ReviewFrontiers in oncology2024
Targeted therapy approaches for epithelial-mesenchymal transition in triple negative breast cancer.
Review in Frontiers in oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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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.
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
19 citing papers in PubMed.
- Role of epithelial-mesenchymal transition (EMT) in malignancies: current status and future prospects.Signal transduction and targeted therapy · 2026Review
- Epithelial-Mesenchymal Plasticity in Cancer: Transcriptional Regulation, Biomarker Challenges, and Emerging Therapeutic Opportunities.Cell biochemistry and function · 2026Review
- Nanotechnology in triple-negative breast cancer: a review of nanocarrier systems for enhanced efficacy and reduced toxicity.Nanoscale advances · 2026Review
- Multi-omics single-cell dissection of malignant epithelial heterogeneity identifies GJB2 as an EMT-driving biomarker in triple-negative breast cancer.BMC medical genomics · 2026Article
- Epithelial-mesenchymal transition and its role in drug resistance of cervical cancer.Molecular biology reports · 2026Review
- Bioactive Natural Compounds in Triple-Negative Breast Cancer: Molecular Targets and Therapeutic Perspectives.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Diffuse Alveolar Hemorrhage Caused by Metastatic Breast Cancer.Internal medicine (Tokyo, Japan) · 2026Article
- Emerging Protein Targets in Triple-Negative Breast Cancer: Beyond Conventional Therapy.Cancers · 2026Review
- From in-silico QSAR modeling to in-vitro MTT assay: experimental validation of novel uPAR leads for triple-negative breast cancer (TNBC) and skin cancer.Scientific reports · 2026Article
- Zerumbone mediated CD1d inhibition suppresses epithelial to mesenchymal transition in triple negative breast cancer.Discover oncology · 2026Article
- Article
- Celastrol increases anoikis sensitivity to suppress triple-negative breast cancer via EGFR pathway and p-EMT state regulation.Frontiers in pharmacology · 2026Article
- Emerging Breast Cancer Subpopulations: Functional Heterogeneity Beyond the Classical Subtypes.International journal of molecular sciences · 2025Review
- Targeting the CXCR4/CXCL12 Axis to Overcome Drug Resistance in Triple-Negative Breast Cancer.Cells · 2025Review
- Cytokine Networks in Triple-Negative Breast Cancer: Mechanisms, Therapeutic Targets, and Emerging Strategies.Biomedicines · 2025Review
- Integrating AI/ML and multi-omics approaches to investigate the role of TNFRSF10A/TRAILR1 and its potential targets in pancreatic cancer.Computers in biology and medicine · 2025Article
- Targeting obesity, metabolic syndrome, and prostate cancer: GLP-1 agonists as emerging therapeutic agents.Discover oncology · 2025Review
- [Epithelial-mesenchymal Transition: Biological Basis and Clinical Prospects of Lung Cancer Invasion, Metastasis, and Drug Resistance].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2025Review
- Pharmacological Inhibition of MDM2 Induces Apoptosis in p53-Mutated Triple-Negative Breast Cancer.International journal of molecular sciences · 2025Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Triple-negative breast cancer (TNBC) is distinguished by negative expression of estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2), making it an aggressive subtype of breast cancer and contributes to 15-20% of the total incidence. TNBC is a diverse disease with various genetic variations and molecular subtypes. The tumor microenvironment involves multiple cells, including immune cells, fibroblast cells, extracellular matrix (ECM), and blood vessels that constantly interact with tumor cells and influence each other. The ECM undergoes significant structural changes, leading to induced cell proliferation, migration, adhesion, invasion, and epithelial-to-mesenchymal transition (EMT). The involvement of EMT in the occurrence and development of tumors through invasion and metastasis in TNBC has been a matter of concern. Therefore, EMT markers could be prognostic predictors and potential therapeutic targets in TNBC. Chemotherapy has been one of the primary options for treating patients with TNBC, but its efficacy against TNBC is still limited. Targeted therapy is a critical emerging option with enhanced efficacy and less adverse effects on patients. Various targeted therapy approaches have been developed based on the specific molecules and the signaling pathways involved in TNBC. These include inhibitors of signaling pathways such as TGF-β, Wnt/β-catenin, Notch, TNF-α/NF-κB and EGFR, as well as immune checkpoint inhibitors, such as pembrolizumab, 2laparib, and talazoparib have been widely explored. This article reviews recent developments in EMT in TNBC invasion and metastasis and potential targeted therapy strategies.
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