Kinisha Gala

TL;DR: A comprehensive genetic analysis of two independent cohorts of metastatic ER-positive breast tumors and identified mutations in ESR1 affecting the ligand-binding domain (LBD) in 14 of 80 cases that implicate LBD-mutant forms of ER in mediating clinical resistance to hormonal therapy and suggest that more potent ER antagonists may be of substantial therapeutic benefit.

TL;DR: The basis for HER3 activation in cancer, the different pharmacologic strategies being used, and opportunities for further development are highlighted.

TL;DR: KMT2C is a key regulator of ERα activity whose loss uncouples breast cancer proliferation from hormone abundance, and from a therapeutic standpoint, KMT-depleted cells that develop hormone-independence retain their dependence on ERα, displaying ongoing sensitivity to ERα antagonists.

TL;DR: In this article , the authors evaluated PFS and additional surrogate endpoints for their correlation with OS in localized and advanced TNBC and found that PFS is significantly correlated with OS across diverse therapies.