Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 3 complete abstracts (589 words), 9 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
A malignant form of astrocytoma histologically characterized by pleomorphism of cells, nuclear atypia, microhemorrhage, and necrosis. They may arise in any region of the central nervous system, with a predilection for the cerebral hemispheres, basal ganglia, and commissural pathways. Clinical presentation most frequently occurs in the fifth or sixth decade of life with focal neurologic signs or seizures.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Glioblastomas; Astrocytoma, Grade IV; Astrocytomas, Grade IV; Grade IV Astrocytoma; Grade IV Astrocytomas; Glioblastoma Multiforme; Giant Cell Glioblastoma; Giant Cell Glioblastomas.
Where it fits in the MeSH classification
- Broader topics
- Astrocytoma
Research landscape
PubMed indexes 39,812 records tagged with the MeSH heading “Glioblastoma” (counts retrieved 2026-10-29). 14,444 of them (36.3%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 14,789 records.
Reviews account for 4,598 records (11.5%) and meta-analyses for 260. Randomized controlled trials number 407 (1.0%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 5,274 |
| 2000-2009 | 5,305 |
| 2010-2019 | 14,789 |
| 2020 onward | 14,444 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 4,598 | 11.5% |
| Meta-analyses | 260 | 0.7% |
| Randomized controlled trials | 407 | 1.0% |
Method: PubMed query "Glioblastoma"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in cancer and oncology
Cancer research spans very different kinds of evidence. Laboratory studies in cell lines and animal models reveal mechanisms but often do not translate to patients. Early-phase trials mainly test safety and dosing, while phase 3 randomized trials and their meta-analyses are the usual basis for treatment conclusions. Outcomes also differ in meaning: tumour shrinkage, progression-free survival and overall survival are not interchangeable, and screening studies can be distorted by lead-time and overdiagnosis. When reading a result, check the cancer type and stage studied, the comparison treatment, and which outcome was measured.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Dual tumour-myeloid targeting of glioblastoma with GPNMB CAR-T cells | 2026 | Research article Design not recorded in structured metadata | 4 | cc by PMID 42386964 · DOI · PMC13518245 |
| The critical role of the endogenous immune compartment after CAR T cell therapy in recurrent GBM | 2026 | Research article Design not recorded in structured metadata | 2 | cc by PMID 42296961 · DOI · PMC13401735 |
| Phase 1 dose-escalation trial combining sulfasalazine and stereotactic radiosurgery in patients with recurrent glioblastoma | 2026 | Research article Design not recorded in structured metadata | 2 | cc by PMID 42229231 · DOI · PMC13251504 |
Dual tumour-myeloid targeting of glioblastoma with GPNMB CAR-T cells [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Glioblastoma is a lethal brain tumour for which current multimodal treatment rarely prevents recurrence1.
- Closing excerpt
- By collapsing tumour control and microenvironmental reprogramming, these findings provide a new strategy for antigen selection and targeting in heterogenous, myeloid-rich solid cancers.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (159 words)
Glioblastoma is a lethal brain tumour for which current multimodal treatment rarely prevents recurrence1. Therapeutic failure is driven by extensive intratumoural cellular heterogeneity2 with a microenvironment dominated by tumour-associated macrophages that sustain tumour growth and immunosuppression3. Although chimeric antigen receptor (CAR)-T cell therapies are being developed for glioblastoma, sustained response has been undermined by non-uniform antigen expression, antigen loss and microenvironmental barriers that are not directly engaged by tumour-targeting designs4. These limitations motivate new strategies that address the disease as a coupled tumour-immune system rather than a single malignant compartment. Here we use a multi-omic target discovery platform to identify GPNMB as a dual-compartment antigen in glioblastoma. Anti-GPNMB CAR-T cells showed potent anti-tumour activity, with long-term disease control in orthotopic patient-derived xenografts and syngeneic glioma models through concomitant depletion of GPNMB+ tumour and immunosuppressive myeloid populations. By collapsing tumour control and microenvironmental reprogramming, these findings provide a new strategy for antigen selection and targeting in heterogenous, myeloid-rich solid cancers.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42386964 · DOI · PMC13518245
The critical role of the endogenous immune compartment after CAR T cell therapy in recurrent GBM [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Glioblastoma (GBM) is the most common primary malignant brain tumor in adults, with a median survival of under 15 months and no effective treatment after recurrence.
- Closing excerpt
- These findings indicate that host immune cells play a critical role in CAR T cell therapy for GBM, suggesting that combinatorial strategies modulating the endogenous immune compartment could improve next-generation treatments.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (159 words)
Glioblastoma (GBM) is the most common primary malignant brain tumor in adults, with a median survival of under 15 months and no effective treatment after recurrence. A recent phase 1 trial of intracerebroventricular bivalent chimeric antigen receptor (CAR) T cells in recurrent GBM, registered at ClinicalTrials.gov (NCT05168423), showed promising responses, including tumor reduction and prolonged survival. However, relapse remains common. We performed in-depth profiling of longitudinal cerebrospinal fluid (CSF) and tumor samples from responders and non-responders to characterize immune dynamics following infusion. Our study reveals that, although CAR T cells activate post infusion across all patients, outcomes were defined by divergent remodeling of the endogenous immune landscape. Cytotoxic natural killer cell expansion characterized responders, whereas regulatory T cell expansion and abundant baseline immunosuppressive scavenger myeloid cells characterized non-responders. These findings indicate that host immune cells play a critical role in CAR T cell therapy for GBM, suggesting that combinatorial strategies modulating the endogenous immune compartment could improve next-generation treatments.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42296961 · DOI · PMC13401735
Phase 1 dose-escalation trial combining sulfasalazine and stereotactic radiosurgery in patients with recurrent glioblastoma [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Glioblastoma radioresistance is linked to glutathione, a key antioxidant protecting against oxidative stress.
- Closing excerpt
- TRIAL REGISTRATION: NCT04205357.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (271 words)
Glioblastoma radioresistance is linked to glutathione, a key antioxidant protecting against oxidative stress. Sulfasalazine inhibits the xCT antiporter mediating cystine uptake required for glutathione synthesis in glioma, potentiating radiotherapy in preclinical studies. This trial evaluated safety and therapeutic potential of combining sulfasalazine with stereotactic radiosurgery (SRS) for recurrent glioblastoma. Adults with recurrences were enrolled in a 3 + 3 dose-escalation trial receiving 1.5, 3.0, 4.5, or 6.0 g sulfasalazine orally for 3 days before SRS. Primary endpoint was safety. Secondary endpoints included changes in quality of life (QOL), tumor glutathione-levels, metabolism, and volumes assessed via Functional-Assessment-of-Cancer-Therapy-Brain-questionnaire, glutathione-edited-MR-spectroscopy,11C-Methionine-PET, and MRI. Eleven eligible patients treated with GKRS only due to closed research facilities served as concurrent controls for time to local tumor progression, progression-free survival (PFS), and overall survival (OS). Twelve patients were enrolled and followed until death or consent withdrawal (n = 1). Of 20 adverse events, two were grade 3 (transient lymphocytopenia), four grade 2, and fourteen grade 1. QOL remained stable for 6 months (p = 0.292). Tumor glutathione-levels and metabolic activity were reduced on day 3 (p = 0.010) and 1 month (p = 0.052), respectively. Best RANO-responses were objective (5/11), stable (5/11) or progressive (1/11) for participants vs. stable (2/11) or progressive (9/11) for controls, p = 0.001. Participants had longer local tumor control (median difference: 5.3 months, 95% CI: 1.0-9.6, p < 0.001) and PFS (1.7 months, 95% CI: 0.3-3.0, p = 0.009), with equivalent OS (p = 0.915). In conclusion sulfasalazine and SRS were well tolerated, reducing intratumoral glutathione-levels and associated with more durable local control than SRS alone supporting phase II investigation. TRIAL REGISTRATION: NCT04205357.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42229231 · DOI · PMC13251504
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Association of the Extent of Resection With Survival in Glioblastoma: A Systematic Review and Meta-analysis [4]
- Research article Genome-wide association study of glioma subtypes identifies specific differences in genetic susceptibility to glioblastoma and non-glioblastoma tumors [5]
- Research article Longer-term (≥ 2 years) survival in patients with glioblastoma in population-based studies pre- and post-2005: a systematic review and meta-analysis [6]
- Research article Re-irradiation for recurrent glioblastoma (GBM): a systematic review and meta-analysis [7]
- Research article The clinical trials landscape for glioblastoma: is it adequate to develop new treatments? [8]
- Research article Treatment options for progression or recurrence of glioblastoma: a network meta-analysis [9]
References
- Savage N, Grewal S, Shaikh MV, Zemp FJ, Mckenna D, Mikolajewicz N, et al.. Dual tumour-myeloid targeting of glioblastoma with GPNMB CAR-T cells. . 2026. PMID 42386964 · DOI · PMC13518245
- Freeburg NF, Chafamo D, Konanur Gopikrishna G, Murphy RM, Peng JJ, Parthasarathy S, et al.. The critical role of the endogenous immune compartment after CAR T cell therapy in recurrent GBM. . 2026. PMID 42296961 · DOI · PMC13401735
- Skeie BS, Craig-Craven AR, Grüner ER, Biermann M, Riemer F, Bragstad S, et al.. Phase 1 dose-escalation trial combining sulfasalazine and stereotactic radiosurgery in patients with recurrent glioblastoma. . 2026. PMID 42229231 · DOI · PMC13251504
- Brown TJ, Brennan MC, Li M, Church EW, Brandmeir NJ, Rakszawski KL, et al.. Association of the Extent of Resection With Survival in Glioblastoma: A Systematic Review and Meta-analysis. JAMA Oncol. 2016. PMID 27310651 · DOI · PMC6438173
- Melin BS, Barnholtz-Sloan JS, Wrensch MR, Johansen C, Il'yasova D, Kinnersley B, et al.. Genome-wide association study of glioma subtypes identifies specific differences in genetic susceptibility to glioblastoma and non-glioblastoma tumors. Nat Genet. 2017. PMID 28346443 · DOI · PMC5558246
- Poon MTC, Sudlow CLM, Figueroa JD, Brennan PM. Longer-term (≥ 2 years) survival in patients with glioblastoma in population-based studies pre- and post-2005: a systematic review and meta-analysis. Sci Rep. 2020. PMID 32669604 · DOI · PMC7363854
- Kazmi F, Soon YY, Leong YH, Koh WY, Vellayappan B. Re-irradiation for recurrent glioblastoma (GBM): a systematic review and meta-analysis. J Neurooncol. 2019. PMID 30523605 · DOI
- Vanderbeek AM, Rahman R, Fell G, Ventz S, Chen T, Redd R, et al.. The clinical trials landscape for glioblastoma: is it adequate to develop new treatments?. Neuro Oncol. 2018. PMID 29518210 · DOI · PMC6280141
- McBain C, Lawrie TA, Rogozińska E, Kernohan A, Robinson T, Jefferies S. Treatment options for progression or recurrence of glioblastoma: a network meta-analysis. Cochrane Database Syst Rev. 2021. PMID 34559423 · DOI · PMC8121043
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-29.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.