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Mutations in _ESR1_, which encodes estrogen receptor-α (ERα), drive resistance to approved endocrine therapies in breast cancer. We studied the molecular response to the investigational ERα

antagonist and degrader, giredestrant, in preclinical models and biopsy samples. We found that long-term inhibition or dysfunction of ERα result in cell plasticity with implications for

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support REFERENCES * Martín, M. et al. Giredestrant for estrogen receptor-positive, HER2-negative, previously treated advanced breast cancer: results from the randomized, phase II acelERA

breast cancer study. _J. Clin. Oncol._ 42, 2149–2160 (2024). THIS PAPER REPORTS A TREND TOWARD FAVORABLE BENEFIT AND GOOD TOLERANCE OF GIREDESTRANT IN PATIENTS WITH _ESR1_-MUTATED TUMORS.

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PUBLISHER’S NOTE Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. THIS IS A SUMMARY OF: Liang, J. et al. ERα dysfunction

caused by _ESR1_ mutations and therapeutic pressure promotes lineage plasticity in ER+ breast cancer. _Nat. Cancer_ https://doi.org/10.1038/s43018-024-00898-8 (2025). RIGHTS AND PERMISSIONS

Reprints and permissions ABOUT THIS ARTICLE CITE THIS ARTICLE Inhibition of ERα signaling induces lineage plasticity in vivo. _Nat Cancer_ 6, 237–238 (2025).

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