ReviewOncogene2022
Wild-type isocitrate dehydrogenase under the spotlight in glioblastoma.
Review in Oncogene, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 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
52 citing papers in PubMed, 1 synthesis or guideline pooled it, 78 citations in OpenAlex.
- Efficacy of ketogenic metabolic therapy as an adjuvant to the current standard of care in the treatment of glioblastoma: A systematic review of clinical trials.Medical oncology (Northwood, London, England) · 2025Pooled it
- Fatty Acid Metabolism Rewires Glioblastoma Progression and Treg-Mediated Immune Resistance.Cancers · 2026Review
- Platelet-to-Albumin Ratio and Clinical Outcomes in IDH-Wildtype Grade 4 Diffuse Glioma.Journal of clinical medicine · 2026Article
- Metabolic vulnerabilities and therapeutic opportunities in diffuse large B-cell lymphoma.Oncogenesis · 2026Review
- miR-181d coordinates homologous recombination and anti-tumor immune responses in glioblastoma.iScience · 2026Article
- Isocitrate dehydrogenase mutations as potential tumour agnostic targets.EJC supplements : EJC : official journal of EORTC, European Organization for Research and Treatment of Cancer ... [et al.] · 2026Article
- Dual Targeting of IDH2 and the Ubiquitin-Proteasome System Reveals a Functional Vulnerability in Breast Cancer Models.Cancers · 2026Article
- p300: expanding beyond acetylation to mastermind lactylation-dependent tumorigenesis.Frontiers in cell and developmental biology · 2026Review
- The TRiC/CCT Complex at the Crossroads of Metabolism and Hypoxia in GBM: Implications for IDH-Dependent Therapeutic Targeting.International journal of molecular sciences · 2025Review
- Single-cell multi-omics identifies metabolism-linked epigenetic reprogramming as a driver of therapy-resistant medulloblastoma.Nature communications · 2025Article
- Distinguishing IDH-mutant astrocytomas from IDH-wildtype glioblastomas using qualitative and quantitative MRI features: a WHO CNS5 study.BMC medical imaging · 2025Article
- Characterisation of the expression of P2X7 receptor, cancer stem cell markers and immunological mediators in human high-grade gliomas.BMC neuroscience · 2025Article
- Targeting the Mitochondria in High-Grade Gliomas.Cancers · 2025Review
- UPP1 is a dual biomarker of prognosis and immune microenvironment in IDH wild-type glioblastoma.Scientific reports · 2025Article
- Large-scale bulk and single-cell RNA sequencing combined with machine learning reveals glioblastoma-associated neutrophil heterogeneity and establishes a VEGFABiology direct · 2025Article
- Creating a predictive model and online calculator for high-value care outcomes following glioblastoma resection: incorporating neighborhood socioeconomic status index.Journal of neuro-oncology · 2025Observational
- The research progress on meningeal metastasis in solid tumors.Discover oncology · 2025Review
- Prognostic Biomarkers in Isocitrate Dehydrogenase Wild-Type Glioblastoma: A Focus on B7-H3.Brain sciences · 2025Article
- The promise of mitochondria in the treatment of glioblastoma: a brief review.Discover oncology · 2025Review
- Targeting metabolic reprogramming in glioblastoma as a new strategy to overcome therapy resistance.Frontiers in cell and developmental biology · 2025Review
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 at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Brain tumors actively reprogram their cellular metabolism to survive and proliferate, thus offering potential therapeutic opportunities. Over the past decade, extensive research has been done on mutant IDH enzymes as markers of good prognosis in glioblastoma, a highly aggressive brain tumor in adults with dismal prognosis. Yet, 95% of glioblastoma are IDH wild-type. Here, we review current knowledge about IDH wild-type enzymes and their putative role in mechanisms driving tumor progression. After a brief overview on tumor metabolic adaptation, we present the diverse metabolic function of IDH enzymes and their roles in glioblastoma initiation, progression and response to treatments. Finally, we will discuss wild-type IDH targeting in primary glioblastoma.
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.