ReviewMedical oncology (Northwood, London, England)2025
CXCR4/CXCL12 blockade therapy; a new horizon in TNBC therapy.
Review in Medical oncology (Northwood, London, England), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed.
- Cancer-Associated Fibroblasts Functions as Multifunctional Architects of the Tumor Stroma and Represent Emerging Therapeutic Vulnerabilities.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- CXCL12/ZNF503/GATA3/MMP1 axis promotes tumor progression and metastasis of triple-negative breast cancer.Breast cancer research : BCR · 2026Article
- Review
- The chemokine network in triple-negative breast cancer: its role in immune microenvironment regulation, and prospects for targeted therapy.Frontiers in immunology · 2026Review
- Targeting the CXCR4/CXCL12 Axis to Overcome Drug Resistance in Triple-Negative Breast Cancer.Cells · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The only subtype of breast cancer (BC) without specific therapy is triple-negative breast cancer (TNBC), which represents 15-20% of incidence cases of BC. TNBC encompasses transformed and nonmalignant cells, including cancer-associated fibroblasts (CAF), endothelial vasculature, and tumor-infiltrating cells. These nonmalignant cells, soluble factors (e.g., cytokines), and the extracellular matrix (ECM) form the tumor microenvironment (TME). The TME is made up of these nonmalignant cells, ECM, and soluble components, including cytokines. Direct cell-to-cell contact and soluble substances like cytokines (e.g., chemokines) may facilitate interaction between cancer cells and the surrounding TME. Through growth-promoting cytokines, TME not only enables the development of cancer but also confers therapy resistance. New treatment targets will probably be suggested by comprehending the processes behind tumor development and progression as well as the functions of chemokines in TNBC. In this light, several investigations have shown the pivotal function of the C-X-C motif chemokine ligand 12 (CXCL12 or SDF-1) axis and chemokine receptor type 4 (CXCR4) in the pathophysiology of TNBC. This review provides an overview of the CXCR4/CXCL12 axis' function in TNBC development, metastasis, angiogenesis, and treatment resistance. A synopsis of current literature on targeting the CXCR4/CXCL12 axis for treating and managing TNBC has also been provided.
Indexed as
Identifiers
40216617What 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.