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The Trophoblastic Nature of Cancer and Pregnancy Cycle
 as the Basis for the Enzyme Treatment of Cancer

by Roger Cathey        

This paper is written for the lay person. If you are a doctor, there is a more technical article on page one of our Science Papers page.

Part One The primary basis of the enzyme treatment of cancer emanates from a recognition that cancer cells share properties with placental cells found in pregnancy. These placental cells are completely rejected by both fetus and mother by the time of delivery. Therefore it was reasoned that whatever factor or factors which underlay the rejection of the placenta could play a similar role in the body's rejection or remission of cancer cells. Other observations lead the earliest thinker along these lines, Embryologist John Beard (1857-1924), to believe that the pancreatic enzymes of fetus and mother combine to bring about this event. Thus the basis of enzyme therapy for cancer was first derived from the idea that enzymes play a role in causing birth.

These placental cells are called trophoblasts and are the first cells to differentiate from the fertilized egg. In this creation of trophoblasts it is important to note that they are a fully parasitic and a distinct feature surrounding the fetal cells that will form the living individual. In their role, trophoblasts mediate the implantation of the individual, but they are never incorporated into the body of the individual or fetus. Thus it is incorrect to call them "fetal" cells. They will eventually be either destroyed or rendered completely inert as far as the mother and fetus are concerned. These cells are often seen as a thin membrane covering the fetus at birth, the so-called "caul." Again, they never form an integral part of the formative individual.

This fact is important to keep in mind, psychologically, because the same holds true of the cancer cell which does not in its incursion form an integral part of the individual. It has been observed that after some time of enzyme treatment tumors often "shell out," and they can be more readily removed surgically, or they may extrude and drop out by themselves if partially exposed on the outside of the body. Somatic "tumors" or lumps or calluses consist of normal cells that sometimes grow up around the cancer growth in an attempt to mechanically limit their incursion. These types of growths are not affected by enzyme treatment, but are reduced by a morphogenic process of apoptosis or programmed cell death, or they may need to be removed surgically. It is believed that in many cases of radiation therapy, it is these normal cells that are destroyed leaving the hardier cancerous cells with a higher concentration in mass. In enzyme therapy, the cancer cells alone are attacked.

The source cells of these trophoblasts in pregnancy are the most potent cells in the life cycle, i.e., the united sperm and egg result in the original "stem cell," or cell capable of becoming any and every cell in the completed form. Other tissues formed or differentiated from this primal cell may have various powers of expression, but they do not possess the power to become any other cell in the whole system. Most cells of the body are therefore "derived" cells and they are all observed to be of limited potential.

As noted above, in the course of gestation these trophoblasts are rendered completely inert and finally rejected from the host representing the event of birth and probably is also a major cause of birth. This happens despite the fact that the cells seem not to induce any immunological reaction. A prime reason for this was discovered in this century by Currie and Bhagshawe who showed that the trophoblast was surrounded by a coating (sialo-glycoprotein) including a molecule that gave it a negative charge. The molecule can be likened to mucilage and has been termed the sialo-mucinous coat. A negative charge is also found on the white blood cells responsible for immune reactivity. Since two like charges repell we have delineated the primary reason for lack of rejection based on immune responses.  This same type of coating is found on the cancer cell.  And in fact, it is one of the chief reasons for classifying all cancer cells as "trophoblastic."

It bears repeating that although the first trophoblast cell in the life cycle goes on to become the entire placenta, it does not become any part of the oncoming fetus, but is strictly a parasitic mediating and terminal cell or tissue type. Because the cellular trophoblast (cytotrophoblast) can differentiate further, it is said to be pleuripotent, but it is still of limited potential compared to the stem or totipotent cell.

John Beard was the first to organize a theory around the cause of birth and the destruction of cancer cells. First he observed that the invading and eroding trophoblast component of the fertilized unit was remarkably similar to metastatic cancer cells, and other observations lead him to believe there was some intimate relationship between these trophoblasts and cancer cells. Another observation was that the placental trophoblasts seem to take a downturn in activity around the time of the activation of the fetal pancreas, which occurs around the 56th day. Modern research has shown that these trophoblast cells secrete a hormone called human chorionic gonadotropin (hCG), and the quantities of this hormone rise until around the 56th day and then begin to taper off. It is this very hormone that coats the trophoblast and cancer cell to make them both immulogically inert. This hormone of pregnancy is expressed in all types of cancers.

Seeing this change in trophoblast behavior and the onset of activity of the fetal pancreas has more than mere coincidence, Beard began to speculate in his correspondence with physicians about the possibility that the function of both the mother's and the fetus' pancreases were somehow involved in the resolution or destruction of the trophoblast. If that is so, he asked, then might the same be said of cancer cells in the cancer patient? In time Beard's speculations were put to the test by several physicians using pancreatic enzymes. At first they used only the proteolytic enzyme trypsin, but when the reactions of patients to this tended to be severe they then turned to combining trypsin with amylase, the carbohydrate digesting enzyme, and found that the reactions of the patients were much better. (For details on this historic finding go to: http://www.navi.net/~rsc/beard066.htm)

This accentuation of the protein digesting enzymes in many versions of this therapy explains the oft reported periods of nausea and other symptoms resembling pre-eclampsia or morning sickness. Beard and his associates'  final form of therapy always accentuated amylase, sometimes completely eliminating trypsin and other protein digesting enzymes after a certain length of application or during so-called "rest periods" of treatment.

This is logical, because the glycoprotein surrounding the cancer cell, and the circulating hormone form of this glycoprotein (often mistakenly called a "protein" or "fibrin" coat), are fundamentally presenting to the system as carbohydrate complexes. That is, the body sees the carbohydrate side of the molecule, not the protein side, and amylase attacks this before the proteinases can do a thing.

There is then the question of how the cancer/trophoblast comes into being in the non-pregnant individual. Since all stem cells have all potentialities within them, it has been assumed by some researchers that cancer must arise from a residual complement of stem cells in the body. There are a number of observations recorded in the medical literature attesting to the presence of these stem or totipotent cells in the adult body. Others contend that since all cells have the complete genome within them, if they can divide at all, there is the possibility of them re-acquiring totipotency, or simply to directly express the trophoblastic suite of characteristics. That is something for research to definitely establish, and we need not concern ourselves too much on this point. It would appear that anything that can disturb the genome sufficiently, presumably factors not normal to the animal economy, whether parasitic, cytotoxins, or carcinogenic or chronic injury of any kind, is sufficient to bring these properties into expression.  After all, the trophoblast has proven to be the hardiest of expressions of the differentiating zygote as it goes through a gamut of harsh environs of low oxygen, then establishing a place in the uterus and a reliable blood supply. In injury, something of the same harshness exists.

In the next and continuing parts, we will discuss further the means being used today to help control the disease and the adjunctive protocols that may form a part of the overall immuno-enzyme therapy.

 

 

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