Weatherman, R. V., Fletterick, R. J. & Scanlan, T. S. Nuclear-receptor ligands and ligand-binding domains. Annu. Rev. Biochem. 68, 559–581 (1999).
Ring, A. & Dowsett, M. Mechanisms of tamoxifen resistance. Endocr. Relat. Cancer 11, 643–658 (2004).
Kuter, I. et al. Dose-dependent change in biomarkers during neoadjuvant endocrine therapy with fulvestrant: results from NEWEST, a randomized Phase II study. Breast Cancer Res. Treat. 133, 237–246 (2012).
van Kruchten, M. et al. Measuring residual estrogen receptor availability during fulvestrant therapy in patients with metastatic breast cancer. Cancer Discov. 5, 72–81 (2015).
Howell, A., DeFriend, D., Robertson, J., Blamey, R. & Walton, P. Response to a specific antioestrogen (ICI 182780) in tamoxifen-resistant breast cancer. Lancet 345, 29–30 (1995).
Robertson, J. F. & Harrison, M. Fulvestrant: pharmacokinetics and pharmacology. Br. J. Cancer 90(Suppl. 1), S7–S10 (2004).
De Savi, C. et al. Optimization of a novel binding motif to (E)-3-(3,5-difluoro-4-((1R,3R)-2-(2-fluoro-2-methylpropyl)-3-methyl-2,3,4,9-tetra hydro-1H-pyrido[3,4-b]indol-1-yl)phenyl)acrylic acid (AZD9496), a potent and orally bioavailable selective estrogen receptor downregulator and antagonist. J. Med. Chem. 58, 8128–8140 (2015).
Weir, H. M. et al. AZD9496: an oral estrogen receptor inhibitor that blocks the growth of ER-positive and ESR1-mutant breast tumors in preclinical models. Cancer Res. 76, 3307–3318 (2016).
Toy, W. et al. Activating ESR1 mutations differentially affect the efficacy of ER antagonists. Cancer Discov. 7, 277–287 (2017).
Hamilton, E. P. et al. A first-in-human study of the new oral selective estrogen receptor degrader AZD9496 for ER(+)/HER2(-) advanced breast cancer. Clin. Cancer Res. 24, 3510–3518 (2018).
Morrison, G. et al. Therapeutic potential of the dual EGFR/HER2 inhibitor AZD8931 in circumventing endocrine resistance. Breast Cancer Res. Treat. 144, 263–272 (2014).
Fu, X. et al. FOXA1 overexpression mediates endocrine resistance by altering the ER transcriptome and IL-8 expression in ER-positive breast cancer. Proc. Natl. Acad. Sci. USA 113, E6600–E6609 (2016).
Massarweh, S. et al. Tamoxifen resistance in breast tumors is driven by growth factor receptor signaling with repression of classic estrogen receptor genomic function. Cancer Res. 68, 826–833 (2008).
Wang, Y. C. et al. Different mechanisms for resistance to trastuzumab versus lapatinib in HER2-positive breast cancers--role of estrogen receptor and HER2 reactivation. Breast Cancer Res. 13, R121 (2011).
Fu, X. et al. Overcoming endocrine resistance due to reduced PTEN levels in estrogen receptor-positive breast cancer by co-targeting mammalian target of rapamycin, protein kinase B, or mitogen-activated protein kinase kinase. Breast Cancer Res. 16, 430 (2014).
Malorni, L. et al. Blockade of AP-1 potentiates endocrine therapy and overcomes resistance. Mol. Cancer Res. 14, 470–481 (2016).
Arpino, G. et al. Treatment of human epidermal growth factor receptor 2-overexpressing breast cancer xenografts with multiagent HER-targeted therapy. J. Natl. Cancer Inst. 99, 694–705 (2007).
Oesterreich, S. et al. Tamoxifen-bound estrogen receptor (ER) strongly interacts with the nuclear matrix protein HET/SAF-B, a novel inhibitor of ER-mediated transactivation. Mol. Endocrinol. 14, 369–381 (2000).
Ariazi, E. A. et al. Emerging principles for the development of resistance to antihormonal therapy: implications for the clinical utility of fulvestrant. J. Steroid Biochem. Mol. Biol. 102, 128–138 (2006).
Osborne, C. K., Coronado, E., Allred, D. C., Wiebe, V. & DeGregorio, M. Acquired tamoxifen resistance: correlation with reduced breast tumor levels of tamoxifen and isomerization of trans-4-hydroxytamoxifen. J. Natl. Cancer Inst. 83, 1477–1482 (1991).
Osborne, C. K. et al. Comparison of the effects of a pure steroidal antiestrogen with those of tamoxifen in a model of human breast cancer. J. Natl. Cancer Inst. 87, 746–750 (1995).
Creighton, C. J. et al. Proteomic and transcriptomic profiling reveals a link between the PI3K pathway and lower estrogen-receptor (ER) levels and activity in ER+ breast cancer. Breast Cancer Res. 12, R40 (2010).
Cuzick, J. A Wilcoxon-type test for trend. Stat. Med. 4, 87–90 (1985).
Kannan, N. et al. Trefoil factor 3 is oncogenic and mediates anti-estrogen resistance in human mammary carcinoma. Neoplasia 12, 1041–1053 (2010).
Lai, A. et al. Identification of GDC-0810 (ARN-810), an orally bioavailable selective estrogen receptor degrader (SERD) that demonstrates robust activity in tamoxifen-resistant breast cancer xenografts. J. Med. Chem. 58, 4888–4904 (2015).
Garner, F., Shomali, M., Paquin, D., Lyttle, C. R. & Hattersley, G. RAD1901: a novel, orally bioavailable selective estrogen receptor degrader that demonstrates antitumor activity in breast cancer xenograft models. Anticancer Drugs 26, 948–956 (2015).
Wardell, S. E. et al. Efficacy of SERD/SERM Hybrid-CDK4/6 inhibitor combinations in models of endocrine therapy-resistant breast cancer. Clin. Cancer Res. 21, 5121–5130 (2015).
Cristofanilli, M. et al. Fulvestrant plus palbociclib versus fulvestrant plus placebo for treatment of hormone-receptor-positive, HER2-negative metastatic breast cancer that progressed on previous endocrine therapy (PALOMA-3): final analysis of the multicentre, double-blind, phase 3 randomised controlled trial. Lancet Oncol. 17, 425–439 (2016).