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Chromatin and disease

Switching under selection: how CoREST controls endocrine therapy resistance in ER+ breast cancer

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New research shows that the CoREST complex controls the acquisition of endocrine therapy resistance in estrogen receptor-positive breast cancers. Profiling data show that this resistance transition is accompanied by a functional retargeting of CoREST on chromatin in coordination with cJUN and SWI/SNF (cBAF).

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Fig. 1: CoREST coordinates the conversion of therapy-sensitive to therapy-resistant states via a functional switch in binding partners in estrogen-deprived T47D cells.

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Acknowledgements

B.Y.C. and D.C.H. are supported by US National Institutes of Health grants 5T32GM133351 (B.Y.C), R01 CA228211 (D.C.H.), the Pew-Stewart Scholars for Cancer Research (D.C.H.) and the American Cancer Society Research Scholar Award (D.C.H.)

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Correspondence to Diana C. Hargreaves.

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Chick, B.Y., Hargreaves, D.C. Switching under selection: how CoREST controls endocrine therapy resistance in ER+ breast cancer. Nat Struct Mol Biol 29, 1040–1042 (2022). https://doi.org/10.1038/s41594-022-00858-9

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  • DOI: https://doi.org/10.1038/s41594-022-00858-9

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