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PostPosted: Fri Jan 19, 2018 1:32 pm 
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In the annuals of the history of curing cancer there are three Doctors that seemed to have had the best clinical results, Dr. Johanne Budwig (based on linoleic acid supplementation) while Dr. Kelly and Nicholas Gonzalez, MD. championed the trophoblastic theory of cancer involving pancreatic enzyme supplementation. All three seemed to have uncanny success when treating cancer in a clinical setting. I want to suggest that the two theories are connected and should be considered as one whole which as far as I know has never been done. This journal article seems to tie the two together:

Quote:
Stem Cell Rev. 2011 Nov;7(4):898-909. doi: 10.1007/s12015-011-9253-7.
Specific unsaturated fatty acids enforce the transdifferentiation of human cancer cells toward adipocyte-like cells.
Ruiz-Vela A1, Aguilar-Gallardo C, Martínez-Arroyo AM, Soriano-Navarro M, Ruiz V, Simón C.
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Abstract

Differentiation therapy pursues the discovery of novel molecules to transform cancer progression into less aggressive phenotypes by mechanisms involving enforced cell transdifferentiation. In this study, we examined the identification of transdifferentiating adipogenic programs in human cancer cell lines (HCCLs). Our findings showed that specific unsatturated fatty acids, such as palmitoleic, oleic and linoleic acids , trigger remarkable phenotypic modifications in a large number of human cancer cell lines (HCCLs), including hepatocarcinoma HUH-7, ovarian carcinoma SK-OV-3, breast adenocarcinoma MCF-7 and melanoma MALME-3M. In particular, we characterized a massive biogenesis of lipid droplets (LDs) and up-regulation of the adipogenic master regulator, PPARG, resulting in the transdifferentiation of HCCLs into adipocyte-like cells. These findings suggest the possibility of a novel strategy in cancer differentiation therapy via switching the identity of HCCLs to an adipogenic phenotype through unsaturated fatty acid-induced transdifferentiation.



As far as the trophoblastic theory, some interesting tidbits:




Quote:
Reduced Pancreatic Enzyme Secretion

At about 12 weeks of pregnancy, the embryonic trophoblast usually stops growing and the placenta takes over the function of nourishing the fetus. Dr. Beard found that enzymes produced by the fetal and maternal pancreas stop the growth of the trophoblast.

This is the basis for the use of pancreatic enzymes in the treatment of cancer advocated by Dr. William Kelley, DDS and others (Kelley, W.D., 1997). Large quantities of pancreatic enzymes are given by mouth, which inhibit the growth of malignant cells.

The pancreas plays another role. Pancreatic enzymes are needed for proper digestion. A weakened, toxic or depleted pancreas contributes to a toxic liver by failing to provide adequate enzymes for complete food digestion. Many people do not produce enough pancreatic enzymes or they overeat, exceeding their digestive capacity. These pancreatic enzymes are not the same as "food enzymes" found in raw food. Ideally, excess pancreatic enzymes are secreted so that any cancer that begins to develop will be destroyed.

Causes for deficient pancreatic activity are similar to the causes of liver toxicity. They include stress, poor-quality diets, poor eating habits, infections and toxic exposures. For this reason, sauna therapy can be most helpful to restore pancreatic activity.














Jeffrey Dach, M.D. is Board Certified in Diagnostic and Interventional Radiology wrote the below and this has implications to the Kelly and Beard Trophoblastic Theory of Cancer:



Quote:
No Coexistence of Cancer with Circulating Enzymes of Pancreatitis

One last point I am compelled to mention. During my 30 year career as a radiologist much of my time was spent reading images of metastatic cancer on CAT scans. One of the things I noticed was that I never witnessed the presence of metastatic cancer in patients who had pancreatic enzymes circulating freely in the bloodstream from acute or chronic diffuse pancreatitis. Excluded of course was focal pancreatitis caused by an obstructed pancreatic duct due to a small pancreatic cancer. Thus I had independently confirmed the major tenet of John Beard and Ernst Krebs many years before I even heard of the trophoblastic theory of cancer.






Quote:
Apparently, malignant tumours does not form their own pancreas (as they are not really fetus or not real pregnancy). Therefore, there will be no organ within the tumuor that will produce the pancreatic enzymes necessary to control its growth. Most cancer patients also have malfunctioning pancreas– that they also do not have sufficient pancreatic enzymes to digest the cancer proteins. Thus, supplementation of pancreatic enzymes is necessary for all cancer patients. Dr. Kelley studied Dr. Beard’s theory and took it at next level by using Macrobiotic and Pancreatic Enzyme Therapy to treat all types of cancer. What I am not sure of is whether Charlotte Gerson read about Dr. Kelley’s work and added it into his father’s Macrobiotic Therapy (or was it the other way around).
What is more important for me is that Dr. Kelley is not a quack doctor- his findings are based on the works of an earlier scientist, Dr. Beard– whose hypothesis is now being studied as a basis for Cancer Stem Cell- targeted therapies and even Immuno-therpies using Enzymes to digest the tumour cells.

I also believe that the Fungal Theory should also be revisited as we know that Fungi also emits HcG and some of the other cancer lines or factors that causes cell prolifiration and tumour formation. Dr. Beard also mentioned that the tumour has a capability to mimic the organ to which it lies (a capability that fungi also have).

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PostPosted: Sun Aug 09, 2020 11:58 am 
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Quote:
Pancreatic Glandular Therapies: From Absorption to Cellular Interactions in Cancer
By Carrie Decker, ND




Cellular Interactions of Proenzymes and Proteolytic Enzymes
Investigations into the effect of pancreatic glandular substances on malignancies goes back to the late 1800s and the work of John Beard, PhD, an embryologist, who had observed that developmentally, the trophoblast is much like a cancer. Its cells, sheltered from immune attack, invade and implant into the uterine lining, producing their own blood supply much like a malignancy does in tissues surrounding it. He discovered that at the same point the poorly differentiated tissue invading the uterus became the mature placenta, production of pancreatic enzymes begins to occur (confirmed by modern research).32,33 He wondered what caused these cells to essentially “behave”; and upon discovering the embryo production of the enzyme trypsin, he tested his theory by injecting trypsin (diluted in distilled water) into tumor-burdened mice and found their tumors regressed – results which were published in the British Medical Journal in 1906.34 Numerous physicians aware of his research began treating their human cancer patients under his direction, finding success that they also detailed in case study publications.35,36

Interest in this use of pancreatic enzymes has waxed and waned with time, with many doctors, such as the late Nicholas Gonzalez, MD, electing instead to use high oral doses of freeze-dried (lyophilized) pancreatic glandular substances prepared in a manner so the fatty content remained.37,38 Fat, it was suspected, contributed to a more stable product while in a water-containing environment the enzymes were prone to autodigestion. By using these whole freeze-dried glandular materials, in addition to the active enzyme fraction, the proenzymes and cofactors normally present in the tissue also remained.

n recent years, researchers have looked at the interactions that the compounds found in pancreatic glandular substances may have with receptors on the surface of cancer cells and trophoblasts. Protease activated receptors (PARs) have been shown to play a role in both tumor cell invasion and placenta growth and development.39,40 In cancer cells expressing certain PARs, trypsin actually may be pro-oncogenic,41,42 although other studies have shown it to have anti-metastasis, anti-motility, PAR-desensitizing, and pro-cellular differentiation effects.43,44

It also may be that the proenzymes or protease inhibitors found in pancreas glandular products are the substances having anti-oncogenic effects.45,46 Proenzymes have been shown to have angiostatic properties and selectively activate on cancer cells, enabling them to directly deliver their proteolytic action to the tumor cells.47 A combination of proenzymes with their active enzyme form (as found in a crude pancreatic extract) was shown to have a far more dramatic effect on survival than trypsinogen or amylase alone in a murine model of melanoma metastasis. In findings published as recently as 2017, proenzyme preparations have been shown to inhibit angiogenesis, tumor growth, and cancer cell migration and invasiveness as well as promote cell adhesion and differentiation in vitro, and to be well tolerated and effective clinically.48,49

Clearly, many questions remain unanswered as to the biological potential of pancreatic glandular preparations. That said, due to their high level of tolerability and the low incidence of adverse reactions, they continue to be used in difficult-to-treat conditions such as cancer.

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