The Microbiology of Cancer and Its Potential Implications for Early Intervention Ron Falcone Website
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Microbiologia do câncer e implicações na intervenção precoce CWD , L-formas Hypothesis: The Microbiology of Cancer and its Potential Implications for Early Intervention Ron Falcone website Introduction The century's old debate as to whether bacteria are simply opportunistic infections "after the fact" or whether they can initiate cancer has been a contentious one. As early as the 1920's, Thomas Glover isolated a bacterium which he named "Glover's organism". Two decades later, Virginia Livingston believed that a single, ubiquitous pathogen she identified as a Mycobacterium (and which she named Progenitor cryptocides) was the primary cause of most human cancer. A handful of others also claimed discovery of a cancer-causing organism which appeared cameleon like, and seemed to defy one, universal taxonomy. From a mainstream standpoint, scientists disagreed with Glover and his later contemporaries, instead arguing that cancer-related pathogens were simply opportunists, contaminating diseased tissues after the fact. But in the 1990's, Shy Chung Lo of the Armed Services Institute of Pathology cultured Mycoplasma fermentans from cancer, injected the organism into animals, and was then able to induce cancer; in effect, Lo had established Koch's Postulates, proving that bacteria were indeed able to directly cause cancer [1]. Other investigators corroborated Lo's Mycoplasma research. For example, Chan reported the prevalence of mycoplasmal DNA in ovarian cancer[2]; Schmidhauser demonstrated that the p37 gene associated with mouse sarcoma originates from Mycoplasma and that a proportionate increase in malignant invasiveness was related to such exposure[3]; Ushio found that Mycoplasma-infected cells have a higher ability to metastasize in vivo than non-infected cells[4]; and Bogoch demonstrated that Mycoplasma secrete a similar polysaccharide used by cancer antigens to avoid immune-system recognition. Although mainstream scientists generally disregarded the notion of a "cancer germ"---even as late as the 1990's---conclusive evidence now linking H.pylori with stomach cancer has rendered this position obsolete. In addition, science now appears to be moving toward a greater acceptance of multiple species of cancer bacteria implicated in different forms of cancer. For example, Salmonella typhi, Streptococcus bovis and Chlamydia penumoniae[5] are being associated with gallbladder, colorectal, and lung cancer, respectively. And a percursory review of the scientific literature clearly has shown an exponential increase in cancer bacteria-based findings, beginning in the early 1990's and continuing through to the present. As the evidence continues to accumulate, the long held paradigm of microbiology that consigns a specific bacterium to a specific infectious disease may not correlate with the multiple species of bacteria now being associated with cancer. Cancer Bacteria and HCG Beside their potential role in oncogenesis, different genera and species of bacteria have consistently tested positive for the human growth hormone choriogonadotropin (hCG). While bacterial hCG is a finding that's not been actively pursued in mainstream laboratories, we feel it represents a major milestone in the cancer process. The first investigator to discover a bacteria-hCG link was Virginia Livingston in 1974[6]. Her findings were corroborated by Cohen and Strampp two years later[7]. In1987, Acevedo also found HCG but in a majority of different bacterial species isolated from cancer patients, including Streptococcus faecalis, Staphylococcus haemolyticus and Staphylococcus epidermidis as well as gram-negative diptherioids[8]. Acevedo's findings contradicted Livingston's claim of an "ubiquitous" or universal cancer bacterium---and this, in turn, was presented as proof against Livingston's bacterial theory in a report issued by the American Cancer Society (ACS) in 1990[9]. It will be noted, the ACS based its negative conclusions on the fact that different bacterial species could secrete hCG, and also on an inability to isolate Livingston' s specific bacterium, Progenitor cryptocides. However it should also be noted that the ACS did not disprove whether or not Livingston's cultures were actually oncogenic. Fundamentally, Acevedo did agree with Livingston's premise that cancer- associated bacteria have "revertant" forms, lack true cell walls, are filter passing (able to simulate viruses) and also intermittently acid fast---characteristics considered by some to implicate the controversial phenomenon known as "pleomorphism". In additional studies, Acevedo also found evidence of hCG in all cancer cell lines he examined, regardless of their origin[10]. These studies offer compelling proof that hCG is a common cancer marker found in many, or possibly most types of cancer, and its presence is significantly higher in disease tissues than in normal ones[11]. Bacteria, Cancer and HCG: An Unholy Trinity We hypothesize that the relationship between bacteria, cancer and hCG has vast implications both in our understanding of the century's old riddle of how cancer tissues evade host immunity, and equally important, in the potential realm of therapeutic intervention. The discovery of hCG as a viable tumor marker may now solve a riddle which has baffled scientists for more than a century---i.e., how cancer cells grow unchecked with little, or no immune system resistance. When cells become malignant, their surfaces change and become charged with carbohydrate residues. One of these residues---a simple sugar known as an oligosaccharide---combines with another sugar, sialic acid, a key molecule of hCG. Sialic acid, in turn, appears to protect the cancer cell from host immunity because it is a negatively charged molecule; immune system cells are also negatively charged[12]. In effect, HCG creates an "electric shield" (i.e., like poles repel) which appears to have evolved as an ingenious survival mechanism, not only for tumors, but for human life itself. In the latter case, HCG plays a significant role in protecting the developing human embryo from host immunity, just as it does with cancer. Without this effect, the mother's immunity would seek and destroy the fetus[13],[14]---a partly foreign protein in the uterus comprised of both friendly (host) and foreign (DNA) from the mother and father. Other insidious roles of HCG in cancer are tumor angiogenesis (formation of blood networks for malignant tissues), promotion of tumor invasiveness, and nourishment of tumors. Are human cancers quasi-manifestations of fetal life gone berserk, but expressing the same intention to live and grow? The parallels are indeed striking. For example, the primary manufacturers of fetal hCG are specialized placental cells called trophoblasts, whereas in cancer, the exact source of hCG is not clearly understood. Several possibilities include genes coded to produce hCG, or bacteria interfacing with cancer cells through DNA transfer, or via what has been described as a "plasmid vector". It may be that cancer bacteria serve as the biologic equivalents of trophoblasts in some capacity, but the latter arising via the evolution of human life and the former, as an adaptative mechanism of evolution. In the final analysis, cancer shares many similarities with fetal life and it is here that the ultimate solution to this disease may lie. Indeed, this idea has gained support among leading scientists working in the fields of genetics and immunobiology. Dr. Robert Weinberg, the first discoverer of a cancer gene and now an MIT professor of biology stated: It's now increasingly apparent that one mechanism, quite possibly the dominant mechanism, involves the ability by the cancer cell to resurrect early embryonic behavioral programs...This movement in the embryo is superficially similar to metastasis. The way cancer cells acquire this embryonic trait of being able to move throughout the organism depends on their ability to resurrect these early embryonic behavioral programs, which they do through their ability to induce the expression of early embryonic transcription factors [proteins that control the expression of a large number of genes]. In this case, these transcription factors control groups of genes that, when turned on, allow the cancer cells to move, to become invasive, to resist programmed cell death (which otherwise threatens their existence once they leave the primary tumor), and even to release degradative enzymes that break down the [surrounding tissue that] represents an impediment to the forward march of the cancer cells[15]. In a similar vein, Italian researchers wrote in the journal Immunobiology: The model that most resembles the behavior of tumor cells in terms of growth, infiltration and suppression of the immune system of the environment in which they live is undoubtedly that of the embryonic cell. The fetus behaves like an allogenic transplant within the mother's body, using every means it has to escape from and defend itself against the mother's immune system. The majority of these mechanisms are the same as those found in tumor cells (including)...antigenic loss and induction of apoptosis in infiltrating lymphocytes...A careful and comparative study of key mechanisms capable of triggering tolerance or cytotoxicity in both embryonic and tumor cells could prove immensely valuable in designing new strategies for anti-tumor immunotherapy[16]. Deadly Symbiosis: An Additional Role for Cancer Bacteria Bacteria may play another critical role in neoplasia beyond their possible involvement in disease causation and