ReviewCancers2020
Perspectives on Triple-Negative Breast Cancer: Current Treatment Strategies, Unmet Needs, and Potential Targets for Future Therapies.
Review in Cancers, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 177 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
177 citing papers in PubMed, 2 syntheses or guidelines pooled it, 330 citations in OpenAlex.
- Research on therapeutic clinical trials including immunotherapy in triple-negative breast cancer: a bibliometric analysis.Frontiers in oncology · 2024Pooled it
- Signaling Pathways and Natural Compounds in Triple-Negative Breast Cancer Cell Line.Molecules (Basel, Switzerland) · 2022Pooled it
- Investigating potential immune mechanisms of trilaciclib administered prior to chemotherapy in patients with metastatic triple-negative breast cancer.Breast cancer research and treatment · 2023Trial
- MPP8 Facilitates DNA DSB Repair via NHEJ to Promote Chemoresistance of TNBC Independent of Methyl-H3K9 Binding.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Understandability and Actionability of Artificial Intelligence-Assisted Lymphedema Education Material in Patients Undergoing Breast Cancer Surgery: Expert Evaluation.Journal of clinical nursing · 2026Observational
- TOMM40/FADS2 Expression Ratio Predicts the Sensitivity to mTOR Inhibitors in Triple-Negative Breast Cancer.Cancer medicine · 2026Article
- Review
- Next-Generation Therapeutic Targets in Triple-Negative Breast Cancer.European journal of breast health · 2026Article
- Integrated network pharmacology reveal new key curcumin-binding targets in triple-negative breast cancer.Discover oncology · 2026Article
- Clitocine suppresses TNBC progression by boosting CCRL2 to block survival signals and neutrophil-driven inflammation.Journal of biological engineering · 2026Article
- An Update on the Role of Androgens and Androgen Receptor in Triple-Negative Breast Cancer.Cells · 2026Review
- Multicenter Real-World Evaluation of Neoadjuvant Carboplatin in Triple-Negative Breast Cancer.Cancer medicine · 2026Article
- "When symptoms interact and change": longitudinal network analysis of dynamic symptom changes in oral cancer patients.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2026Article
- Article
- Tumor biology, treatment patterns, and recurrence in breast cancer patients aged 70-79 vs ≥ 80 years: a large-scale registry analysis.Archives of gynecology and obstetrics · 2026Article
- The Interplay Between Circadian Clocks and the Tumour Microenvironment in Breast Cancer.Cancers · 2026Review
- Optimizing immunotherapy-radiotherapy synergy in triple-negative breast cancer: mechanisms, clinical evidence, and therapeutic windows.Frontiers in immunology · 2026Review
- Novel Microbiome-Driven Approaches to Counteract Chemotherapy-Induced Mucositis in Breast Cancer Patients.Breast cancer (Dove Medical Press) · 2026Review
- Binding Interaction and Stability Analysis of Quercetin and its Derivatives as Potential Inhibitors of Triple Negative Breast Cancer (TNBC) against PARP1 Protein: AnCurrent pharmaceutical design · 2026Article
- Signalling Pathways and Inhibitors in Triple Negative Breast Cancer: Current Progress.Anti-cancer agents in medicinal chemistry · 2026Review
117 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
16 authors at 13 institutions in 1 country.
Funding
Abstract
Triple-negative breast cancer (TNBC), characterized by the absence or low expression of estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor (HER2), is the most aggressive subtype of breast cancer. TNBC accounts for about 15% of breast cancer cases in the U.S., and is known for high relapse rates and poor overall survival (OS). Chemo-resistant TNBC is a genetically diverse, highly heterogeneous, and rapidly evolving disease that challenges our ability to individualize treatment for incomplete responders and relapsed patients. Currently, the frontline standard chemotherapy, composed of anthracyclines, alkylating agents, and taxanes, is commonly used to treat high-risk and locally advanced TNBC. Several FDA-approved drugs that target programmed cell death protein-1 (Keytruda) and programmed death ligand-1 (Tecentriq), poly ADP-ribose polymerase (PARP), and/or antibody drug conjugates (Trodelvy) have shown promise in improving clinical outcomes for a subset of TNBC. These inhibitors that target key genetic mutations and specific molecular signaling pathways that drive malignant tumor growth have been used as single agents and/or in combination with standard chemotherapy regimens. Here, we review the current TNBC treatment options, unmet clinical needs, and actionable drug targets, including epidermal growth factor (EGFR), vascular endothelial growth factor (VEGF), androgen receptor (AR), estrogen receptor beta (ERβ), phosphoinositide-3 kinase (PI3K), mammalian target of rapamycin (mTOR), and protein kinase B (PKB or AKT) activation in TNBC. Supported by strong evidence in developmental, evolutionary, and cancer biology, we propose that the K-RAS/SIAH pathway activation is a major tumor driver, and SIAH is a new drug target, a therapy-responsive prognostic biomarker, and a major tumor vulnerability in TNBC. Since persistent K-RAS/SIAH/EGFR pathway activation endows TNBC tumor cells with chemo-resistance, aggressive dissemination, and early relapse, we hope to design an anti-SIAH-centered anti-K-RAS/EGFR targeted therapy as a novel therapeutic strategy to control and eradicate incurable TNBC in the future.
Indexed as
Identifiers
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.