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Prior work showed that 17\u03b2-estradiol (E2), the predominant premenopausal hormone, promotes BM of tumors intrinsically unresponsive to E2, in part through modulating estrogen receptor-alpha expressing (ER\u03b1\u207a) glial cells. However, how E2 reshapes the brain tumor microenvironment (TME), particularly microglia\u2011mediated immunity, and its impact on BM progression remains unclear.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Single-cell RNA (scRNA) sequencing and multiparametric flow cytometry were used to define the impact of E2 and E2-suppression on brain immune-cell populations across different stages of BM progression using spontaneous and experimental models of BM. Depletion of microglia and T-cell co-cultures were used to study microglia\u2019s role in E2-induced BM. The effects of E2-suppression alone or in combination with whole-brain radiotherapy were tested in preclinical models mimicking late-stage BM.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>E2 repressed immune surveillance and immune activation programs in microglia from early to late stages of brain metastatic progression, suppressing recruitment of effector immune cells to BM. Estrogen suppression, in turn, reactivated anti-tumoral signaling in microglia and increased recruitment of effector immune cells to the brain. Microglia from E2-treated BM-bearing mice showed a reduced capacity to promote T-cell expansion, effector potential, and CD8\u207aT cell-mediated tumor cell killing. Conversely, E2-suppression reactivated an effective anti-tumoral response and synergized with RT to significantly decrease BM progression.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>These findings reveal a previously unrecognized mechanism by which E2 accelerates BCBM progression through microglial immunosuppression and support evaluation of endocrine therapies as adjunct treatments for ER\u207b breast cancer brain metastases.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1093\/neuonc\/noag173","type":"journal-article","created":{"date-parts":[[2026,7,28]],"date-time":"2026-07-28T11:15:09Z","timestamp":1785237309000},"source":"Crossref","is-referenced-by-count":0,"title":["Estradiol reprograms microglia to create an immune\u2011suppressed niche permissive to breast cancer brain 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