ArticleNature communications2023
Monocyte depletion enhances neutrophil influx and proneural to mesenchymal transition in glioblastoma.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 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
45 citing papers in PubMed, 52 citations in OpenAlex.
- Macrophage Plasticity in Cancer Therapy: Function, Timing, and Tradeoffs.International journal of molecular sciences · 2026Review
- Circulating immune profiling reveals impaired monocyte states and trajectories driving immunosuppression in glioblastoma.Journal of neuroinflammation · 2026Article
- Integrative bulk and single-cell analyses implicate ASL in MIF-associated myeloid programs in glioblastoma.Functional & integrative genomics · 2026Article
- Emerging roles of ferroptosis in modulating the immune landscape of glial tumours.Nature cell biology · 2026Review
- Consensus statement on microglial and macrophage functions in gliomas.Acta neuropathologica · 2026Review
- Mismatch repair deficiency drives malignant progression and alters the tumor immune microenvironment in glioblastoma models.The Journal of clinical investigation · 2026Article
- Immunosuppressive mechanisms and therapeutic interventions shaping glioblastoma immunity.Nature cancer · 2026Review
- The immunosuppressive tumor microenvironment in glioblastoma.Frontiers in immunology · 2026Review
- Decoding the dual roles of monocytes in tumor immunity: from immunosurveillance to immune evasion.Frontiers in immunology · 2026Review
- Next-generation immunotherapy biologics for glioblastoma.Frontiers in immunology · 2026Review
- NAT10-mediated N4-acetylcytidine (ac4C) modification of PIK3R2 mRNA promotes malignant progression of glioblastoma.Cell death & disease · 2025Article
- Glioblastoma insights: Focus on crosstalk with the suppressive tumor microenvironment and advanced therapeutic strategies.Medicine · 2025Review
- Glioportal: a comprehensive transcriptomic resource unveiling ligand-mediated mesenchymal transition in glioblastoma.Neuro-oncology · 2025Article
- Pan-cancer single-cell and spatial transcriptomics implicate cancer-associated fibroblasts in neutrophil immunosuppressive phenotypic transitions and immunotherapy resistance.Functional & integrative genomics · 2025Article
- Immune microenvironment in hepatocellular carcinoma: from pathogenesis to immunotherapy.Cellular & molecular immunology · 2025Review
- Single-cell dissection of the genotype-immunophenotype relationship in glioblastoma.Brain : a journal of neurology · 2025Article
- Review
- Quantitative Proteomic Analysis Reveals Different Functional Subtypes amongJournal of proteome research · 2025Article
- The mechanisms and clinical significance of CD8Cancer biology & medicine · 2025Review
- Machine learning and multi-omics analysis reveal key regulators of proneural-mesenchymal transition in glioblastoma.Scientific reports · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
19 authors at 3 institutions in 1 country.
Funding
Abstract
Myeloid cells comprise the majority of immune cells in tumors, contributing to tumor growth and therapeutic resistance. Incomplete understanding of myeloid cells response to tumor driver mutation and therapeutic intervention impedes effective therapeutic design. Here, by leveraging CRISPR/Cas9-based genome editing, we generate a mouse model that is deficient of all monocyte chemoattractant proteins. Using this strain, we effectively abolish monocyte infiltration in genetically engineered murine models of de novo glioblastoma (GBM) and hepatocellular carcinoma (HCC), which show differential enrichment patterns for monocytes and neutrophils. Eliminating monocyte chemoattraction in monocyte enriched PDGFB-driven GBM invokes a compensatory neutrophil influx, while having no effect on Nf1-silenced GBM model. Single-cell RNA sequencing reveals that intratumoral neutrophils promote proneural-to-mesenchymal transition and increase hypoxia in PDGFB-driven GBM. We further demonstrate neutrophil-derived TNF-a directly drives mesenchymal transition in PDGFB-driven primary GBM cells. Genetic or pharmacological inhibiting neutrophils in HCC or monocyte-deficient PDGFB-driven and Nf1-silenced GBM models extend the survival of tumor-bearing mice. Our findings demonstrate tumor-type and genotype dependent infiltration and function of monocytes and neutrophils and highlight the importance of targeting them simultaneously for cancer treatments.
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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.