Current and emerging estrogen receptor-targeted therapies for the treatment of breast cancer

被引:26
作者
Haines, Corinne N. [1 ]
Wardell, Suzanne E. [1 ]
McDonnell, Donald P. [1 ]
机构
[1] Duke Univ, Sch Med, Dept Pharmacol & Canc Biol, Durham, NC 27710 USA
来源
EXPLORING NUCLEAR RECEPTORS | 2021年 / 65卷 / 06期
关键词
DENDRITIC CELL-DIFFERENTIATION; GROWTH-FACTOR RECEPTOR; FIRST-LINE THERAPY; POSTMENOPAUSAL WOMEN; ENDOCRINE THERAPY; CONFORMATIONAL-CHANGES; STRUCTURAL BASIS; HORMONE-THERAPY; ER MODULATORS; TUMOR-GROWTH;
D O I
10.1042/EBC20200174
中图分类号
Q5 [生物化学];
学科分类号
071010 ; 081704 ;
摘要
Nearly 80% of all breast cancers are estrogen receptor positive (ER+) and require the activity of this transcription factor for tumor growth and survival. Thus, endocrine therapies, which target the estrogen signaling axis, have and will continue to be the cornerstone of therapy for patients diagnosed with ER+ disease. Several inhibitors of ER activity exist, including aromatase inhibitors (AIs), selective estrogen receptor modulators (SERMs), selective estrogen receptor degraders/down-regulators (SERDs), and ER proteolysis-targeting chimeras (ER PROTACs); drugs which differ in the mechanism(s) by which they inhibit this signaling pathway. Notwithstanding their significant impact on the management of this disease, resistance to existing endocrine therapies remains a major impediment to durable clinical responses. Although the mechanisms of resistance are complex and varied, dependence on ER is typically retained after progression on SERMs and AIs, suggesting that ER remains a bona fide therapeutic target. The discovery and development of orally bioavailable drugs that eliminate ER expression (SERDs and ER PROTACs) will likely aid in treating this growing patient population. All of the existing endocrine therapies were developed with the intent of inhibiting the cancer cell intrinsic actions of ER and/or with the objective of achieving extreme estrogen deprivation and most achieve that goal. A longstanding question that remains to be addressed, however, is how actions of existing interventions extrinsic to the cancer cells influence tumor biology. We believe that these issues need to be addressed in the development of strategies to develop the next generation of ER-modulators optimized for positive activities in both cancer cells and other cells within the tumor microenvironment (TME).
引用
收藏
页码:985 / 1001
页数:17
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