The two studies below show that bacteria seems to play a role in cancer. The bacteria in its different forms may cause inflammation which also plays a role in cancer. If this subject interests you, you may want to read The Cancer Microbe by Alan Cantwell. He is also the author of the second study on this page.Many people with chronic Lyme disease or other chronic lowgrade infections, often can develop cancer. Would proper allopathic antibiotic treatment or herbal antibiotic treatment keep cancers from developing? Would a proper diet devoid of sugar and other refined foods make the body less hospitable to these microbes?
This is a quote from Cantwell's book "Virologists study viruses; and bacteriologists study bacteria. Virologists don't comprehend that viruses can originate from bacteria. And bacteriologists don't comprehend that bacteria can originate from viruses. And few physicians understand that "mycoplasmas" comprise the borderline stages between viruses and bacteria. It is pathetic that close minded scientists cannot see the vital interconnections between these branches of microbiology."
I read Cantwell's book several years ago and it must have been his statement above concerning mycoplasmas being the borderline stage between viruses and bacteria, that got me to thinking about the Lyme bacteria and its connection to mycoplasma. I was told by a molecular biologist that 60% of Lyme disease patients also harbor different types of mycoplasma. I noticed that doxycycline worked for both mycoplasma and Lyme disease and that Gulf War Illness patients(mycoplasma infected) and Lyme disease patients were both being denied proper antibiotic treatment. Some Gulf war illness veterans were also being diagnosed with Lyme disease. Because of the pleomorphic nature of Lyme disease and the way it can morph into a mycoplasma like sphere, I wondered if they could be different forms of the same microbe. One mycoplasma expert said that yes this was possible and the other one I asked said no...mycoplasma and the sphere form of Lyme disease are two separate entities. Its just something to think about.
This is just a wild statement I am making but is it possible that the retrovirus XMRV and or the EBV virus could be somehow related to different forms of the lyme bacteria? Many Lyme patients are coinfected with these organisms.
2010 May 26;5(5):e10850.
Bacteria peptidoglycan promoted breast cancer cell invasiveness and adhesiveness by targeting toll-like receptor 2 in the cancer cells.
Xie W, Huang Y, Xie W, Guo A, Wu W.
Biology Research Institute of the United Laboratories International Holdings Limited, Zhuhai, China. firstname.lastname@example.org
Chronic bacterial infection increased the risk of many solid malignancies and the underlying mechanism is usually ascribed to bacterial-caused inflammation. However, the direct interaction of infectious bacteria with cancer cells has been largely overlooked. We identified that highly metastatic breast cancer MDA-MB-231 cells expressed high level of Toll-like receptor 2 (TLR2) in contrast to poorly metastatic breast cancer cells and homogenous untransformed breast cells. TLR2 in MDA-MB-231 cells were actively triggered by peptidoglycan (PGN) from infectious bacterium Staphylococcus aureus (PGN-SA), resulting in the promoted invasiveness and adhesiveness of the cancer cells in vitro. PGN-SA induced phosphorylation of TAK1 and IkappaB in the TLR2-NF-kappaB pathway of the cancer cells and stimulated IL-6 and TGF-beta secretion in MDA-MB-231 cells. All these effects were abrogated by TLR2 blockade. Further investigation showed that the NF-kappaB, STAT3 and Smad3 activities were augmented sequentially in MDA-MB-231 cells after PGN-SA stimulation. Phosphorylation of NF-kappaBp65 was initially increased and then followed by phosphorylation of STAT3 and Smad3 in the delayed 4 or 6 hours. NF-kappaB inhibition attenuated STAT3 and Smad3 activities whereas PGN-SA-stimulated cell culture supernatants reversed these inhibitory effects. Our study indicated that TLR2 activation by infectious bacterial PGN played an important role in breast cancer cell invasiveness and illustrated a new link between infectious bacteria and the cancer cells, suggesting the importance of antibiotic therapy to treat cancer with bacterial infection.
J Dermatol Surg Oncol. 1981 Jun;7(6):483-91.
Microbial findings in cancers of the breast and in their metastases to the skin. Implications for etiology.
Cantwell AR Jr, Kelso DW.
In four cases of carcinoma of the breast, variably acid-fast coccoid forms were found in sections from their metastases to the skin and in one of these cases in sections of the primary carcinoma. In this one case, similar-appearing corcoid forms were observed within the sections of the primary malignancy. In this same case, Staphylococcus epidermidis was cultured and studied at once and as it aged for development of forms comparable to those found in the microscopic sections of the neoplastic process. The implications of the findings for etiology of carcinoma of the breast are discussed.