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A new class of agents for estrogen-receptor-positive breast cancer

Breast cancer is the most common cancer in women [1], and accounts for 15% of all new cancer diagnoses in the United States (www.seer.cancer.gov) [1]. In the United States alone, there will be an estimated 252,710 new cases of breast cancer and 40,610 deaths in 2017 (www.seer.cancer.gov). The majority of breast cancers (70–80%) express ERα [2,3]. While ERα is activated by estrogenic ligands and is important for normal female breast development, it is also the primary molecular driver of breast cancer [4,5]. Indeed, drugs targeting either the production of estrogen or those targeting the estrogen (ligand)-binding domain of ERα are the mainstay of therapies against ERα+ breast cancer [6,7]. Like other steroid receptors, ERα has a modular protein structure, with a transactivation domain at the amino terminus, a ligand-binding domain (LBD) that binds estrogens with a high-affinity at the carboxy terminus and a DNAbinding domain in between, which enables ERα binding to cognate estrogen response elements (EREs) in target genes [8–10]. In the canonical pathway, following estrogen binding, ERα undergoes a conformational change, dimerizes, and interacts with several coregulatory proteins [11,12]. The coregulatory proteins interact with and modulate the activity of ERα and thus function either as coactivators or corepressors [11,12].