Estrogen Receptor-Positive (ER+) Breast Cancers

Dear Colleagues,

The majority of breast cancers express estrogen and/or progesterone receptors (ER and PR). ER is the primary transcription factor driving oncogenesis in hormone receptor-positive (HR+) breast cancer; it is both the predictor and the target of response to antiestrogen therapy. In tumors without concomitant HER2 amplification, endocrine therapy, aimed at the therapeutic blockade of ER signaling, forms the backbone of treatment for all disease stages; adjuvant endocrine therapy alone reduces the relative risk of recurrence by nearly 40%. Endocrine therapies include aromatase inhibitors (AIs), gonadotropin-releasing hormone (GnRH) agonists, selective ER modulators (SERMs), and selective ER downregulators (SERDs). Despite its wide therapeutic efficacy, endocrine therapy eventually fails in the majority of patients with metastatic and in a proportion of patients with ER+, HER2- early breast cancer who develop endocrine resistance, resulting in disease recurrence. A number of resistance mechanisms can lead to estrogen-independent growth of HR+ breast cancer as a result of genetic and epigenetic alterations, which could be exploited as novel therapeutic targets. This Special Issue focuses on the biology of ER and the implications of ESR1 mutations in HR+ breast cancer, the role of neoadjuvant therapy, the use of multigene assays to select treatment for early disease, the optimal management of premenopausal patients with ER+ breast cancer, the role of extended adjuvant endocrine therapy, the molecular mechanisms mediating endocrine resistance emphasizing the prominent role of the PI3K/Akt/mTOR and CDK4/6/retinoblastoma protein pathways in cancer cell growth and survival, the molecularly targeted agents to overcome or delay endocrine resistance, and potential predictive biomarkers for accurate patient stratification.

Prof. Dr. Christos Papadimitriou
Prof. Dr. Dimitrios Mavroudis
Prof. Dr. Nicholas Pavlidis
Guest Editors

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