ArticleCancer immunology research2020
Matrix-Targeting Immunotherapy Controls Tumor Growth and Spread by Switching Macrophage Phenotype.
Article in Cancer immunology research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
What it found
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Who cites it
43 citing papers in PubMed, 59 citations in OpenAlex.
- Cancer-associated adipocytes: metabolic reprogramming, crosstalk and therapeutic implications in tumor progression.Signal transduction and targeted therapy · 2026Review
- PU.1 is a mediator of the reactive stromal response associated with castration-resistant prostate cancer.Communications biology · 2026Article
- Biochemical signals from the extracellular matrix in inflammation and tumour immunology.Nature reviews. Immunology · 2026Review
- Tenascin-C orchestrates radiotherapy-induced head and neck tumor regression.EMBO molecular medicine · 2026Article
- Spatial transcriptomics and multi-omics reveal relapse and resistance mechanisms of EndMT-derived CAFs mediated by TNC and FLNC in glioblastoma.Journal of translational medicine · 2025Article
- Tumor-Associated Macrophage in Breast Tumor Microenvironment.International journal of molecular sciences · 2025Review
- Macrophages and fibroblasts as regulators of the immune response in pancreatic cancer.Nature immunology · 2025Review
- Tumor-associated macrophages in colon cancer immunotherapy: mechanisms, natural product interventions, and microenvironment remodeling.Frontiers in immunology · 2025Review
- Targeting innate and adaptive immunity to suppress lung cancer metastasis.Frontiers in immunology · 2025Review
- Targeting the MAtrix REgulating MOtif abolishes several hallmarks of cancer, triggering antitumor immunity.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- CAF-induced physical constraints controlling T cell state and localization in solid tumours.Nature reviews. Cancer · 2024Review
- Immune Checkpoint Inhibitor Therapy for Metastatic Melanoma: What Should We Focus on to Improve the Clinical Outcomes?International journal of molecular sciences · 2024Review
- The Tumor Stroma of Squamous Cell Carcinoma: A Complex Environment That Fuels Cancer Progression.Cancers · 2024Review
- MTDH enhances radiosensitivity of head and neck squamous cell carcinoma by promoting ferroptosis based on a prognostic signature.Journal of radiation research · 2024Article
- Biology of Tenascin C and its Role in Physiology and Pathology.Current medicinal chemistry · 2024Review
- Reprogramming the tumor microenvironment - macrophages emerge as key players in breast cancer immunotherapy.Frontiers in immunology · 2024Review
- Tenascin-C in Tissue Repair after Myocardial Infarction in Humans.International journal of molecular sciences · 2023Article
- Investigating Chemokine-Matrix Networks in Breast Cancer: Tenascin-C Sets the Tone for CCL2.International journal of molecular sciences · 2023Article
- Extracellular matrix remodeling in tumor progression and immune escape: from mechanisms to treatments.Molecular cancer · 2023Review
- The mechanical phenotypic plasticity of melanoma cell: an emerging driver of therapy cross-resistance.Oncogenesis · 2023Review
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 2 countries.
Funding
Abstract
The interplay between cancer cells and immune cells is a key determinant of tumor survival. Here, we uncovered how tumors exploit the immunomodulatory properties of the extracellular matrix to create a microenvironment that enables their escape from immune surveillance. Using orthotopic grafting of mammary tumor cells in immunocompetent mice and autochthonous models of breast cancer, we discovered how tenascin-C, a matrix molecule absent from most healthy adult tissues but expressed at high levels and associated with poor patient prognosis in many solid cancers, controls the immune status of the tumor microenvironment. We found that, although host-derived tenascin-C promoted immunity via recruitment of proinflammatory, antitumoral macrophages, tumor-derived tenascin-C subverted host defense by polarizing tumor-associated macrophages toward a pathogenic, immune-suppressive phenotype. Therapeutic monoclonal antibodies that blocked tenascin-C activation of Toll-like receptor 4 reversed this phenotypic switch
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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.