Recent observations indicate that the pathogenesis and prognosis of hormone-receptor breast cancer is not only dictated by the properties of the malignant cells but also by immune and microbial parameters. Thus, the immunosurveillance system retards the development of hormone-positive breast cancer and contributes to the therapeutic efficacy of estrogen receptor antagonists and aromatase inhibitors. Moreover, the anticancer immune response is profoundly modulated by the local and intestinal microbiota, which influences cancer cell-intrinsic signaling pathways, affects the composition and function of the immune infiltrate present in the tumor microenvironment and modulates the metabolism of estrogens. Indeed, specific bacteria in the gut produce enzymes that affect the enterohepatic cycle of estrogen metabolites, convert estrogens into androgens or generate estrogen-like molecules. The knowledge of these circuitries is in its infancy, calling for further in-depth analyses.
Keyphrases
- positive breast cancer
- estrogen receptor
- immune response
- induced apoptosis
- signaling pathway
- cell cycle arrest
- healthcare
- microbial community
- ms ms
- endoplasmic reticulum stress
- pi k akt
- optical coherence tomography
- oxidative stress
- dendritic cells
- epithelial mesenchymal transition
- toll like receptor
- mesenchymal stem cells
- cell death
- weight gain
- physical activity
- body mass index