ReviewCells2023
Monocyte and Macrophage in Neuroblastoma: Blocking Their Pro-Tumoral Functions and Strengthening Their Crosstalk with Natural Killer Cells.
Review in Cells, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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.
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Who cites it
15 citing papers in PubMed, 21 citations in OpenAlex.
- Bioengineered cell therapies for pediatric solid tumors: unmet needs and a measurement-integrated approach.Progress in biomedical engineering (Bristol, England) · 2026Review
- The B7-H3/CD3 immune phenotype identifies prognostic subgroups in neuroblastoma.Frontiers in immunology · 2026Article
- Inhibition of CDK1 Promotes Immunogenic Cell Death in Neuroblastoma.Cancer management and research · 2026Article
- NK cell hyperactivation drives macrophage repolarization and limits M2 bias in pemphigus vulgaris.Frontiers in immunology · 2026Article
- Membrane IL-18 identifies a human macrophage subset with distinct proteomic and functional traits.Oncoimmunology · 2025Article
- Exploring the mechanisms of mutual influence between lactylation and macrophage polarization in the context of disease.Clinical and translational medicine · 2025Review
- M344 Suppresses Histone Deacetylase-Associated Phenotypes and Tumor Growth in Neuroblastoma.International journal of molecular sciences · 2025Article
- Review
- Exosomes and immune modulation: implications for neuroblastoma immunotherapy.Frontiers in immunology · 2025Review
- Amyloid precursor-like protein 2 expression in macrophages: differentiation and M1/M2 macrophage dynamics.Frontiers in oncology · 2025Article
- Tumor-associated macrophages correlate with better outcome in SHH medulloblastoma.Frontiers in oncology · 2025Article
- The neuroblastoma tumor microenvironment: From an in-depth characterization towards novel therapies.EJC paediatric oncology · 2024Article
- Shikonin reduces M2 macrophage population in ovarian cancer by repressing exosome production and the exosomal galectin 3-mediated β-catenin activation.Journal of ovarian research · 2024Article
- NF-κB: Governing Macrophages in Cancer.Genes · 2024Review
- B7-H3 in Pediatric Tumors: Far beyond Neuroblastoma.Cancers · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Over the past decade, immunotherapy has represented an enormous step forward in the fight against cancer. Immunotherapeutic approaches have increasingly become a fundamental part of the combined therapies currently adopted in the treatment of patients with high-risk (HR) neuroblastoma (NB). An increasing number of studies focus on the understanding of the immune landscape in NB and, since this tumor expresses low or null levels of MHC class I, on the development of new strategies aimed at enhancing innate immunity, especially Natural Killer (NK) cells and macrophages. There is growing evidence that, within the NB tumor microenvironment (TME), tumor-associated macrophages (TAMs), which mainly present an M2-like phenotype, have a crucial role in mediating NB development and immune evasion, and they have been correlated to poor clinical outcomes. Importantly, TAM can also impair the antibody-dependent cellular cytotoxicity (ADCC) mediated by NK cells upon the administration of anti-GD2 monoclonal antibodies (mAbs), the current standard immunotherapy for HR-NB patients. This review deals with the main mechanisms regulating the crosstalk among NB cells and TAMs or other cellular components of the TME, which support tumor development and induce drug resistance. Furthermore, we will address the most recent strategies aimed at limiting the number of pro-tumoral macrophages within the TME, reprogramming the TAMs functional state, thus enhancing NK cell functions. We also prospectively discuss new or unexplored aspects of human macrophage heterogeneity.
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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.