Hormone receptor-positive breast cancer (HR+ BC) accounts for approximately 75% of new BC diagnoses. Despite the undisputable progresses obtained in the treatment of HR+ BC in recent years, primary or acquired resistance to endocrine therapies still represents a clinically relevant issue, and is largely responsible for disease recurrence after curative surgery, as well as for disease progression in the metastatic setting. Among the mechanisms causing primary or acquired resistance to endocrine therapies is the loss of estrogen/progesterone receptor expression, which could make BC cells independent of estrogen stimulation and, consequently, resistant to estrogen deprivation or the pharmacological inhibition of estrogen receptors. This review aims at discussing the molecular mechanisms and the clinical implications of HR loss as a result of the therapies used in the neoadjuvant setting or for the treatment of advanced disease in HR+ BC patients.

Hormone Receptor Loss in Breast Cancer: Molecular Mechanisms, Clinical Settings, and Therapeutic Implications / E. Zattarin, R. Leporati, F. Ligorio, R. Lobefaro, A. Vingiani, G. Pruneri, C. Vernieri. - In: CELLS. - ISSN 2073-4409. - 9:12(2020), pp. 2644.1-2644.23. [10.3390/cells9122644]

Hormone Receptor Loss in Breast Cancer: Molecular Mechanisms, Clinical Settings, and Therapeutic Implications

E. Zattarin
Co-primo
;
R. Leporati
Co-primo
;
F. Ligorio;R. Lobefaro;A. Vingiani;G. Pruneri
Penultimo
;
C. Vernieri
2020

Abstract

Hormone receptor-positive breast cancer (HR+ BC) accounts for approximately 75% of new BC diagnoses. Despite the undisputable progresses obtained in the treatment of HR+ BC in recent years, primary or acquired resistance to endocrine therapies still represents a clinically relevant issue, and is largely responsible for disease recurrence after curative surgery, as well as for disease progression in the metastatic setting. Among the mechanisms causing primary or acquired resistance to endocrine therapies is the loss of estrogen/progesterone receptor expression, which could make BC cells independent of estrogen stimulation and, consequently, resistant to estrogen deprivation or the pharmacological inhibition of estrogen receptors. This review aims at discussing the molecular mechanisms and the clinical implications of HR loss as a result of the therapies used in the neoadjuvant setting or for the treatment of advanced disease in HR+ BC patients.
breast cancer; hormone receptors; conversion; intratumor heterogeneity; clonal selection; endocrine therapies; (neo)adjuvant therapy; tumor recurrences; re-characterization
Settore MED/06 - Oncologia Medica
Settore MED/08 - Anatomia Patologica
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2434/939428
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