Mechanisms of tamoxifen resistance
Open accessAbstract
The anti-oestrogen tamoxifen is the most commonly used treatment for patients with oestrogen-receptor (ER)-positive breast cancer. Although many patients benefit from tamoxifen in the adjuvant and metastatic settings, resistance is an important clinical problem. The target of tamoxifen in vivo is the ER. Over the last decade many advances have been made in our understanding of the biology of the ER which may help to explain how resistance to tamoxifen develops. Such mechanisms may include changes in the expression of ERα or ERβ, alterations in co-regulatory proteins, and the influences of cellular kinase signal transduction pathways. The experimental and clinical evidence supporting these mechanisms of tamoxifen resistance are discussed in this review.
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- Authors
- Ring, A., & Dowsett, M.
- Affiliations
- Royal Marsden Hospital (GB)
- Institute of Cancer Research (GB)
- Venue
- Endocrine-Related Cancer
- Publisher
- Bioscientifica
- Published
- 2004-12-01
- Volume
- 11
- Issue
- 4
- Pages
- 643-658
- ISSN
- 1351-0088 (ISSN-L)
- 1479-6821
- OpenAlex
- W2128605357
- Cited by
- 651
- References
- 119
- Citations by year
- 2026: 10 · 2025: 14 · 2024: 16 · 2023: 33 · 2022: 25 · 2021: 40 · 2020: 41 · 2019: 22 · 2018: 37 · 2017: 33 · 2016: 48 · 2015: 37 · 2014: 45 · 2013: 42 · 2012: 39
- FWCI
- 2.24
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Endocrine Related Cancer (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Breast Cancer Treatment Studies
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Advanced Breast Cancer Therapies
- Keywords
- tamoxifen resistance, oestrogen receptor, estrogen receptor-positive breast cancer, estrogen receptor alpha, estrogen receptor beta, antiestrogen therapy
- MeSH terms
- Breast Neoplasms, Estrogen Antagonists, Female, Humans, Receptors, Estrogen, Tamoxifen, Transcription, Genetic, Signal Transduction, Antineoplastic Agents, Hormonal, Drug Resistance, Neoplasm
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