Activating ESR1 mutations in hormone-resistant metastatic breast cancer
Open accessAbstract
Breast cancer is the most prevalent cancer in women, and over two-thirds of cases express estrogen receptor-α (ER-α, encoded by ESR1). Through a prospective clinical sequencing program for advanced cancers, we enrolled 11 patients with ER-positive metastatic breast cancer. Whole-exome and transcriptome analysis showed that six cases harbored mutations of ESR1 affecting its ligand-binding domain (LBD), all of whom had been treated with anti-estrogens and estrogen deprivation therapies. A survey of The Cancer Genome Atlas (TCGA) identified four endometrial cancers with similar mutations of ESR1. The five new LBD-localized ESR1 mutations identified here (encoding p.Leu536Gln, p.Tyr537Ser, p.Tyr537Cys, p.Tyr537Asn and p.Asp538Gly) were shown to result in constitutive activity and continued responsiveness to anti-estrogen therapies in vitro. Taken together, these studies suggest that activating mutations in ESR1 are a key mechanism in acquired endocrine resistance in breast cancer therapy.
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Gain-of-function ERα LBD mutations are frequently found in metastatic endocrine-resistant breast cancers and recruit elevated SRC coactivators to EREs.
“The gain-of-function ERα LBD mutations are frequently found in metastatic endocrine-resistant breast cancers (Jeselsohn et al., 2014; Robinson et al., 2013; Spoerke et al., 2016; Toy et al., 2013; Zhang et al., 1997) and recruit elevated levels of the SRC coactivators to EREs (Gates et al., 2018).”
From Structural Insights of Transcriptionally Active, Full-Length Androgen Receptor Coactivator Complexes (2020) · cites this paper as Robinson et al., 2013
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“…the eR, rather than inhibition, is beneficial for treating cancers as it effectively counter-acts resistance mechanisms and alleviates the paradoxical “estrogen-agonistic” side effects observed with long-term use of traditional hormonal agents like tamoxifen (Robinson et al. 2013; toy et al. 2013).”
- Authors
- Robinson, D. R., Wu, Y.-M., Vats, P., Su, F., Lonigro, R. J., Cao, X., Kalyana-Sundaram, S., Wang, R., Ning, Y., Hodges, L., Gursky, A., Siddiqui, J., Tomlins, S. A., Roychowdhury, S., Pienta, K. J., Kim, S. Y., Roberts, J. S., Rae, J. M., Van Poznak, C. H., Hayes, D. F., Chugh, R., Kunju, L. P., Talpaz, M., Schott, A. F., & Chinnaiyan, A. M.
- Affiliations
- University of Michigan (US)
- Howard Hughes Medical Institute (US)
- The Ohio State University (US)
- Johns Hopkins University (US)
- Corresponding author
- Chinnaiyan, Arul M
- ORCID
- Venue
- Nature Genetics
- Published
- 2013-11-03
- Volume
- 45
- Issue
- 12
- Pages
- 1446-1451
- ISSN
- 1061-4036 (ISSN-L)
- 1546-1718
- PMC
- PMC4009946
- OpenAlex
- W2073367400
- Cited by
- 1,145
- References
- 43
- Citations by year
- 2026: 41 · 2025: 75 · 2024: 62 · 2023: 84 · 2022: 79 · 2021: 93 · 2020: 108 · 2019: 105 · 2018: 101 · 2017: 114 · 2016: 125 · 2015: 93 · 2014: 55 · 2013: 6
- FWCI
- 61.31
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Genetics (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Howard Hughes Medical Institute
- National Human Genome Research Institute (UM1HG006508)
- National Cancer Institute (U01CA111275)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Advanced Breast Cancer Therapies
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Breast Cancer Treatment Studies
- Keywords
- ESR1 mutations, estrogen receptor alpha, ligand-binding domain, metastatic breast cancer, hormone resistance, endocrine therapy resistance, antiestrogen therapy, constitutively active receptor, endometrial cancer, clinical sequencing
- MeSH terms
- Adult, Aged, Breast Neoplasms, DNA Mutational Analysis, Female, Humans, Middle Aged, Mutation, Neoplasm Metastasis, Antineoplastic Agents, Hormonal, Drug Resistance, Neoplasm, Estrogen Receptor alpha, Protein Interaction Domains and Motifs
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