ArticleThe Journal of clinical investigation2017
A proangiogenic signaling axis in myeloid cells promotes malignant progression of glioma.
Article in The Journal of clinical investigation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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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
26 citing papers in PubMed, 47 citations in OpenAlex.
- Signaling pathways and targeted interventions for precancers.Signal transduction and targeted therapy · 2026Review
- Single-dose radiotherapy is more effective than fractionation when combined with anti-PD-1 immunotherapy in glioblastoma.Scientific reports · 2025Article
- ID2-ETS2 axis regulates the transcriptional acquisition of pro-tumoral microglia phenotype in glioma.Cell death & disease · 2024Article
- Glioblastoma microenvironment-from biology to therapy.Genes & development · 2024Review
- SorLA restricts TNFα release from microglia to shape a glioma-supportive brain microenvironment.EMBO reports · 2024Article
- Microbes, macrophages, and melanin: a unifying theory of disease as exemplified by cancer.Frontiers in immunology · 2024Review
- Radiotherapy Plus Temozolomide With or Without Nimotuzumab Against the Newly Diagnosed EGFR-Positive Glioblastoma: A Retrospective Cohort Study.The oncologist · 2023Article
- Direct and indirect regulation of the tumor immune microenvironment by VEGF.Journal of leukocyte biology · 2022Review
- Effectiveness and safety of tumor-treating fields therapy for glioblastoma: A single-center study in a Chinese cohort.Frontiers in neurology · 2022Article
- VEGFR2 activity on myeloid cells mediates immune suppression in the tumor microenvironment.JCI insight · 2021Article
- Phenotypic plasticity of myeloid cells in glioblastoma development, progression, and therapeutics.Oncogene · 2021Review
- Targeting Myeloid-Derived Suppressor Cells to Enhance the Antitumor Efficacy of Immune Checkpoint Blockade Therapy.Frontiers in immunology · 2021Review
- Metabolic Remodeling in Glioma Immune Microenvironment: Intercellular Interactions Distinct From Peripheral Tumors.Frontiers in cell and developmental biology · 2021Review
- Retrospective Study of the Safety and Efficacy of Anlotinib Combined With Dose-Dense Temozolomide in Patients With Recurrent Glioblastoma.Frontiers in oncology · 2021Article
- Cellular Plasticity and Tumor Microenvironment in Gliomas: The Struggle to Hit a Moving Target.Cancers · 2020Review
- Article
- Targeting Myeloid-Derived Suppressor Cell, a Promising Strategy to Overcome Resistance to Immune Checkpoint Inhibitors.Frontiers in immunology · 2020Review
- Is Visible Aminolevulinic Acid-Induced Fluorescence an Independent Biomarker for Prognosis in Histologically Confirmed (World Health Organization 2016) Low-Grade Gliomas?Neurosurgery · 2019Article
- Article
- Targeting Myeloid Cells in Combination Treatments for Glioma and Other Tumors.Frontiers in immunology · 2019Review
Corrections and comments
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Authors and funding
23 authors at 3 institutions in 1 country.
Funding
Abstract
Tumors are capable of coopting hematopoietic cells to create a suitable microenvironment to support malignant growth. Here, we have demonstrated that upregulation of kinase insert domain receptor (KDR), also known as VEGFR2, in a myeloid cell sublineage is necessary for malignant progression of gliomas in transgenic murine models and is associated with high-grade tumors in patients. KDR expression increased in myeloid cells as myeloid-derived suppressor cells (MDSCs) accumulated, which was associated with the transformation and progression of low-grade fibrillary astrocytoma to high-grade anaplastic gliomas. KDR deficiency in murine BM-derived cells (BMDCs) suppressed the differentiation of myeloid lineages and reduced granulocytic/monocytic populations. The depletion of myeloid-derived KDR compromised its proangiogenic function, which inhibited the angiogenic switch necessary for malignant progression of low-grade to high-grade tumors. We also identified inhibitor of DNA binding protein 2 (ID2) as a key upstream regulator of KDR activation during myeloid differentiation. Deficiency of ID2 in BMDCs led to downregulation of KDR, suppression of proangiogenic myeloid cells, and prevention of low-grade to high-grade transition. Tumor-secreted TGF-β and granulocyte-macrophage CSF (GM-CSF) enhanced the KDR/ID2 signaling axis in BMDCs. Our results suggest that modulation of KDR/ID2 signaling may restrict tumor-associated myeloid cells and could potentially be a therapeutic strategy for preventing transformation of premalignant gliomas.
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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.