Therapeutic resistance to anti-oestrogen therapy in breast cancer

被引:91
作者
Will, Marie [1 ,2 ]
Liang, Jackson [3 ]
Metcalfe, Ciara [4 ]
Chandarlapaty, Sarat [1 ,2 ]
机构
[1] Mem Sloan Kettering Canc Ctr, Human Oncol & Pathogenesis Program, New York, NY 10065 USA
[2] Mem Sloan Kettering Canc Ctr, Dept Med, New York, NY 10065 USA
[3] Genentech Inc, Dept Oncol Biomarker Dev, South San Francisco, CA USA
[4] Genentech Inc, Dept Discovery Oncol, South San Francisco, CA 94080 USA
基金
美国国家卫生研究院;
关键词
ESTROGEN-RECEPTOR-ALPHA; CELL-CYCLE PROGRESSION; ACQUIRED ENDOCRINE RESISTANCE; ACTIVATING ESR1 MUTATIONS; GROWTH-FACTOR; AROMATASE INHIBITORS; POSTMENOPAUSAL WOMEN; CDK4/6; INHIBITORS; ELACESTRANT RAD1901; ANTITUMOR-ACTIVITY;
D O I
10.1038/s41568-023-00604-3
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Although selective antagonism of oestrogen receptor signalling in breast cancer has been one of the most successful therapeutic approaches in oncology, resistance is a major clinical challenge. In this Review, Will et al. explore mechanisms of oestrogen-receptor-& alpha;-targeted therapeutic resistance and strategies to overcome it. The hormone receptor oestrogen receptor-& alpha; (ER) orchestrates physiological mammary gland development, breast carcinogenesis and the progression of breast tumours into lethal, treatment-refractory systemic disease. Selective antagonism of ER signalling has been one of the most successful therapeutic approaches in oncology, benefiting patients as both a cancer preventative measure and a cancer treatment strategy. However, resistance to anti-oestrogen therapy is a major clinical challenge. Over the past decade, we have gained an understanding of how breast cancers evolve under the pressure of anti-oestrogen therapy. This is best depicted by the case of oestrogen-independent mutations in the gene encoding ER (ESR1), which are virtually absent in primary breast cancer but highly prevalent (20-40%) in anti-oestrogen-treated metastatic disease. These and other findings highlight the 'evolvability' of ER+ breast cancer and the need to understand molecular processes by which this evolution occurs. Recent development and approval of next-generation ER antagonists to target ESR1-mutant breast cancer underscores the clinical importance of this evolvability and sets a new paradigm for the treatment of ER+ breast cancers.
引用
收藏
页码:673 / 685
页数:13
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