A drug used in hormone replacement therapy can target estrogen receptors that have become resistant to breast cancer treatments.

A novel first-in-class small molecule (ERX-11) that interacts with and disrupts the interactome of the estrogen receptor (ER), blocks the growth of ER-positive breast cancers, including those that are resistant to currently approved hormonal agents.

Two common mutant versions of estrogen receptor alpha achieve constitutive activity and hormone-resistance by preferentially adopting a suite of conformations that expose the coregulator-binding surface.

Activation of the Estrogen Receptor by estra-2-diol results in sustained binding and the previously described cyclical response kinetics are likely an artefact of observing a highly variable process without replicates.

Anti-inflammatory effects of resveratrol are mediated by the estrogen receptor to coordinate a complex array of transcriptional coregulators, suggesting that estrogenic effects must be considered in the complex polypharmacology of resveratrol.

Cyclic estrogen signaling in oviduct epithelial cells suppresses oviduct luminal protease activity to allow survival and development of preimplantation embryos

GDC-0810 is a novel, orally bioavailable SERD that exhibits robust pre-clinical activity in models of ER+ breast cancer, including models of tamoxifen resistance, and those that express the ERα mutations, ER.Y537S and ER.D538G.

Driving melanoma differentiation through G protein-coupled estrogen receptor signaling decreases proliferative capacity, decreases expression of the oncodriver and stem cell marker c-Myc, and increases the effectiveness of immunotherapy.

Loss of RUNX1, a key regulator of estrogen receptor-positive luminal breast cells, impairs mammary epithelial differentiation and contributes to luminal breast cancer via genetic interactions with a loss of p53 or RB1.