the role of the sialic acids on the hormone hCG and the action of amylase
on potentiation of the action of trypsin).
Once these proteins are unmasked, the circulating plasma proteases may
attack the peptide linkages to which they are specific, and to which they
had little or no access prior to the amylase enzyme action[i]. It is then that the
contact immune cells, the killer T cells, the Helper cells, and other
components of the specific immune system are activated, and this constitutes
the rejection process in full force. Nevertheless, it requires 9 months of
continuous action to consummate this superiority, and obviously in some
cases this threshold is not reached. What transpires then is an
"intractable syncytium", or retained trophoblast with the concomitant
possibility of the most malignant form of cancer known:
chorion-epithelioma[j] Since the resolution of the trophoblast is not self
induced, and its normal activity cannot but be invasive, erosive, metastatic
and antagonistic to the uterine tissues, its control can never be intrinsic,
but extrinsic, and such an eventuality as chorionepithelioma must follow
when the defensive forces are not total and absolute in their eradicating
functions.
Thus, by enzymatic digestion ... parenteral digestion ...we have true
anti-biotic action not based however on enzyme inhibition. This approach
will work when it comes to virus, protozoa or germs as well as it does with
trophoblast [k]. In so-far-as the alternative interpretation, wherein
anti-biotic is based on enzyme inhibition, it would appear that it does not
take place in man or beast to any appreciable extent, or as an accident of
consumption of bacteriophage, or intentional use of marketed mold produced
antibiotics.
Evolutionarily speaking, the body could not depend on the tactic of enzyme
inhibition, that is, inhibition of the enzymes required for synthesis of
parts of the invading organism because of the possibility of also acting on
similar or identical enzymes required for the human host. Many millions of
different enzymes can be synthesized that will synthesize the same cell
coats, but the components of the cell coats are always bound to be suitable
substrates to the regularly occurring enzymes of the host. Thus an enzyme
like trypsin that attacks linkages of two amino-acids in a sequence will
always find utility, and there will not be regular resistance. The body
does regularly inhibit its own enzymes. The cancer cell also inhibits
enzymes: the attacking enzymes of the body. HCG occupies the enzymes to such
an extent they are slowed from completely deshielding the cell coat...long
enough for the cell to synthesize replacement components.
Concentration of enzyme is therefore essential for success, and this is
provided by the combined action of fetal and maternal enzymes, and in cancer
therapy, supplementation of enzymes from food and synthesized sources.
Besides enzyme concentration, there is also the possibility that cofactors
can be brought in that reactivate the inhibited enzymes. Hydrogen cyanide
has been observed to have a unique accelerating and life-extending effect on
the protein-digesting enzymes of papayap[24], and tests done by the author of
this paper indicate that it also accelerates digestion of carbohydrates by
amylase. Having the ability to reactivate these enzymes repetitively and
thereby recycle them into the tumor milieu makes HCN-bearing compounds
potent anti-cancer adjuncts. In addition, the HCN is directly toxic to
cancer cells during their aerobic phase, while being relatively non-toxic to
normal cells due to the absence in cancer cells of an enzyme that detoxifies
HCN into thiocyanate. This HCN detoxifying enzyme (rhodanese) is present in
the normal cell. It has been shown that hCG inhibits this enzyme, therefore
it is logical that cancer cells which rely on hCG production for defense
cannot also support rhodanese. From this researchers have taken nitrilosides
or cyanophoric glycosides found in many seeds and vegetables to be an
important dietary factor for enzyme functionality because they carry HCN in
a harmless form. On these grounds, it has even been proposed that
nitrilosides answer to the description of a vitamin, since in their absence
susceptibility to proliferating trophoblasts is many times greater, and the
simple observation that where ever nitrilosides are ingested in higher
amounts cancer incidence also is much lower or entirely absent. However that
may be, it may simply fit into a new category of nutritional science that
may be termed adjunctive-catalytic factors. If vitamins are co-enzymes, and
metals cofactors, these simple molecules could be termed colytic factors.
Other molecules in this category could be gluthione, dimethyl sulfoxide
(DMSO), ethylene disulphonate, thiocyanate (a by-product of HCN
detoxification), nitric oxide, glyoxilide. It is interesting to note that
sulphur bearing compounds seem especially to have this potential, and it is
possible that the special potential of HCN may be in the entire cycle of
detoxification with consequent evolution of thiocyanate, which is also known
to accelerate proteolysis. However, studies done early in this century
showed that in regards to its effect on enzyme reactivation, it seems more
to do with the lability of hydrogen or the ease of exchange of the hydrogen
between the enzyme and the cyanide radical than to the cyanide radical
itself.
The tumor or placenta responds to enzyme attack by producing multiple nuclei
both by cellular fusion, and nuclear division, for the sake of greater
transcription to replace the continuously digested cell coats at the limb of
the placenta or the cancer tumor. In addition to multiplication of nuclei,
it appears that by means of desmosomes or gated channels that this form of
trophoblast may take on characteristics of the cells with which they fuse
that are entirely normal until such hybridization. At this point it may be
that we see the appearance of odd numbers of genes, pleuripoidy, anuploidy,
etc. as if the syncytial phase -- which we might term the defensive and
relatively benign, or non-metastatic phase of "trophoblastism" -- takes
selected components or gene-sectors and multiplies them. This is the
source of the seemingly unlimited variety of cancers that exist. It is also
this hybridized component that perhaps forms the most difficult aspect of
healing from cancer. For how can the body differentiate between a normal
cell and one having both components in one? Since hCG forms part of the
makeup of both the pure trophoblast and the hybridized cells, it may be that
this is the one defining characteristic that determines body-knowledge that
this tissue is active, and the enzymes that can attack this have some
feedback mechanism to insure activation and proliferation to clear them
out.
If the forces that induced this syncytial/hybrid phase should fall back,
this phase may return to an actively dividing phase, but now with the
hybridized characters picked up during its syncytial, plasmodial phase.
This characteristic of cancer cells to show relentlessly the characteristics
of their site of origin actually represents their site of conversion from
the highly malignant, and metastatic or cytotrophoblast phase, to the less
malignant, but hybridizing phase (syncytiotrophoblast). Thus the metastatic
cell found in the lung that appears to be a prostatic cell, indicates two
possibilities: 1. A somatic prostate cell has by some means been induced to
totipotency, and activated the trophoblastic alleles along with its
characteristic, or limited potency; 2. A totipotent cell has undergone
direct differentiation into trophoblast somewhere in the body by means of
sufficient activating factors[l]. This pure trophoblastic source cell has
metastasized, then at some implantation site, has undergone enzymatic
attack, with consequent differentiation to the syncytial phase, wherein
hybridization may take place. Then a period of battle:
enzyme-inhibition/digestion takes place. If the body wins, the cancer is
erased. If the cancer cell wins, we have a metastatic recurrence, and the
cell shows the characteristic of the first entrenchment site, not truly and
necessarily the origin of the first cancer cell.[m]
Assuming some probity to this postulate, the metastatic characteristic,
which is constant, represents already that the body can conquer this cell in
it's most vicious---although most rarely seen---phase.
In cancer, this trophoblastic invasion, as opposed to the pregnancy type, is
an "auto-graft", or autologous evolution of trophoblast. This poses in
contrast to pregnancy, a more dangerous condition, since the criterion for
antigenicity is absent as such: the entire genetic code of the trophoblast
is derived from the individual (except where caused by a parasitic or viral
insertion as activator). It would have to be by another criterion that the
body attacks this cell, or sees it as "not self" than a genetic variation.
Beard postulated it was simply because this cell is a suitable substrate for
digestion, and that its suitability was related to stereochemistry[n]. It
should be pointed out, that in actual allografting, or transplantation, the
incidence of cancer amongst these individuals is about 8 times greater or
more frequent. And usually takes the form of lymphomas, a wandering cell
with properties already very similar to cancer cells (Norman, 1999).
Onset of Fetal pancreatic function and the appearance of anti-trophoblastic
action: Implications of Therapeutic anecdotes for mechanisms of the cause of
birth
We could derive the mechanisms of the cause of birth for realization of
similar modes to the resolution of cancer. Fortunately, experimentation
instigated by Beard obviates the need to recapitulate such a model
theoretically. Believing it was the onset of function of the fetal pancreas
that marked the beginning of the end of the placental trophoblast, it was
logical for him to instigate the attempt to insert such enzymes into the
cancer environs. The observations made by physicians utilizing these
enzymes, once properly prepared, did conform to a general outline provided
by the process of pregnancy and birth itself.
Complications of pregnancy and protease therapy in cancer:
Beard worked with Italian physicians in the year 1905-6 and found that
patients undergoing enzyme injections of a proteolytic type alone were
experiencing symptoms identical to "eclampsia"(pre-eclampsia)[22]. Beard
realized that the fetal pancreas did not secrete amylase, and that in
pregnancy the problems of morning sickness and eclampsia only begin after
onset of fetal function. The fetus does not need amylase until after
weaning, when his or her foods incorporate complex carbohydrates. When
Beard suggested they add amylase, the bad effects disappeared.
Clinical Experience using Enzymes for Chronic, metabolic Diseases
Clinical Experiences using pancreatic and plant enzymes for cancer has a
continuously developing resume of success. A compendium developed by
Klaschka[23] details the development of the use of enzymes for other
diseases that evolved into a program for cancer. The unifying basis of
trophoblast as cancer by means of Beard's insights was rediscovered later by
these experimental approaches, but Beard's approach represents the first
rational treatment for cancer. It is evident now that it can enable a wide
variety of rational approaches through recognition of trophoblastic
mechanisms involved in all cancers.
Conclusion:
In the mutual and exclusively shared properties between cancer and pregnancy
trophoblasts, as distinct from normal somatic cells, a simple axiom comes
into definition: two things equal to a third thing are equal to each other.
In a historical context, we may ascribe the multitudes of different cancers
that have been delineated as the description of a universe of hybridized
trophoblast and somatic tissues. The criterion of malignancy can be derived
from the purest form of trophoblast that acts outside its normal
constraints: chorionepithelioma. All other forms of cancer that may arise
would represent a diminishing grade of malignancy. Furthermore, all other
cancers would represent a model of the site of origin or the first
implantation site. The actual mechanisms of origin of that first cancer
cell are not understood, but we may suspect that any stem cell can give rise
to the trophoblast with far greater ease than a specialized cell. If a
specialized cell gives rise to trophoblast, then that will determine the
hybridized characteristics. If an undetermined stem cell gives rise to a
trophoblast cell, then it may land anywhere and implant itself. Thenceforth,
the metastatic cell line represents the character of that cancer and it will
not change.
In the history of medicine, not one chronic, metabolic[o] disease has ever
responded to surgery, radiation, or intervention by agents foreign to the
evolutionary experience. All preventative or curative measures have been
agents or factors normal to the animal economy or experience: food factors
such as proteins, fats, carbohydrates, vitamins, minerals or natural light,
fresh air and water. This translates to factors pertaining to nutrition or
normal metabolic function. Thus scurvy responded to vitamin C and nothing
else. And pernicious anemia to a B vitamin or factors pertaining to the
pathways in which it is an integral part. Kwashiorkor, a protein deficiency
disease, can not be cured by anything but protein (and after a certain
point, protein cannot cure either, but pure amino acids have to be
introduced.) On the basis of factors relevant to the animal economy or
pertaining to normal function we must look for the resolution of cancer as
well. We do not have an adequate model in our way of thinking about cancer
in modern medical science. It is part and parcel to a problem of internal
gestation, and this in turn goes to an issue of controlled parasitism. We
should not be surprised to learn that once it arises the cancer cell, a cell
normal to the lifecycle, can become a pernicious, viscious attacking cell in
the absence of its normal controls. Experience in the clinic and the
internal evidence both attest to the basic truth Beard first enunciated:
cancer, like the rejection process of birth itself, is a process that
depends on extrinsic factors belonging to the mother and eventually the
fetus as well. A process that is primarily enzymatic, and dependant on
proper nutrition most of all.
Glossary:
trophoblast: the most primitive cell in the life cycle, arising after the
sperm and egg unit to form the zygote, which will later differentiate into
the fetus and germ cell lines.
hCG : human chorionic gonadotropin, a glycoprotein expressed by
trophoblasts, that acts both a biochemical messenger and enzyme inhibitor.
The uterine tissues that would normally be sloughed off are preserved under
the action of this hormone. Also: hCG-holo: complete hCG; hCG-Beta/CTP: the
beta-subunit that is unique to pregnancy trophoblast with
carboxy-terminal-peptide. The alpha subunit is shared with a variety of
different hormones not of trophoblastic origin.
biomarkers: in this context, molecules that can be used to mark the
presence of trophoblasts due to their exclusive expression by trophoblasts
and not by other tissues. Since only cancer and trophoblasts express hCG,
hCG serves as a biomarker of both pregnancy and cancer. Other factors must
be factored in to distinguish between a pregnant woman who has cancer and a
woman who simply has cancer.
enzymes: catalytic agents that come in one of several classes, all of which
lower the activation energy for a spontaneous chemical reaction.
hydrolysis: a form of catalysis by means of a hydrolytic enzyme, which
insert a water molecule between one between peptides. In the process, the
water is split, thus one end of the peptides is hydroxylated (an -OH is
added), and the other protonated (an H+) is added, thus H + OH = H2O. The
reverse of this is condensation. immune augmentation: In this context, the
enzymes of the pancreas are suggested as potentiating the function of the
plasma or immune cells.
hybridization: The merging of two specialized cell lines into a mixed cell
line, whose characteristics will then be passed down as the new phenotype.
In this context, the cancer cell merges.
catalysis: The speeding of a spontaneous reaction by lowering the energy
required for its activation.
degradation: The tearing apart of a molecule into two or more products. In
enzymology, the act of hydrolysis is a degradation of a linear peptide
chain.
inhibitors: Inhibitors can be substrates to enzymes that are not easily
dislodged from the catalytic site on the enzyme; or molecules that occupy a
site on the enzyme that change its shape and thus the enzymes catalytic
power is lost.
Footnotes:
[a] Augustus Weismann developed the concept that there were basically two cell
lines: the somatic cell line, which was mortal and restricted to the
individual life-span; and the germ cell line, which is immortal, passing on
from time immemorial the "side-chains" of numberless individuals.
Scientists are now recognizing that the body carries a residue of totipotent
cells, or stem cells, and thus theoretically the individual could be
reproduced in place just as the race is by sexual exchanges.
[b] No relation to John Beard.
[c] Aschheim-Zondek Tests.
[d] A term that encompasses the concept of a graft between genetically
different individuals as well as a transplantation as of a whole organ. In
this sense, however, it is one individual en toto, originated by the most
primitive of all grafts: that of the genome of the father into the mother's
prepared egg.
[e] Since there seem to be numerous advantages to the bearing individual, as
well as to the race if we will, then "parasite" cannot accurately reflect
this relationship. It is not a commensal relationship, and so we must
conclude in reality this is a symbiotic relationship, and the fetus is the
symbiote, while the placental tissue, namely the trophoblast is a parasitic
tissue. This is what is rejected ultimately, since there is no anatomic
contact between fetus and mother.
[f] Major Histocompatability (MHC) receptors are notably lacking in the
syncytio-tropohoblast. The precise cause of this is unknown.
[g] Various means have been contemplated to summarize quickly the concept of
cancer in relation to immunity, and for this purpose we will take recourse to
this term, since Beard's concept most closely comports to the process as
conceived herein.
[h] Researchers who worked at the Pasteur Institute in the early part of this
Century.
[i] The action of trypsin is probably not entirely dependent on amylase, since
there is good evidence that the action of this enzyme alone is much more
capable of stripping the sialomucins off than EDTA, as shown by Anghileri LJ, and
Dermietzel: Oncology 33: 17-23 (1976) Cell Coat in Tumor Cells - Effects of
Trypsin and EDTA. However, this stripping loads the plasma with large
glycoprotein conjugates that raise the osmotic pressure on the blood, induce
high arterial tension, strain the function of the kidneys and causes
edematous extrasavation, and probably contributes to the classic early
symptoms of morning sickness, pre-eclampsia, and ultimately eclampsia. See,
Beard, 1906; Krebs and Bartlett, 1949.
[j] Chorioepithelioma is, we think, the proper term, and not chorio-carcinoma.
As it is the thesis that cancer it trophoblastic, it is meaningless or a
tautology to say "the cancer of cancer" as is implied in the terms
chorio-carcinoma, or trophoblastic carcinoma. One may as well say cancerous
cancer.
[k] A doctor working in Burma at the turn of the century, F.W. Lambelle, MD,
reported the use of amylase and trypsin for the treatment of malaria, with
100% success against the relapsing disease:
[l] E.T. Krebs, Jr., insisted, after Weismann's dogma, that as all cells are
derived from like cells, it would be a thermodynamic impossibility for a
determined cell to become a totipotent cell. Thus he was forced to
contemplate and propose that something akin to the original process of
evolution of the germ cell via reduction division, with consequential
refusion, or irritation, acted as a kind of parthenogenesis of the
trophoblast, assuming incorrectly that trophoblast was a haploid tissue. In
the original development of trophoblast, it was observed that the sperm tail
is compulsively in only one half of the first division, and not both. It
would appear that this extra factor induces a totally different expression
from the nucleus of that side as opposed to the other. One marked difference
being that on the side that will become the fetus, and germ cells, only the
mother's mitochondria will exist. of course, on this basis, we must assume
that all mitochondria are derived from a woman, and that woman came first,
not man, and out of Eve's side came the rib that became Adam. Be that as it
may, the mitochondria that had come from the father's mother, does not become
incorporated in the son or daughter of this couple, which have thereafter
only the mother's mother...etc.....mitochondrial heritage. Further to
this, we might postulate that something akin to the inclusion of an added
energy source as takes place in this lopsided zygote might be an inducer of
activation of this trophoblastic property latent in every cell that has a
complete genome.]
[m] If that first cell were destroyed right off, we would never be the wiser,
but sensitive detection techniques might enable clinicians to be aware of
their existence, and that would be the time to initiate enzyme
supplementation, such as the mother gets from her own fetus. More of which in
text.
[n] We will not be able to digress to examine this postulate in any depth in
this paper, but a brief description of Beard's concept is warranted.
Stereochemical differences between species might represent a niche in the
evolutionary sense of taking advantage of available resources. For example,
Beard believed the reason that our own pancreatic enzymes do not digest
normal tissues of the body is because the proteins and carbohydrates
composing our bodies are of the opposite conformation of the proteins and
carbohydrates we see as food. This is not entirely correct, but it is not
entirely incorrect.
[o] Cancer is a chronic, metabolic disease. Chronic: a condition that does not
go away of it's own accord; metabolic: is confined to the metabolism, is not
contagious.
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22. URL: http://www.navi.net/~rsc/beard066.htm
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Acceleration of Proteolysis by
HCN, J.Biol.Chem, Vol. 8:177-213, 1910
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