ReviewOncoTargets and therapy2014
ER-α36: a novel biomarker and potential therapeutic target in breast cancer.
Review in OncoTargets and therapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
33 citing papers in PubMed, 36 citations in OpenAlex.
- The Bidirectional Role of Cellular Senescence in the Treatment of Ovarian Cancer.Biomedicines · 2026Review
- Cannabidiol enhances tamoxifen efficacy via CREB-mediated suppression of ERα signaling in ER-positive breast cancer cells.Cell & bioscience · 2026Article
- Progress of estrogen receptor and splice variants in ovarian carcinoma.Journal of ovarian research · 2026Review
- Study of Estrogen Receptor Alpha Gene Polymorphisms (International journal of molecular sciences · 2026Article
- More than alternative estrogen receptors: the emerging role of GPER-1 and ERα36 in breast cancer.Exploration of targeted anti-tumor therapy · 2026Review
- ER‑α36 knockdown is associated with lysosomal dysfunction and proliferation inhibition in liver cancer cells.Molecular medicine reports · 2025Article
- ERα36 PromotesInternational journal of molecular sciences · 2025Article
- Ovarian Cancer-Epidemiology, Classification, Pathogenesis, Treatment, and Estrogen Receptors' Molecular Backgrounds.International journal of molecular sciences · 2025Review
- Review
- Characteristic Binding Landscape of Estrogen Receptor-α36 Protein Enhances Promising Cancer Drug Design.Biomolecules · 2023Article
- Vitamin D, Th17 Lymphocytes, and Breast Cancer.Cancers · 2022Review
- Estrogen Receptors-Mediated Apoptosis in Hormone-Dependent Cancers.International journal of molecular sciences · 2022Review
- The essential role of YAP in ERα36-mediated proliferation and the epithelial-mesenchymal transition in MCF-7 breast cancer cells.Frontiers in pharmacology · 2022Article
- Identification of Hub Genes Associated With the Development of Stomach Adenocarcinoma by Integrated Bioinformatics Analysis.Frontiers in oncology · 2022Article
- Steroid Hormone Receptors: Links With Cell Cycle Machinery and Breast Cancer Progression.Frontiers in oncology · 2021Review
- Article
- Broussoflavonol B fromMolecules (Basel, Switzerland) · 2020Article
- A Role for Estrogen Receptor alpha36 in Cancer Progression.Frontiers in endocrinology · 2020Review
- Fatostatin in Combination with Tamoxifen Induces Synergistic Inhibition in ER-Positive Breast Cancer.Drug design, development and therapy · 2020Article
- ERα, A Key Target for Cancer Therapy: A Review.OncoTargets and therapy · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Estrogen receptor-alpha36 (ER-α36) is a 36-kDa variant of estrogen receptor-alpha (ER-α) firstly identified and cloned by Wang et al in 2005. It lacks both transactivation domains (activation function 1 and activation function 2) and has different biological characteristics compared to traditional ER-α (ER-α66). ER-α36 primarily locates on plasma membrane and cytoplasm and functions as a mediator in the rapid membrane-initiated non-genomic signaling pathway. Additionally, it inhibits the traditional genomic signaling pathway mediated by ER-α66 in a dominant-negative pattern. Accumulating evidence has demonstrated that ER-α36 regulates the physiological function of various tissues. Thus, dysregulation of ER-α36 is closely associated with plenty of diseases including cancers. ER-α36 is recognized as a molecular abnormality which solidly correlates to carcinogenesis, aggressiveness, and therapeutic response of breast cancer. Additionally, special attention has been paid to the role of ER-α36 in endocrine therapy resistance. Therefore, ER-α36 provides a novel biomarker of great value for diagnosis, prognosis, and treatment of breast cancer. It may also be a potential therapeutic target for breast cancer patients, especially for those who are resistant to endocrine therapy. In this review, we will overview and update the biological characteristics, underlying mechanism, and function of ER-α36, focusing on its biological function in breast cancer and endocrine therapy resistance. We will evaluate its application value in clinical practice.
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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.