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

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).

Automated summary

Recent research reveals that the CoREST complex plays a crucial role in regulating the acquisition of endocrine therapy resistance in estrogen receptor-positive breast cancers. Profiling data demonstrate that this resistance transition is associated with the functional retargeting of CoREST on chromatin, which occurs in coordination with cJUN and SWI/SNF (cBAF).