ArticleThe Journal of experimental medicine2008
"Re-educating" tumor-associated macrophages by targeting NF-kappaB.
Article in The Journal of experimental medicine, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 428 papers, 2 of them syntheses that pooled it.
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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.
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Who cites it
428 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Promising effects of parasite-derived compounds on tumor regression: a systematic review of in vitro and in vivo studies.Environmental science and pollution research international · 2022Pooled it
- The metabolic addiction of cancer stem cells.Frontiers in oncology · 2022Pooled it
- Challenges in Developing a Microglial NF-Kappa B Conditional Mouse Model for Glioblastoma Studies.Cells · 2026Article
- Next-generation macrophage engineering in cancer therapy: From TAM reprogramming to CAR-macrophages.Molecular therapy. Nucleic acids · 2026Review
- Inflammatory bone marrow microenvironment impairs the therapeutic effect of daratumumab-lenalidomide in multiple myeloma.Biomarker research · 2026Article
- Noninvasive in vivo imaging of NF-κB activation predicts immunotherapy response in solid tumors.Npj imaging · 2026Article
- The double-edged sword role of tumor-associated macrophages: preventing or causing resistance to immunotherapy.Journal of experimental & clinical cancer research : CR · 2026Review
- Harnessing nanomedicine to target NF-κB signalling in cancer: at the intersection of inflammatory signalling, metabolic reprogramming, and therapeutic innovation.Cell communication and signaling : CCS · 2026Review
- Quantitative Cell Type-Specific Immunopeptidome Analysis of Macrophage and Tumor Coevolution Reveals Therapeutic MHC-I Peptides in Glioblastoma.Cancer research · 2025Article
- Intracellular Calcium as a Regulator of Polarization and Target Reprogramming of Macrophages.International journal of molecular sciences · 2025Review
- The Pivotal Role of NF-κB in Glioblastoma: Mechanisms of Activation and Therapeutic Implications.International journal of molecular sciences · 2025Review
- NF-κB in inflammation and cancer.Cellular & molecular immunology · 2025Review
- Chemoradiation-Altered Micromilieu of Glioblastoma Cells Particularly Impacts M1-like Macrophage Activation.International journal of molecular sciences · 2025Article
- Radiation-induced rescue effect on human breast carcinoma cells is regulated by macrophages.Biochemistry and biophysics reports · 2025Article
- Immunosuppressive tumor microenvironment in pancreatic cancer: mechanisms and therapeutic targets.Frontiers in immunology · 2025Review
- Inhibition of HMGB1/NF-κB signaling restores Th17/Treg balance via dendritic cell modulation in liver transplant rejection.Frontiers in immunology · 2025Article
- Evaluation of Immunostimulatory Effects of Bacterial Lysate Proteins on THP-1 Macrophages: Pro-inflammatory Cytokine Response and Proteomic Profiling.Journal of immunology research · 2025Article
- The Regulatory Network of Transcription Factors in Macrophage Polarization.ImmunoTargets and therapy · 2025Review
- Immunocytes in the tumor microenvironment: recent updates and interconnections.Frontiers in immunology · 2025Review
- The Bidirectional Interaction Between NF-Journal of immunology research · 2025Review
368 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors.
Funding
Abstract
The nuclear factor kappaB (NF-kappaB) signaling pathway is important in cancer-related inflammation and malignant progression. Here, we describe a new role for NF-kappaB in cancer in maintaining the immunosuppressive phenotype of tumor-associated macrophages (TAMs). We show that macrophages are polarized via interleukin (IL)-1R and MyD88 to an immunosuppressive "alternative" phenotype that requires IkappaB kinase beta-mediated NF-kappaB activation. When NF-kappaB signaling is inhibited specifically in TAMs, they become cytotoxic to tumor cells and switch to a "classically" activated phenotype; IL-12(high), major histocompatibility complex II(high), but IL-10(low) and arginase-1(low). Targeting NF-kappaB signaling in TAMs also promotes regression of advanced tumors in vivo by induction of macrophage tumoricidal activity and activation of antitumor activity through IL-12-dependent NK cell recruitment. We provide a rationale for manipulating the phenotype of the abundant macrophage population already located within the tumor microenvironment; the potential to "re-educate" the tumor-promoting macrophage population may prove an effective and novel therapeutic approach for cancer that complements existing therapies.
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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.