ReviewTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2013
Current understanding of the role and targeting of tumor suppressor p53 in glioblastoma multiforme.
Review in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers, 1 of them a synthesis that pooled it.
What it found
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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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
86 citing papers in PubMed, 1 synthesis or guideline pooled it, 155 citations in OpenAlex.
- Expression and Prognostic Significance of p53 in Glioma Patients: A Meta-analysis.Neurochemical research · 2016Pooled it
- Synthesis and Biological Evaluation of a Novel Dual-Targeting Small Molecule Drug Conjugate Modulating the Crosstalk between α5β1 Integrin and MDM2 in Glioblastoma.ACS medicinal chemistry letters · 2026Article
- A Comprehensive Analysis of Natural Bioactive Molecules for the Treatment and Control of Glioblastoma Multiforme (GBM) Targeting Underlying Molecular Mechanism.Chemistry & biodiversity · 2026Review
- Cut the fat: targeting cholesterol and lipid metabolism in glioblastoma.Cell death & disease · 2025Review
- Exploring the therapeutic role of carnosol in cancer: from molecular insights to clinical promise.Medical oncology (Northwood, London, England) · 2025Review
- The subventricular zone structure, function and implications for neurological disease.Genes & diseases · 2025Review
- Key genes altered in glioblastoma based on bioinformatics (Review).Oncology letters · 2025Review
- Cytolethal distending toxin from Glaesserella parasuis induces ferroptosis in porcine alveolar macrophages and mice.Veterinary research · 2025Article
- Metformin and glioma: Targeting metabolic dysregulation for enhanced therapeutic outcomes.Translational oncology · 2025Review
- Cinnamaldehyde impacts key cellular signaling pathways for induction of programmed cell death in high-grade and low-grade human glioma cells.BMC research notes · 2025Article
- In vivo mouse models for adult brain tumors: Exploring tumorigenesis and advancing immunotherapy development.Neuro-oncology · 2024Review
- Hemoglobin, albumin, lymphocytes and platelets (HALP) score as a predictor of survival in patients with glioblastoma (GBM).BMC neurology · 2024Article
- Mutations in glioblastoma proteins do not disrupt epitope presentation and recognition, maintaining a specific CD8 T cell immune response potential.Scientific reports · 2024Article
- UBE2C enhances temozolomide resistance by regulating the expression of p53 to induce aerobic glycolysis in glioma.Acta biochimica et biophysica Sinica · 2024Article
- Metabolic Roles of HIF1, c-Myc, and p53 in Glioma Cells.Metabolites · 2024Review
- Review
- Review
- Liquid biopsy: creating opportunities in brain space.British journal of cancer · 2023Review
- Systems Medicine for Precise Targeting of Glioblastoma.Molecular biotechnology · 2023Review
- Unraveling the signaling mechanism behind astrocytoma and possible therapeutics strategies: A comprehensive review.Cancer reports (Hoboken, N.J.) · 2023Review
26 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
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma multiforme (GBM) is the most common primary malignancy in the brain and confers a uniformly poor prognosis. Despite decades of research on the topic, limited progress has been made to improve the poor survival associated with this disease. GBM arises de novo (primary GBM) or via dedifferentiation of lower grade glioma (secondary GBM). While distinct mutations are predominant in each subtype, alterations of tumor suppressor p53 are the most common, seen in 25-30 % of primary GBM and 60-70 % of secondary GBM. Various roles of p53 that protect against neoplastic transformation include modulation of cell cycle, DNA repair, apoptosis, senescence, angiogenesis, and metabolism, resulting in an extremely complex signaling network. Mutations of p53 in GBM are most common in the DNA-binding domain, namely within six hotspot mutation sites (codons 175, 245, 248, 249, 273, and 282). These alterations generally result in loss-of-function, gain-of-function, and dominant-negative mutational effects for p53, however, the distinct effect of these mutation types in GBM pathogenesis remain unclear. Signaling alterations downstream from p53 (e.g., MDM2, MDM4, INK4/ARF), p53 isoforms (e.g., p63, p73), and microRNAs (e.g., miR-34) also play critical roles in modulating the p53 pathway. Despite novel mouse models of GBM showing that p53 combined with other mutation generate tumors de novo, the role of p53 as a molecular marker of GBM remains controversial with most studies failing to show an association with prognosis. Regarding treatment in GBM, p53 targeted-gene therapy and vaccinations have reached phase I clinical trials while therapeutic drugs are still in preclinical development. This review aims to discuss the most recent findings regarding the impact of p53 mutations on GBM pathogenesis, prognosis, and treatment.
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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.