ReviewJournal of advanced research2023
A review of biological targets and therapeutic approaches in the management of triple-negative breast cancer.
Review in Journal of advanced research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers, 1 of them a synthesis 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
70 citing papers in PubMed, 1 synthesis or guideline pooled it, 115 citations in OpenAlex.
- Advancements in Zebrafish Models for Breast Cancer Research: Unveiling Biomarkers, Targeted Therapies, and Personalized Medicine.Medical science monitor : international medical journal of experimental and clinical research · 2023Pooled it
- Apatinib plus etoposide in pretreated patients with advanced triple-negative breast cancer: a phase II trial.BMC cancer · 2023Trial
- Article
- Tumor Mechanical Remodeling via Bidirectional Calcium Redistribution Enables Deep Photothermal-Immunotherapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Cryptotanshinone Directly Targets MEK1 to Inhibit Migration and Invasion of Breast Cancer Cells Through Down-Regulating ERK/EMT Axis.Phytotherapy research : PTR · 2026Article
- circZNF148 Drives Glucose Metabolism Reprogramming to Enhance Metastasis and Immune Evasion via HK1 Stabilization in Triple-Negative Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- CK2 in triple-negative breast cancer: oncogenic signaling networks and emerging CK2 inhibitor-based combination therapies.Clinical and experimental medicine · 2026Review
- Targeting RSK2 enhances the efficacy of IGF1R inhibitor against triple-negative breast cancer via antagonizing IGF1/IGF1R signaling mediated by GATA3-IGFBP5 pathway.Acta pharmacologica Sinica · 2026Article
- MCPB-21 targets glycogenin-2 to regulate fatty acid oxidation and promote ferroptosis of breast cancer.American journal of cancer research · 2026Article
- Discrimination of Triple-Negative Breast Cancer: A Robust Clinical Baseline versus Multimodal Magnetic Resonance Imaging Integrated Models with Assessment of Generalizability.Breast cancer (Dove Medical Press) · 2026Article
- Konjac petroleum ether extract inhibits triple-negative breast cancer cell migration and invasion by attenuatingFrontiers in pharmacology · 2026Article
- HMGB1 reduce DNA damage by binding KU70 to activate NHEJ pathway in colorectal cancer cells after radiation.PloS one · 2026Article
- Signalling Pathways and Inhibitors in Triple Negative Breast Cancer: Current Progress.Anti-cancer agents in medicinal chemistry · 2026Review
- Largazole targets Musashi protein expression via miR-125b-5p and sensitizes triple-negative breast cancer cells to radiation.Frontiers in pharmacology · 2026Article
- Minibeam radiation therapy remodels tumor microenvironment and suppresses HIF-1α/VEGFR axis to overcome radioresistance in triple-negative breast cancer.NPJ precision oncology · 2025Article
- Identification of a super enhancer associated gene signature for the prognosis prediction and regulatory mechanism exploration in breast cancer.Scientific reports · 2025Article
- Emerging Nanozyme Strategies for Precision Breast Cancer Treatment.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- CircATP5C1 promotes triple-negative breast cancer progression by binding IGF2BP2 to modulate CSF-1 secretion.Cancer biology & therapy · 2025Article
- NRG1/PDGFC loop between fibroblasts and cancer cells drives paclitaxel resistance via ferroptosis suppression in breast cancer.Cell death discovery · 2025Article
- A dual-targeting peptide-drug conjugate based on CXCR4 and FOLR1 inhibits triple-negative breast cancer.Acta pharmaceutica Sinica. B · 2025Article
10 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
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTriple-negative breast cancer (TNBC) is a heterogeneous, aggressive phenotype of breast cancer with associated chemoresistance. The development of chemo- or radioresistance could be attributed to diverse tumor microenvironments, overexpression of membrane proteins (transporters), epigenetic changes, and alteration of the cell signaling pathways/genes associated with the development of cancer stem cells (CSCs). AIM OF REVIEW: Due to the diverse and heterogeneous nature of TNBC, therapeutic response to the existing modalities offers limited scope and thus results in reccurance after therapy. To establish landmark therapeutic efficacy, a number of novel therapeutic modalities have been proposed. In addition, reversal of the resistance that developed during treatment may be altered by employing appropriate therapeutic modalities. This review aims to discuss the plethora of investigations carried out, which will help readers understand and make an appropriate choice of therapy directed toward complete elimination of TNBC. KEY SCIENTIFIC CONCEPTS OF REVIEW: This manuscript addresses the major contributory factors from the tumor microenvironment that are responsible for the development of chemoresistance and poor prognosis. The associated cellular events and molecular mechanism-based therapeutic interventions have been explained in detail. Inhibition of ABC transporters, cell signaling pathways associated with CSCs, and epigenetic modification offers promising results in this regard. TNBC progression, invasion, metastasis and recurrence can also be inhibited by blocking multiple cell signaling pathways, targeting specific receptors/epigenetic targets, disrupting bioenergetics and generating reactive oxygen species (ROS).
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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.