New research from the University of Virginia suggests that an inflamed bowel without a bacterial physiological flora makes breast cancer much more invasive and spreads more quickly to other parts of the body.
Melanie Rutkowski of the Department of Microbiology, Immunology and Cancer Biology of UVA, discovered that the destruction of the microbiome of mice caused a greater aggressiveness of breast cancer positive to hormonal receptors.
The alteration of the microbiome (microorganisms that live in the intestine and elsewhere) has had dramatic effects on the body, causing the spread of cancer.
The reason why some patients with breast cancer (HR +) have a more aggressive and invasive disease is unknown.
Predicting whether these tumors will spread to other parts of the body (a process called metastasis) represents a major challenge in the medical field. Important indications of the patient’s clinical characteristics can be derived at the time of diagnosis.
It is known that metastatic spread occurs early in the disease and is facilitated by alterations in the tissue environment, suggesting that undefined host intrinsic factors improve early dissemination and the likelihood of developing a metastatic disease.
In the study, researchers identified commensal dysbiosis as an intrinsic host factor associated with metastatic spread.
During the studies, it was observed that the destruction of the balance of the microbiome in mice by chronic treatment with antibiotics, caused both systemic and internal inflammation in the breast tissue.
In the presence of inflammation, the tumor cells more easily spread from the tissue to the blood and to the lungs (an important site of metastasis for breast carcinoma).
Commensal dysbiosis promotes early inflammation within the mammary gland, an inflammation that feeds on the progression of HR + breast cancer.
In addition, dysbiosis increased fibrosis and collagen deposition both systemically and locally within the tumor microenvironment and induced significant myeloid infiltration in the mammary gland.
These effects were caused by the direct action on intestinal microbes, the use of no absorbable antibiotics or the fecal microbiota transplant (cecal dysbiotic), which demonstrates the direct impact of intestinal dysbiosis in the spread of breast cancer.
The majority of breast cancers, 65 percent or more, are hormone receptor positive. This means that its growth is fueled by a hormone, estrogen or progesterone (the good news is that these types of tumors respond well to hormone therapy such as tamoxifen).
The creation of an imbalance in the microbiome has caused long-term inflammation within the tissue. The study in question identifies dysbiosis as a pre-existing regulator, intrinsic to tissue inflammation and the tumor environment.
These results suggest that a deficient microbiome can be considered an early indicator of invasive or metastatic breast cancer.
For the purposes of this study, antibiotics have been used as a simple means, a direct way to create a long-term imbalance in the microbiome, similar to what individuals can experiment with chronically compromised microbiomes.
Rutkowski’s research, along with other studies on the subject, could be a starting point to implement actions aimed at manipulating the microbiome for the benefit of patients.
But the key message is the importance of a healthy microbiome. The discovery adds to growing evidence that a healthy microbiome is vital to many aspects of health. In general, precautions are recognized to promote a healthy microbiome: a healthy diet, rich in fiber, along with physical exercise and good quality sleep.
The continuous intake of yogurt, kefir, fermented beverages, foods with added lactic ferments can contribute to a competent microbiome.
In cases of more severe dysbiosis, it is recommended to take probiotics and prebiotics during cycles of at least three months to restore a functional and healthy microbiome in several anatomical districts.