ArticleOncoimmunology
Mammary tumor-derived CCL2 enhances pro-metastatic systemic inflammation through upregulation of IL1β in tumor-associated macrophages.
Article in Oncoimmunology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.
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Who cites it
75 citing papers in PubMed, 102 citations in OpenAlex.
- Blocking IL-1β reverses the immunosuppression in mouse breast cancer and synergizes with anti-PD-1 for tumor abrogation.Proceedings of the National Academy of Sciences of the United States of America · 2019Trial
- MLK4 orchestrates macrophage-induced triple-negative breast cancer invasion and ECM remodeling via enhanced paracrine signaling and NF-κB-MMP axis activation.Cell death & disease · 2026Article
- The role of tumor-associated macrophages in cancer development and their significance as prognostic markers.Clinical and experimental medicine · 2026Review
- Understanding and reversing mammary tumor-driven reprogramming of myelopoiesis to reduce metastatic spread.Cancer cell · 2025Article
- Invasion and metastasis in cancer: molecular insights and therapeutic targets.Signal transduction and targeted therapy · 2025Review
- Article
- Triple-negative breast cancer modifies the systemic immune landscape and alters neutrophil functionality.NPJ breast cancer · 2025Article
- Chemokines as key mediators in RIPI: pathophysiology and translational potential.Frontiers in immunology · 2025Review
- Review
- Tumor associated macrophages as key contributors and targets in current and future therapies for melanoma.Expert review of clinical immunology · 2024Review
- An update to experimental and clinical aspects of tumor-associated macrophages in cancer development: hopes and pitfalls.Clinical and experimental medicine · 2024Review
- The Tumor Immune Microenvironment in Breast Cancer Progression.Acta oncologica (Stockholm, Sweden) · 2024Review
- Article
- Melanoma-derived cytokines and extracellular vesicles are interlinked with macrophage immunosuppression.Frontiers in molecular biosciences · 2024Article
- Spatial and Temporal Mapping of Breast Cancer Lung Metastases Identify TREM2 Macrophages as Regulators of the Metastatic Boundary.Cancer discovery · 2023Article
- Intestinal IL-1β Plays a Role in Protecting against SARS-CoV-2 Infection.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Review
- Innate lymphoid cells and innate-like T cells in cancer - at the crossroads of innate and adaptive immunity.Nature reviews. Cancer · 2023Review
- Investigating Chemokine-Matrix Networks in Breast Cancer: Tenascin-C Sets the Tone for CCL2.International journal of molecular sciences · 2023Article
- An innovative risk index based on neutrophils and macrophages can effectively predict prognosis and immunotherapy response in patients with muscle-invasive bladder cancer.Translational cancer research · 2023Article
15 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 2 countries.
Funding
Abstract
Patients with primary solid malignancies frequently exhibit signs of systemic inflammation. Notably, elevated levels of neutrophils and their associated soluble mediators are regularly observed in cancer patients, and correlate with reduced survival and increased metastasis formation. Recently, we demonstrated a mechanistic link between mammary tumor-induced IL17-producing γδ T cells, systemic expansion of immunosuppressive neutrophils and metastasis formation in a genetically engineered mouse model for invasive breast cancer. How tumors orchestrate this systemic inflammatory cascade to facilitate dissemination remains unclear. Here we show that activation of this cascade relies on CCL2-mediated induction of IL1β in tumor-associated macrophages. In line with these findings, expression of
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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.