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Are infections the cause of cancer? Well, in many cases this is a proven fact. Usually the infectious agent is a virus that takes over the genetic machinery of a cell and turns it cancerous. Some researchers down through many years have contended that bacteria may also be involved. Usually those claims have been dismissed without much serious consideration.
Now research out of China shows a relationship between metastatic breast cancer (pictured above) and a bacteria. Antibiotics may be effective in such a case, or more natural immune enhancing therapies.
Read more about it in the following abstracts, one from 2010,
the other going back to 1981.
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. xiewj75@126.com
Abstract
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.
Abstract
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.
PMID: 6166642 [PubMed - indexed for MEDLINE]
Alan Cantwell M.D.
alancantwell@sbcglobal.net
author of THE CANCER MICROBE
www.ariesrisingpress.com
Xie W, Huang Y, Xie W, Guo A, Wu W.
Biology Research Institute of the United Laboratories International Holdings Limited, Zhuhai, China. xiewj75@126.com
Abstract
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.
Abstract
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.
PMID: 6166642 [PubMed - indexed for MEDLINE]
Alan Cantwell M.D.
alancantwell@sbcglobal.net
author of THE CANCER MICROBE
www.ariesrisingpress.com
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