ArticleBreast (Edinburgh, Scotland)2019
Endocrine therapy resistance: new insights.
Article in Breast (Edinburgh, Scotland), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07387861 (Immunohistochemical Evaluation of p-AKT and p-S6 as Surrogate Markers of PI3K/AKT/mTOR Pathway Activation in ER-Positive, HER2-Negative Breast Carcinoma), which is not on this map. Cited by 72 papers, 2 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.
Immunohistochemical Evaluation of p-AKT and p-S6 as Surrogate Markers of PI3K/AKT/mTOR Pathway Activation in ER-Positive, HER2-Negative Breast Carcinoma
Who cites it
72 citing papers in PubMed, 2 syntheses or guidelines pooled it, 118 citations in OpenAlex.
- The Role of Estrogen Receptor-Targeted PET with 16α-Journal of nuclear medicine : official publication, Society of Nuclear Medicine · 2026Pooled it
- BCAR4 Expression as a Predictive Biomarker for Endocrine Therapy Resistance in Breast Cancer.Clinical breast cancer · 2024Pooled it
- Elacestrant in ER+, HER2- Metastatic Breast Cancer with ESR1-Mutated Tumors: Subgroup Analyses from the Phase III EMERALD Trial by Prior Duration of Endocrine Therapy plus CDK4/6 Inhibitor and in Clinical Subgroups.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024Trial
- Entinostat, a class I selective histone deacetylase inhibitor, plus exemestane for Chinese patients with hormone receptor-positive advanced breast cancer: A multicenter, randomized, double-blind, placebo-controlled, phase 3 trial.Acta pharmaceutica Sinica. B · 2023Trial
- Real-world estrogen receptor alpha 1 (ESR1) testing patterns and results for ER+/HER2- metastatic breast cancer in the United States, 2018-2024.Breast cancer research and treatment · 2026Observational
- Regulation of PSAT1 and PHGDH by m6A in endocrine-resistant breast cancer cells.Biochimica et biophysica acta. Molecular basis of disease · 2026Article
- CDKN1B inactivation impacts ER signaling and drives resistance to endocrine therapy in breast cancer.British journal of cancer · 2026Article
- Progesterone receptors drive advanced breast cancer phenotypes including circulating tumor- and stem-like cell expansion in the context of ESR1 mutation.NPJ breast cancer · 2026Article
- Shu Gan Jie Yu herbal combination enhances tamoxifen sensitivity in breast cancer cells via modulation of the SNCG/Frontiers in pharmacology · 2026Article
- Robust dPCR Hyper-Plexing Approach by Color Combination for Detection of 17 ESR1 Mutations in Breast Cancer Patient Samples.Methods in molecular biology (Clifton, N.J.) · 2026Article
- Recent Advances (2020-2025) in Estrogen and ER-Positive Breast Cancer: Receptor Signaling, Tumor Microenvironment, Endocrine Therapy Resistance and Innovative Treatment Strategies-A Comprehensive Review.Cancer management and research · 2026Review
- Aberrant cytoplasmic localization of MLH1 characterizes a cell population that seeds breast cancer recurrence.Nature communications · 2025Article
- Progesterone receptors drive advanced breast cancer phenotypes including circulating tumor- and stem-like cell expansion in the context ofbioRxiv : the preprint server for biology · 2025Article
- IKZF3 promotes gastric cancer progression via Hedgehog signaling activation and is targetable by SANT-1.Acta biochimica et biophysica Sinica · 2025Article
- Emerging Mechanisms of Therapy Resistance in Metastatic ER+ Breast Cancer.Endocrinology · 2025Review
- Detection rate for ESR1 mutations is higher in circulating-tumor-cell-derived genomic DNA than in paired plasma cell-free DNA samples as revealed by ddPCR.Molecular oncology · 2025Article
- Gene expression associated with endocrine therapy resistance in estrogen receptor-positive breast cancer.Scientific reports · 2025Article
- Article
- Genomic hallmarks of endocrine therapy resistance in ER/PR+HER2- breast tumours.Communications biology · 2025Article
- Clinical characteristics of male patients with breast cancer in the Latino population.Breast cancer research and treatment · 2025Article
12 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 2 institutions in 1 country.
Funding
Abstract
The estrogen receptor positive (ER+) subset is the dominant contributor to global deaths from breast cancer which now exceeds 500,000 deaths annually. Lethality is driven by endocrine resistance, which has been shown to be associated with high mutational rates and extreme subclonal diversity. Treatment forces subclonal selection until the patient eventually succumbs to metastatic treatment-resistant disease. Recently, we have been addressing several questions related to this process: What is the cause of the increased mutation rate in lethal ER+ breast cancer? Why is endocrine therapy resistance related to mutational load? What are the functions of the somatic mutations that are eventually selected in the treatment resistant and metastatic clones? These questions have provoked new mechanistic hypotheses that link resistance to endocrine agents to: (1) Specific defects in single strand break repair are associated with increased mortality from ER+ breast cancer [1,2]; (2) Loss/mutations of certain single strand break repair proteins that disrupt estrogen-regulated cell cycle control through the ATM, CHK2, CDK4 axis [1,2] thereby directly coupling endocrine therapy resistance to specific DNA repair defects; (3) Acquired mutations that drive metastasis include the generation of in-frame ESR1 gene fusions that activate epithelial-to-mesenchymal transition (EMT) driven metastasis as well as endocrine drug-resistant proliferation [3].
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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.