ReviewNature reviews. Clinical oncology2015
ESR1 mutations—a mechanism for acquired endocrine resistance in breast cancer.
Review in Nature reviews. Clinical oncology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07753954 (Imaging to Re-evaluate Elacestrant Clinical Application), which is not on this map. Cited by 398 papers, 5 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Imaging to Re-evaluate Elacestrant Clinical Application
Who cites it
398 citing papers in PubMed, 5 syntheses or guidelines pooled it, 659 citations in OpenAlex.
- Dynamic circulating tumor DNA profiling of ESR1 mutations in HR+/HER2- advanced breast cancer: from prognostic biomarker to clinical decision-making - a comprehensive review.Frontiers in oncology · 2026Pooled it
- A systematic review of progress toward unlocking the power of epigenetics in breast cancer: latest updates and perspectives.Frontiers in pharmacology · 2025Pooled it
- Diagnostic accuracy of ESR1 mutation detection by cell-free DNA in breast cancer: a systematic review and meta-analysis of diagnostic test accuracy.BMC cancer · 2024Pooled it
- Efficacy of CDK4/6 inhibitors combined with endocrine therapy in HR+/HER2- breast cancer: an umbrella review.Journal of cancer research and clinical oncology · 2024Pooled it
- The adverse events of CDK4/6 inhibitors for HR+/ HER2- breast cancer: an umbrella review of meta-analyses of randomized controlled trials.Frontiers in pharmacology · 2024Pooled it
- ctDNA and tumor-based biomarkers of giredestrant response in acelERA breast cancer.Nature communications · 2026Trial
- Trial
- Imlunestrant, an oral selective estrogen receptor degrader, in combination with HER2 directed therapy, with or without abemaciclib, in ER-positive, HER2-positive advanced breast cancer: results from the phase 1a/1b EMBER study.Breast cancer research : BCR · 2025Trial
- Assessing endocrine resistance: monitoring circulating ESR1 mutations in Irosustat-treated ER positive breast cancer.Breast cancer research and treatment · 2025Trial
- Continuous versus Standard Palbociclib Treatment and Molecular Profiling of Solid Tissues and Liquid Biopsies in the CCTG MA.38 Trial in Advanced Breast Cancer.Cancer research communications · 2025Trial
- Giredestrant for Estrogen Receptor-Positive, HER2-Negative, Previously Treated Advanced Breast Cancer: Results From the Randomized, Phase II acelERA Breast Cancer Study.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2024Trial
- Trial
- Landscape of Baseline and Acquired Genomic Alterations in Circulating Tumor DNA with Abemaciclib Alone or with Endocrine Therapy in Advanced Breast Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024Trial
- Efficacy and exploratory biomarker analysis of entinostat plus exemestane in advanced or recurrent breast cancer: phase II randomized controlled trial.Japanese journal of clinical oncology · 2023Trial
- AMEERA-1 phase 1/2 study of amcenestrant, SAR439859, in postmenopausal women with ER-positive/HER2-negative advanced breast cancer.Nature communications · 2022Trial
- Identification of benzoxazine scaffold derivatives as novel CDK4 inhibitors for the treatment of cancer.Journal of enzyme inhibition and medicinal chemistry · 2026Article
- Effects of short-course preoperative endocrine therapy on tumour morphology and immunohistochemical profile in oestrogen receptor-positive, HER2-negative breast cancer.Histopathology · 2026Article
- Toward targeted therapeutics for lobular breast cancer.The Journal of clinical investigation · 2026Review
- Nuclear SOX9 Expression and Short-Term Survival Outcomes in Early-Stage Luminal Breast Cancer: An Immunohistochemical and Retrospective Cohort Analysis.International journal of molecular sciences · 2026Article
- Standardized Analytical Verification of ctDNA ESR1 Mutation Testing in Metastatic HR+/HER2- Breast Cancer: A European Multicentre Study Using dPCR and NGS-Based Liquid Biopsy.Molecular diagnosis & therapy · 2026Article
338 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Approximately 70% of breast cancers are oestrogen receptor α (ER) positive, and are, therefore, treated with endocrine therapies. However, about 25% of patients with primary disease and almost all patients with metastases will present with or eventually develop endocrine resistance. Despite the magnitude of this clinical challenge, the mechanisms underlying the development of resistance remain largely unknown. In the past 2 years, several studies unveiled gain-of-function mutations in ESR1, the gene encoding the ER, in approximately 20% of patients with metastatic ER-positive disease who received endocrine therapies, such as tamoxifen and aromatase inhibitors. These mutations are clustered in a 'hotspot' within the ligand-binding domain (LBD) of the ER and lead to ligand-independent ER activity that promotes tumour growth, partial resistance to endocrine therapy, and potentially enhanced metastatic capacity; thus, ER LBD mutations might account for a mechanism of acquired endocrine resistance in a substantial fraction of patients with metastatic disease. In general, the absence of detectable ESR1 mutations in patients with treatment-naive disease, and the correlation between the frequency of patients with tumours harbouring these mutations and the number of endocrine treatments received suggest that, under selective treatment pressure, clonal expansion of rare mutant clones occurs, leading to resistance. Preclinical and clinical development of rationale-based novel therapeutic strategies that inhibit these ER mutants has the potential to substantially improve treatment outcomes. We discuss the contribution of ESR1 mutations to the development of acquired resistance to endocrine therapy, and evaluate how mutated ER can be detected and targeted to overcome resistance and improve patient outcomes.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.