Chromatin architecture reprogramming reveals novel epigenetic dependencies in breast cancer [Cut&Run]

To address this, we tracked chromatin structure dynamics during the progression of endocrine resistance in ER+ breast cancer using Hi-C, chromatin accessibility, epigenomic, and transcriptomic profiling. We uncovered a critical role for H3K9 methylation and the demethylase KDM4C in driving proliferation of cells fated to become resistant through a non-genomic estrogen-mediated mechanism.

These findings highlight the mechanistic contribution of chromatin regulation in therapy resistance and offer a blueprint for studying similar processes in cancer, development, and cell fate decisions.