ReviewOncotarget2017
Potential therapeutic targets of triple-negative breast cancer based on its intrinsic subtype.
Review in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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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.
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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.
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Who cites it
39 citing papers in PubMed.
- RAD51B-EZH2 axis as a potential therapeutic target for TNBC through cell fate conversion.Cell death & disease · 2025Article
- Targeting GD2 with naxitamab overcomes GD3 synthase-driven immune suppression in triple-negative breast cancer.NPJ breast cancer · 2025Article
- Defining the regulatory logic of breast cancer using single-cell epigenetic and transcriptome profiling.Cell genomics · 2025Article
- CRISPR Screening of Transcribed Super-Enhancers Identifies Drivers of Triple-Negative Breast Cancer Progression.Cancer research · 2024Article
- Defining the Regulatory Logic of Breast Cancer Using Single-Cell Epigenetic and Transcriptome Profiling.bioRxiv : the preprint server for biology · 2024Article
- Influence of copper(I) nicotinate complex on the Notch1 signaling pathway in triple negative breast cancer cell lines.Scientific reports · 2024Article
- Receptor tyrosine kinases in breast cancer treatment: unraveling the potential.American journal of cancer research · 2024Review
- A molecular approach to triple-negative breast cancer: targeting the Notch signaling pathway.Einstein (Sao Paulo, Brazil) · 2024Review
- Emergence of Nanotechnology as a Powerful Cavalry against Triple-Negative Breast Cancer (TNBC).Pharmaceuticals (Basel, Switzerland) · 2022Review
- Molecular targets and therapeutics in chemoresistance of triple-negative breast cancer.Medical oncology (Northwood, London, England) · 2021Review
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- Delivery of miR-424-5p via Extracellular Vesicles Promotes the Apoptosis of MDA-MB-231 TNBC Cells in the Tumor Microenvironment.International journal of molecular sciences · 2021Article
- CRISPR/Cas9 based genome editing for targeted transcriptional control in triple-negative breast cancer.Computational and structural biotechnology journal · 2021Review
- Down-Regulation of Toll-Like Receptor 5 (TLR5) Increased VEGFR Expression in Triple Negative Breast Cancer (TNBC) Based on Radionuclide Imaging.Frontiers in oncology · 2021Article
- [EGFR tyrosine kinase inhibitor HS-10296 induces autophagy and apoptosis in triplenegative breast cancer MDA-MB-231 cells].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2020Article
- NOTCH1 activation compensates BRCA1 deficiency and promotes triple-negative breast cancer formation.Nature communications · 2020Article
- Machine learning analysis identifies genes differentiating triple negative breast cancers.Scientific reports · 2020Article
- RAC1B Induces SMAD7 via USP26 to Suppress TGFβ1-Dependent Cell Migration in Mesenchymal-Subtype Carcinoma Cells.Cancers · 2020Article
- Novel Medicinal Mushroom Blend as a Promising Supplement in Integrative Oncology: A Multi-Tiered Study using 4T1 Triple-Negative Mouse Breast Cancer Model.International journal of molecular sciences · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Triple-negative breast cancer (TNBC) is an aggressive subgroup of human breast cancer, which is characterized as estrogen receptor (ER) negative, progesterone receptor (PR) negative, and human epidermal growth factor receptor 2 (HER2) negative. TNBC is the most difficult breast cancer subgroup to treat, due to its unresponsiveness to current clinical targeted therapies, high rate of recurrence, and poor prognosis. Thus, there is an urgent medical need to identify therapeutic targets and develop more effective stratified medicine for the treatment of TNBC. Here we review the potential therapeutic targets for TNBC based on its intrinsic subtype. We also review the aberrant activated signals found in different subgroups of TNBC, including androgen receptor (AR) and PI3K/AKT/mTOR, Notch, Wnt/β-catenin, Hedge-hog, and TGF-β signaling pathways, which play essential roles in multiple development stages of TNBC. The careful analysis of these signaling pathways and therapeutic targets would have significant impact on the drug development and clinical trials, leading to effective therapies for this deadly disease.
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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.