ArticleNeuro-oncology2013
Increase in tumor-associated macrophages after antiangiogenic therapy is associated with poor survival among patients with recurrent glioblastoma.
Article in Neuro-oncology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 151 papers.
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Who cites it
151 citing papers in PubMed, 222 citations in OpenAlex.
- Randomized Phase II and Biomarker Study of Pembrolizumab plus Bevacizumab versus Pembrolizumab Alone for Patients with Recurrent Glioblastoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2021Trial
- Angiogenic and immunomodulatory biomarkers in axitinib-treated patients with advanced renal cell carcinoma.Future oncology (London, England) · 2020Trial
- Improved tumor oxygenation and survival in glioblastoma patients who show increased blood perfusion after cediranib and chemoradiation.Proceedings of the National Academy of Sciences of the United States of America · 2013Trial
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- Cellular and inflammatory characteristics of patient‑derived glioblastoma organoids duringOncology reports · 2026Article
- Consensus statement on microglial and macrophage functions in gliomas.Acta neuropathologica · 2026Review
- Cellular Allies Against Glioblastoma: Therapeutic Potential of Macrophages and Mesenchymal Stromal Cells.Pharmaceutics · 2026Review
- The blood-brain tumor barrier as a spatial immune checkpoint in glioblastoma: leukocyte entry, perivascular retention, and therapeutic implications.Frontiers in immunology · 2026Review
- Single-cell analysis reveals KLF10-high macrophages induced by glioblastoma cells are associated with tumor progression.Frontiers in immunology · 2026Article
- PLX3397 attenuated tumor growth and remodeled tumor microenvironment of recurrent glioblastoma.Scientific reports · 2025Article
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- Inhibition of NFE2L1 Enables the Tumor-Associated Macrophage Polarization and Enhances Anti-PD1 Immunotherapy in Glioma.CNS neuroscience & therapeutics · 2025Article
- Breaking Down Glioma-Microenvironment Crosstalk.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2025Review
- Targeting HIF-2α in glioblastoma reshapes the immune infiltrate and enhances response to immune checkpoint blockade.Cellular and molecular life sciences : CMLS · 2025Article
- Advances in the Repurposing and Blood-Brain Barrier Penetrance of Drugs in Pediatric Brain Tumors.Cancers · 2025Review
- Single-cell RNA sequencing identifies a subtype of FN1 + tumor-associated macrophages associated with glioma recurrence and as a biomarker for immunotherapy.Biomarker research · 2024Article
- Unveiling the Inflammatory Landscape of Recurrent Glioblastoma through Histological-Based Assessments.Cancers · 2024Review
- Pediatric glioma immune profiling identifies TIM3 as a therapeutic target in BRAF fusion pilocytic astrocytoma.The Journal of clinical investigation · 2024Article
- Review
91 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
19 authors at 4 institutions in 1 country.
Funding
Abstract
Antiangiogenic therapy is associated with increased radiographic responses in glioblastomas, but tumors invariably recur. Because tumor-associated macrophages have been shown to mediate escape from antiangiogenic therapy in preclinical models, we examined the role of macrophages in patients with recurrent glioblastoma. We compared autopsy brain specimens from 20 patients with recurrent glioblastoma who received antiangiogenic treatment and chemoradiation with 8 patients who received chemotherapy and/or radiotherapy without antiangiogenic therapy or no treatment. Tumor-associated macrophages were morphologically and phenotypically analyzed using flow cytometry and immunohistochemistry for CD68, CD14, CD163, and CD11b expression. Flow cytometry showed an increase in macrophages in the antiangiogenic-treated patients. Immunohistochemical analysis demonstrated an increase in CD68+ macrophages in the tumor bulk (P < .01) and infiltrative areas (P = .02) in antiangiogenic-treated patients. We also observed an increase in CD11b+ cells in the tumor bulk (P < .01) and an increase in CD163+ macrophages in infiltrative tumor (P = .02). Of note, an increased number of CD11b+ cells in bulk and infiltrative tumors (P = .05 and P = .05, respectively) correlated with poor overall survival among patients who first received antiangiogenic therapy at recurrence. In summary, recurrent glioblastomas showed an increased infiltration in myeloid populations in the tumor bulk and in the infiltrative regions after antiangiogenic therapy. Higher numbers of CD11b+ cells correlated with poor survival among these patients. These data suggest that tumor-associated macrophages may participate in escape from antiangiogenic therapy and may represent a potential biomarker of resistance and a potential therapeutic target in recurrent glioblastoma.
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