ReviewTrends in cancer2022
Mechanism and therapeutic potential of tumor-immune symbiosis in glioblastoma.
Review in Trends in cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
57 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.
- Focused ultrasound-induced blood-brain barrier modulation for drug delivery in recurrent glioblastoma: A systematic review.The Indian journal of medical research · 2026Pooled it
- Glioma microenvironment: Cellular crosstalk, immunosuppression, and novel therapeutic perspectives.Chinese medical journal · 2026Review
- Galanin impairs tumor immunity in glioblastoma by promoting infiltration and ferroptosis resistance of myeloid-derived suppressor cells.Nature cancer · 2026Article
- Leptomeningeal fibroblasts promote glioblastoma progression by regulating cerebrospinal fluid dynamics.Nature communications · 2026Article
- Integrated PANoptosis Profiling Identifies Immunosuppressive Subtypes and a Prognostic Signature With Functional Validation of MLKL in Glioblastoma.Annals of clinical and translational neurology · 2026Article
- Time-staggered chemo-immunotherapy via engineered nanofiber resists postoperative dynamic immunosuppression in glioblastoma.Nature communications · 2026Article
- Review
- Complement C5a/C5aR1 pathway facilitates glioblastoma progression via fostering glioma stem cell-macrophage symbiosis.Journal of neuroinflammation · 2026Article
- Symbiotic exclusivity between CLOCK and TFPI2 drives stemness and immunosuppression in glioblastoma models.The Journal of clinical investigation · 2026Article
- Accumulation of Siglec10European journal of immunology · 2026Article
- Oligodendrocyte transcription factor 2 orchestrates glioblastoma immune evasion by suppressing CXCL10 and CD8+ T cell activation.The Journal of clinical investigation · 2026Article
- AI-driven radiomics and radiogenomics: supporting the assessment and differentiation of pseudoprogression in cellular immunotherapy for glioblastoma.Frontiers in immunology · 2026Review
- Meningeal immunity and "Interstitial" therapy: a new paradigm for immunotherapy in glioblastoma.Frontiers in immunology · 2026Review
- Glioblastoma insights: Focus on crosstalk with the suppressive tumor microenvironment and advanced therapeutic strategies.Medicine · 2025Review
- Combined Tumor Cell and Lysate-Based Vaccines for Immunotherapy of Primary and Recurrent Glioblastoma (GBM).Cancers · 2025Review
- Neuropeptide adrenomedullin remodels stemness and macrophage dynamics in glioblastoma.Cell reports · 2025Article
- Single-cell dissection of the genotype-immunophenotype relationship in glioblastoma.Brain : a journal of neurology · 2025Article
- Inhibition of Extracellular Matrix Protein Fibulin-3 Reduces Immunosuppressive Signaling and Increases Macrophage Activation in Glioblastoma.Cancer research communications · 2025Article
- Therapeutic potential of targeting macrophages and microglia in glioblastoma.Trends in pharmacological sciences · 2025Review
- Glycoprotein NMB mediates bidirectional GSC-TAM interactions to promote tumor progression.JCI insight · 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
4 authors at 1 institution in 1 country.
Funding
Abstract
Glioblastoma (GBM) is the most aggressive and lethal form of brain tumor in human adults. Myeloid-lineage cells, including macrophages, microglia, myeloid-derived suppressor cells (MDSCs), and neutrophils, are the most frequent types of cell in the GBM tumor microenvironment (TME) that contribute to tumor progression. Emerging experimental evidence indicates that symbiotic interactions between cancer cells and myeloid cells are critical for tumor growth and immunotherapy resistance in GBM. In this review, we discuss the molecular mechanisms whereby cancer cells shape a myeloid cell-mediated immunosuppressive TME and, reciprocally, how such myeloid cells affect tumor progression and immunotherapy efficiency in GBM. Moreover, we highlight tumor-T cell symbiosis and summarize immunotherapeutic strategies intercepting this co-dependency in GBM.
Indexed as
Identifiers
What OpenQuestion holds
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.