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.
Cell Stress (CES) emerges as a peer-reviewed publishing platform for high-impact research. CES publishes articles of extraordinary novelty and significance, including research papers and reviews that cover heterogenous topics in the field of cellular pathophysiology.
CES is an open access online journal that thus allows its readership and general public around the world to read, download, store, distribute or print any article free of charge. Long-term archiving and accessibility of all published articles is secured through partnership with different repositories, including PubMed Central.
At the same time, our open access policy ensures fast publication as well as high visibility and broad divulgence of the author’s published research. The financing of this policy is sustained by charging a publication fee/article processing charges (APCs). By pursuing an open access approach and the universal accessibility to scientific knowledge, we support the return to one of the essential values of science: the free exchange of ideas.
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