ReviewCancer research2015
The Role of TLR4 in Chemotherapy-Driven Metastasis.
Review in Cancer research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 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
59 citing papers in PubMed, 120 citations in OpenAlex.
- Protective effect of hesperetin against myelosuppression and splenic inflammation via modulating TLR4/MYD88/NF-κB signaling: molecular docking and experimental validation.Frontiers in pharmacology · 2026Article
- Molecular mechanisms underlying cyclophosphamide-induced ovarian injury and protective strategies.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Elucidating the association between TLR-4 expression and the clinical course of glioblastoma leptomeningeal disease.British journal of cancer · 2025Article
- The role of TLR-4 in chemoresistance of cancer.Discover oncology · 2025Review
- Paclitaxel, interferons and functional reprogramming of tumor-associated macrophages in optimized chemo-immunotherapy.Journal for immunotherapy of cancer · 2025Review
- Fruquintinib saddles tumor immune tolerance by curbing pro-tumoral immature myeloid cell populations.Frontiers in immunology · 2025Article
- Expression of toll-like receptors and inflammatory mediators in primary human glioma cells (low- and high-grade) compared to primary cells from epileptic human brain.Iranian journal of basic medical sciences · 2025Article
- TLR4/MyD88 expression patterns and novel genetic variants: association with aggressive clinicopathological features in colorectal cancer.Frontiers in oncology · 2025Article
- Mitochondrial rewiring with small-molecule drug-free nanoassemblies unleashes anticancer immunity.Nature communications · 2024Article
- Toll-like Receptors: Key Players in Squamous Cell Carcinoma Progression.Journal of clinical medicine · 2024Article
- Analysis of Selected Toll-like Receptors in the Pathogenesis and Advancement of Non-Small-Cell Lung Cancer.Journal of clinical medicine · 2024Article
- Clinicopathological Significance and Prognostic Role of High Mobility Group Box 1 (HMGB1), Toll-Like Receptor (TLR) 2 and TLR4 in Breast Cancer.Acta histochemica et cytochemica · 2024Article
- Imbalance between Actin Isoforms Contributes to Tumour Progression in Taxol-Resistant Triple-Negative Breast Cancer Cells.International journal of molecular sciences · 2024Article
- SESN1 functions as a new tumor suppressor gene via Toll-like receptor signaling pathway in neuroblastoma.CNS neuroscience & therapeutics · 2024Article
- Low-dose metronomic cisplatin as an antiangiogenic and anti-inflammatory strategy for cancer.British journal of cancer · 2024Article
- Chemotherapy-induced metastasis: molecular mechanisms and clinical therapies.Acta pharmacologica Sinica · 2023Review
- Microfluidic Microcirculation Mimetic for Exploring Biophysical Mechanisms of Chemotherapy-Induced Metastasis.Micromachines · 2023Article
- High-Dose Paclitaxel and its Combination with CSF1R Inhibitor in Polymeric Micelles for Chemoimmunotherapy of Triple Negative Breast Cancer.Nano today · 2023Article
- Cooperative NF-κB and Notch1 signaling promotes macrophage-mediated MenaINV expression in breast cancer.Breast cancer research : BCR · 2023Article
- Targeting ATAD3A-PINK1-mitophagy axis overcomes chemoimmunotherapy resistance by redirecting PD-L1 to mitochondria.Cell research · 2023Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Tumor resistance to cytotoxic drugs is one of the main obstacles to successful cancer therapy. Emerging evidence suggests that chemoresistance is promoted by substances released from dead and damaged cells that activate the host repair program orchestrated by Toll-like receptor-4 (TLR4). TLR4 is often overexpressed in malignant and tumor-infiltrating immune cells. In addition to endogenous ligands released by therapy-induced tumor destruction, TLR4 is directly activated by paclitaxel, one of the most commonly used chemotherapeutic drugs against various human cancers. TLR4 activation promotes local and systemic inflammation, leading to induction of multiple circuits that create a regenerative environment favoring local recurrence and metastasis. Of particular importance is TLR4-mediated recruitment of endothelial progenitors derived from immature myeloid cells. These cells play a major role in rebuilding tumor-associated lymphatic and blood vessels, thereby promoting lymphatic and hematogenous metastasis. The latter is further enhanced by the premetastatic niche generated by mobilization of myeloid provascular cells to distant organs. This review summarizes the recent evidence demonstrating that paclitaxel and other clinically used anticancer drugs actively induce metastasis even while shrinking the primary tumor. Better understanding of the mechanisms underlying TLR4-dependent chemotherapy-driven metastasis might be the key to overcoming challenges of cancer eradication.
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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.