Archive for December, 2016

Further Evidence for Cancer as a Cell-Wall-Deficient Mycobacterial Disease

December 5, 2016

A.P. Lysenko PhD, L. Broxmeyer MD, V.V. Vlasenko PhD, P.A. Krasochko PhD, A.P.Lemish PhD, and E.A. Krasnikova

Further Evidence for Cancer as a Cell-Wall-Deficient Mycobacterial Disease.pdf

Corresponding author:
Lawrence Broxmeyer, M.D

© Under License of Creative Commons Attribution 3.0 License


Received: October 07, 2016; Accepted: November 03, 2016; Published: November
14, 2016



In 2014, Buehring reported that Bovine Leukemic Virus (BLV), a common oncogenic retrovirus of cattle, was present in some humans, primarily localized to the breast epithelium  ―  the  very  cell  type  from  which  most  breast  malignancies  arise.  By 2015, there appeared data (Buehring, 2015) supporting that as many as 37% of human breast cancer cases could be attributable to BLV exposure. But if recent estimates suggest over 83% of U.S. dairy operations are currently positive for BLV, they also show that approximately 68% are positive for cell-wall-deficient Mycobacterium avium subspecies paratuberculosis (MAP). Although tubercular lung infection has been said to cause 11 times the incidence of lung cancer as normal control subjects, it is its cell-wall-deficient (CWD) forms (also called L-forms) that have recently repeatedly been found through genetic analysis and appropriate stains in such cancer tissue ― suggesting that CWD tuberculosis or atypical tuberculosis “is likely to be involved in the occurrence or development of lung carcinoma”. A similar relationship between tubercular L-forms and the genesis of the very breast cancer addressed in the aforementioned BLV viral trials. This is not a coincidence. L-forms (CWD forms) predominate and are crucial to the survival of mycobacteria in vivo and they have been documented by fluorescence microscopy in all intracellular macrophage-grown M. tuberculosis observed. From its origin, the very concept of the “BLV leukemic virus” has been on shaky, unstable ground. In 1969, veterinarians Janice and Lyle Miller from the University of Wisconsin-Madison spotted C-shaped “virus-like” particles in cattle lymphosarcoma insisting that these were similar to other C-type viruses “regarded as the cause of leukemia in other species.” But by 1978, scientists at Downstate reported atypical mycobacterial forms, including its preferred filterable virus-sized “L” or cell-wall-deficient (CWD) forms in not only leukemia but all other malignancies ― all having, as their common denominator the continuous presence of mycobacterial C-shaped forms.

Tracing back to techniques similar to Miller and Millers original BLV study we found in the very lyophilized antigens present in commercial kits for the diagnosis of BLV (AgBLV), these very same CWD (cell-wall-deficient) mycobacteria and mycobacterial DNA in all BLV samples ― which when introduced into guinea pigs stimulated the same antibody as occurred when mycobacteria-infected internal organ homogenates themselves were injected into other guinea pigs. It is therefore assumed that the Bovine Leukemic Virus (BLV) is being mistaken for viral-like forms of cell-wall-deficient (CWD) atypical tubercular mycobacteria. Since latent tubercular infection, as well as the administration of BCG and tuberculin also results in persistent CWD forms, their possible role in carcinogenesis is also considered.

KEYWORDS: Cancer; Mycobacterium tuberculosis; Bovine Leukemic Virus; BLV; Mycobacteriophages



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