ReviewNature reviews. Neurology2018
Multidimensional communication in the microenvirons of glioblastoma.
Review in Nature reviews. Neurology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 375 papers, 2 of them syntheses 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
375 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- T cell immunity in glioma and potential implications for immunotherapy: A systematic review.Neuro-oncology · 2026Pooled it
- Pooled it
- Biomimetic membrane-coated metal nanoplatforms for enhanced BBB penetration and targeted glioblastoma therapy.International journal of pharmaceutics: X · 2026Review
- The 15-year bibliometric landscape of glioblastoma vaccines: Emergence of combinatorial immunotherapy.Human vaccines & immunotherapeutics · 2026Review
- FXYD5 promotes the growth of glioblastoma by targeting the PI3K/AKT/ACSL4 signaling axis.Oncology reports · 2026Article
- IL-17D reprograms CD93Cellular & molecular immunology · 2026Article
- Glioma microenvironment: Cellular crosstalk, immunosuppression, and novel therapeutic perspectives.Chinese medical journal · 2026Review
- Biomimetic Scaffold-Based 3D Models for Decoding Cancer Biology and Advancing Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Detection of mutant cancer-derived circRNAs in extracellular vesicles by rolling circle amplification.Molecular therapy. Nucleic acids · 2026Article
- Review
- Lactate-Induced K370 Lactylation of STING Inhibits STING-TBK1 Signaling and Dampens Anti-Tumor Immunity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Tumor microenvironment-responsive nanocarriers for enhanced glioblastoma immunotherapy.Journal of nanobiotechnology · 2026Review
- Exosome Secretion Drives Chemo-Resistance of Temozolomide in Glioblastoma.Journal of extracellular biology · 2026Article
- Complement C5a/C5aR1 pathway facilitates glioblastoma progression via fostering glioma stem cell-macrophage symbiosis.Journal of neuroinflammation · 2026Article
- Spatial and single-cell characterization of human glioblastoma tumor microenvironment reveals malignant cellular communities.Nature neuroscience · 2026Article
- Extracellular Vesicles in the Biology and Liquid Biopsy Diagnostics of Pediatric High-Grade Glioma - Emerging Findings and Opportunities.Journal of extracellular biology · 2026Review
- CCL5 promotes colon cancer progression via PI3K/AKT signaling and is negatively regulated by STAT1.Journal of gastrointestinal oncology · 2026Article
- Modeling glioblastoma relapse in vitro: a critical journey from 2D models to organ-on-chip alternatives.NPJ precision oncology · 2026Review
- Review
- Single-cell profiling reveals distinct populations of tumor-associated macrophages and metastatic tumor cells in breast cancer brain metastasis.Cell death & disease · 2026Article
315 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Glioblastomas are heterogeneous and invariably lethal tumours. They are characterized by genetic and epigenetic variations among tumour cells, which makes the development of therapies that eradicate all tumour cells challenging and currently impossible. An important component of glioblastoma growth is communication with and manipulation of other cells in the brain environs, which supports tumour progression and resistance to therapy. Glioblastoma cells recruit innate immune cells and change their phenotype to support tumour growth. Tumour cells also suppress adaptive immune responses, and our increasing understanding of how T cells access the brain and how the tumour thwarts the immune response offers new strategies for mobilizing an antitumour response. Tumours also subvert normal brain cells - including endothelial cells, neurons and astrocytes - to create a microenviron that favours tumour success. Overall, after glioblastoma-induced phenotypic modifications, normal cells cooperate with tumour cells to promote tumour proliferation, invasion of the brain, immune suppression and angiogenesis. This glioblastoma takeover of the brain involves multiple modes of communication, including soluble factors such as chemokines and cytokines, direct cell-cell contact, extracellular vesicles (including exosomes and microvesicles) and connecting nanotubes and microtubes. Understanding these multidimensional communications between the tumour and the cells in its environs could open new avenues for therapy.
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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.