=========================================================================== A point-for-point response from RCRS to data found at: http://catalog.com/bri/bri.htm ============================================================================== "Antineoplastons ---General Overview" "The most exciting and promising new direction of cancer research is into the body's own natural defense systems against cancer." ============================================================================== This is true, but the approach is not new unless we are thinking in evolutionary terms. The fact of the matter is that since 1902 we have had a rational, biological anti-cancer program in the pancreatic enzymes as proposed by Embryologist John Beard of the University of Edinburgh Medical School. (Lancet, 21 June, 1902 & Oct 29, 1904). This program languished until the 1940s, when Drs. Ernst T. Krebs, Sr. and Jr. began an extensive study of Beard's work and presented their findings beginning in 1949 in the Medical Record, Science, and other scientific journals. ============================================================================== "Most cancer experts believe we all develop cancer hundreds if not millions of times in our lifetimes. Given the trillions of developing cells, the millions of errors that can occur in the differentiating (maturing) process of each cell, and our constant exposure to carcinogenic substances (smoke, car fumes, radiation, etc.), the laws of probability dictate that mis-developing cells must occur frequently in the life of each individual. It stands to reason that a healthy body has a corrective system to "reprogram" newly-developed cancer cells into normal differentiation pathways before the cancer can take hold." ============================================================================== This is conceptually true, but inaccurate with regard to frank cancer cells. Normal cells undergoing differentiation or actively dividing are capable of abnormal development or expression of different specializations due to malnutrition, toxins, etc. Sometimes when this occurs such cells undergo such extensive alterations they are not recognized as "self" by the immune system, and they are killed and digested. Other pathways are possible in which apoptosis, or so-called "programmed" cell death is all that happens. For example, a deficiency in vitamin A will alter the development of the underlying or basal epithelial cells of the ducts of the pancreas and salivary glands. Instead of this normal differentiation, these cells will undergo differentiation towards keratinizing squamous cells. This is referred to as squamous metaplasia, caused by retinoid (Vitamin A) deficiency. These cells persist as long as they are fully functional in their albeit alternative mode of life. Administration of Vitamin A will provide for the reappearance of normal epithelial cells...but it does not cause the metaplasias to "reverse" or de-differentiate; rather they drop away to make room for new normal cells as these develop and apoptosis is elicited. Furthermore, these metaplasias are not capable of differentiation into cancer as such. Cancer is itself a highly differentiated, although primitive, cell line in the life-cycle. In fact cancer is the most primitive differentiation in the life-cycle. It only arises from a competent cell capable of meiotic or reduction division. Such a precursor or competent cell is called totipotent. And highly differentiated cells are not totipotent. What may be presumed to occur in the tumorigenesis in the locality of metaplasias may go something like this: a keratinized cellular process, unable to perform adequately the normal functions of the organs or tissues to which they are attached triggers a partial response of the immune cells. The lymphocytes or leucocytes may infiltrate these and in the process of digestion or the killing of these trigger inflammation. Such inflammatory processes (due in part to histidine-histamine-histiocyte pathways) causes a collection of fibrin on the surfaces of confining membranes or in the afferent vessels surrounding the areas in question. These in turn collect steroidal reactants such as estrogen. Estrogen is the primary inductor of meiotic or reduction division. If in these tissues competent totipotent cells are to be found, these will then undergo meiosis with consequent evolution of haploid gametogenous cells whose only alternative to death is differentiation into trophoblast, and trophoblast is cancer. In a persistent deficiency of retinoids, then, we will have a chronic expression of these processes with adequate collection of estrogens towards evolution of trophoblast...cancer. We will lay aside for now the potential of specialized cells to revert to totipotency, but such would certainly be required before trophoblast could evolve from them. Also, note that most carcinogens are estrogenic in general character. Also, these metaplasias will have an altered functionality with regard to toxins, and may selectively localize adventitious toxins on their surfaces, eliciting similar responses noted above. Now if the intrinsic, endogenous serine enzymes are weak (due to chromium deficiency for example, or amino-acid deficiency, or presence of parasitic or heavy metal inhibitors) these frank trophoblast cells are free to develop normally just as they do in normal pregnancy. And you now have cancer. Since deficiency in one area is usually accompanied by deficiencies in other areas, we can expect that not only are the serine enzymes suppressed, but the immune system will be suppressed. Leucocyte development depends on adequate nutrition, along with their functional co-factors which are synthesized elsewhere in the body, such as amylase (diastase) and trypsin and chymotrypsin, factors whose synthesis is possible from adequate nutrition alone. The body cannot create de novo essential dietary factors like tri-valent chromium (GTF:glucose tolerance factor), vitamin A, vitamin B-17, vitamin B-15, B-12, or vitamin C. Therefore these metaplasias as spoken of here are expressions of a nutritional deficiency. There is no need for "reprogramming" the genome to correct the problem. Adequate nutrition is required. Epigenetic pathways are obviously invoked for the proper transformation of various specialized cells into other normal specializations; as well as in abnormalities. This is true even with normal trophoblast, which are transformed by means of pancreatic enzymes to differentiate into a terminal, non-dividing phase (syncytiotrophoblast); correspondingly through a lack of adequate exogenetic trypsin and amylase, pregnancy trophoblast will fail to so transform and thus remain in its invasive, erosive, proliferative, metastasizing phase..and you have choriocarcinoma. But trophoblast (cancer) cannot be induced to become any normal cell functionally a part of the body, any more than it does in pregnancy, wherein its normal role is to form the contact-epithelium or chorion of the placenta. These tissues are not in any way integrated into the baby's body, or the mother's...they are not fetal cells as is so commonly said; and trophoblastic exhibition in either environment outside pregnancy is not experienced as anything except as cancer. Needless perhaps to say, abnormalities in the cancer cell gene expressions are also possible, with subsequent dysfunction or degeneration, playing a role both in failed pregnancies and toxemias, but also in so-called spontaneous regressions of cancer. ============================================================================== "Cancer cells differ from healthy cells in that they are, in effect, immortal. While healthy cells live a short while and then die, cancer cells continue dividing. The program for cell death is never activated." ============================================================================== This is true of any asexual generation, whether a protozoa, or the asexual generation of any animal. ============================================================================== "Antineoplastons are peptides, small proteins and amino-acid derivatives found naturally in human blood. Cancer patients tend to have low levels -- as little as 2% that of healthy individuals...." ============================================================================== This follows in Beardian terms from the obligative deficiency of break-down products from action of such proteinases as pepsin, trypsin, and chymotrypsin. Since pepsin is the first-acting proteinase, it's insufficiency provides an obligative reduction of adequate action by trypsin, which is not a first-acting proteinase. This is a vicious cycle: inadequate function of the pancreatic serine enzymes will not provide adequate release of amino acids from the gut towards proper synthesis by the stomach of pepsinogens. Conversely, toxins introduced to the gut, such as aluminum, anti-acids, heavy metals, etc. will completely inhibit or decrease the activity of pepsin, trypsin and so on. The system begins a slow starvation cycle which is highly exacerbated by the presence of trypsin- and other enzyme inhibitors secreted by the cancer cells, which results in cachexia in the cancer patient. ============================================================================== "Antineoplastons work by "reprogramming" cancer cells to die like normal cells. Healthy cells are not affected." ============================================================================== We are not in this expressing any undue criticism of the possible adjunctive utility of such a program. What we are suggesting is that normal immuno-responses are provided only by adequate function of the pancreatic/digestive system, in conjunction with adequate nutrition. The body will produce it's own "anti-neoplastins" in that case. But it would be foolhardy to deny the trial of such a program in any case because: 1) It is non-toxic...no reason not to beyond practical costs, and deferment of superior methods. 2) It has been empirically demonstrated to have positive effects beyond what might be expected from a statistical assessment; however, similar assessments have demonstrated that, in some cancers, doing nothing at all yields positive effects. Thus as to whether these effects with respect to antineoplastins issue from the specified pathways or not, or other factors we lack sufficient data to evaluate. ============================================================================== "Antineoplastons have a two-pronged mechanism of activity. They suppress the activity of the oncogenes that cause cancer, while at the same time stimulating the activity of the tumor-suppressor genes that stop cancer." ============================================================================== Insufficient data to evaluate. However, if trophoblastic transformation from the cytotrophoblastic phase into the syncytial or plasmoditrophoblast phase can be said to be dependent on gene activation or suppression, then the exogenetic factors which trigger this (pancreatic enzymes) can be said to "suppress" or "activate" various "oncogenes" towards a positive result. No exotic manipulation of the genome, or extrinsic adaptations of endogenous proteins or peptides is required for such action. Only introduction (parenterally or enterally) of supplemental serine enzymes or their potentiators (such as GTF and B-17) is required. Thus in terms of prevention, as well as clinical protocols adequate nutrition is absolutely required. ============================================================================== "Antineoplastons A10 and AS2-1 seem particularly effective against brain cancer and non-hodgkins lymphoma." ============================================================================== Insufficient data to evaluate. ============================================================================== "For more information please call (713) 597-0111 or FAX (713) 597-1166" "Burzynski Research Institute 12000 Richmond Ave. Houston TX 77082 Copyright (C) 1995 Burzynski Research Institute All rights reserved." ============================================================================== Final thoughts: Empirical empetus towards research is perfectly valid, and the majority of research being done today is based on empirical evidence provided from hundreds of years of collected datums. The empirical concoctions from the pharmaceutical and manuals of practice from the last 300 years, the accumulated knowledge bank of medicine itself, based on purely empirical data up until only very recently, is the subject of thousands of Doctoral Theses, and the subject of countless hours of public and proprietary research. Anecdotal reports fall under the same domain, with the same objective: as empetus to convert empirical streams of data into rational and practical components of our knowledge. The theories of researchers like Dr. Bryzynski or of Dr. Gold and his hydrazine sulfate, and other programs may be correct or incorrect. Only a prior and independent establishment of all the points of their contentions and experiment can fully validate any thesis. It would be a shame to deny their formulations testing or licensure just because their theories are not perfect if, nonetheless, the compounds themselves are effective. There are obviously complex and alternate pathways by which the body acheives similar, if not optimal, ends. For example, as noted, addition of chromium in biologically active form plays a crucial role in the activity of trypsin on protein particalization. One structure for GTF is complexed with cysteine, glycine and glutamic acids. This same complex goes into the structure of glutathione, and glutathione is known for it's ability to reactivate deactivated trypsin. Hydrogen sulfide, which may be reduced from hydrogen sulfate--a component of hydrazine sulfate moiety--is also a trypsin reactivator, just as hydrogen cyanide is. These factors are not currently taken into account in the promotion of the utility of hydrazine or chromium in cancer therapies. End of point-for-point response from the RCRS