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We reveal that estrogen causes obtainable chromatin and ER binding at a subset of enhancers, which form higher-order very enhancers that are essential for ER signaling. ER definitely correlates with active enhancers in primary tumors, and tumors had been effectively classified into molecular subtypes with chromatin availability characteristics and ER-dependent gene signature. ARID1A binds within ER-bound enhancers and regulates ER-dependent transcription. Knockdown of ARID1A or fulvestrant therap
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