Study links microbial imbalance with breast cancer

After comparing breast tumour tissue and normal tissue from the same patient, the researchers found that the bacterium Methylobacterium radiotolerans​ was relatively enriched in tumour tissue, while the bacterium Sphingomonas yanoikuyae​ was relatively enriched in paired normal tissue. The results suggested there had been a microbial dysbiosis, or imbalance, within the tumour tissue.

The Californian researchers said the dramatic reduction in bacterial load found in breast tumour tissue compared to healthy breast tissue implied that bacterial load may be used along with current methods to monitor the progression of breast cancer and to help stage the disease.

“Furthermore, it is tempting to speculate that a decrease in bacterial load in a healthy individual may be a signal of heightened breast cancer risk,”​ they wrote.

The study follows previous research suggesting a link between microbiota imbalance and various human diseases including obesity, diabetes and colon cancer. Human microbiota are microbes residing on and in the skin, in saliva, oral mucosa, conjunctiva and gastrointestinal tracts, sometimes dubbed ‘friendly bacteria’.

Maintaining health levels ​

The study’s quantitative survey of breast microbiota found that the amount of bacteria was not significantly different in paired normal tissue of breast cancer patients and healthy individuals. However, compared to both of these healthy tissues, breast tumour tissue had significantly reduced amounts of bacteria.

The researchers said this coincided with the, “reduced expression of one-third of antibacterial response genes surveyed”​.

“Taken together, these data suggest that bacteria may have a role in maintaining healthy breast tissue through stimulation of host inflammatory responses,”​ the researchers wrote. 

Source: Plos One​

Published January 08, 2014, DOI: 10.1371/journal.pone.0083744​

'Microbial Dysbiosis Is Associated with Human Breast Cancer'​
Authors: C. Xuan, J. M. Shamonki, A. Chung, M. L. DiNome, M. Chung, P. A. Sieling, D. J. Lee