Estrogen receptor (ER)? exhibits an antitumor activity in multiple cancer types in both tumor-intrinsicand -extrinsic manners. However, little is known as to how such activity can be harnessed with high efficacyand precision, nor is it clear which host cell type(s) mediates the tumor-extrinsic function of ER?. These majorknowledge gaps hamper efforts to unleash ER? antitumor activity for cancer therapies. We recently discovereda phosphotyrosine-dependent signaling axis that controls ER? antitumor activity.
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