ArticleOncogene2000
p53 gene mutation and ink4a-arf deletion appear to be two mutually exclusive events in human glioblastoma.
Article in Oncogene, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 144 citations in OpenAlex.
- Cystic glioblastoma IDH-wildtype: genetic alterations and outcomes.Journal of neuro-oncology · 2025Article
- Novel sights on therapeutic, prognostic, and diagnostics aspects of non-coding RNAs in glioblastoma multiforme.Metabolic brain disease · 2023Review
- New phase therapeutic pursuits for targeted drug delivery in glioblastoma multiforme.Exploration of targeted anti-tumor therapy · 2022Review
- Utilisation of semiconductor sequencing for the detection of predictive biomarkers in glioblastoma.PloS one · 2022Article
- Mechanisms of TP53 Pathway Inactivation in Embryonic and Somatic Cells-Relevance for Understanding (Germ Cell) Tumorigenesis.International journal of molecular sciences · 2021Review
- Hsa_circ_0080229 upregulates the expression of murine double minute-2 (MDM2) and promotes glioma tumorigenesis and invasion via the miR-1827 sponging mechanism.Annals of translational medicine · 2021Article
- Genomic destabilization and its associated mutagenesis increase with senescence-associated phenotype expression.Cancer science · 2021Review
- Heme Oxygenase-1 in Central Nervous System Malignancies.Journal of clinical medicine · 2020Review
- The p53 Pathway in Glioblastoma.Cancers · 2018Review
- Joint Covariate Detection on Expression Profiles for Selecting Prognostic miRNAs in Glioblastoma.BioMed research international · 2017Article
- Structural mutation analysis of PTEN and its genotype-phenotype correlations in endometriosis and cancer.Proteins · 2016Article
- The failure in the stabilization of glioblastoma-derived cell lines: spontaneous in vitro senescence as the main culprit.PloS one · 2014Article
- Using a preclinical mouse model of high-grade astrocytoma to optimize p53 restoration therapy.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- P14ARF inhibits human glioblastoma-induced angiogenesis by upregulating the expression of TIMP3.The Journal of clinical investigation · 2012Article
- Integrins and p53 pathways in glioblastoma resistance to temozolomide.Frontiers in oncology · 2012Article
- Deregulated signaling pathways in glioblastoma multiforme: molecular mechanisms and therapeutic targets.Cancer investigation · 2012Review
- Review
- Acquisition of p53 mutations in response to the non-genotoxic p53 activator Nutlin-3.Oncogene · 2011Article
- Radioresistance of human glioma spheroids and expression of HSP70, p53 and EGFr.Radiation oncology (London, England) · 2011Article
- NFKBIA deletion in glioblastomas.The New England journal of medicine · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
P16 and P14ARF are two tumor suppressors encoded by the locus ink4a-arf which is frequently deleted in human tumors. Recent experiments performed with mouse embryonic fibroblasts have shown that P14ARF is an upstream regulator of the P53 pathway. This raises the question as to whether in human tumors the loss of p14arf and mutation of p53 are mutually exclusive events which segregate with genetic alterations at other loci. To examine this question we performed a multigenic analysis on 29 gliomas. We analysed p53 and p14arf in relation with five other genetic loci encoding the most frequently mutated genes in human gliomas: cdkn2a, mdm2, egfr, pten and the chromosomal regions 10q23.3 and 10q25-26. Our study shows for the first time that p53 mutations and p14arf deletions appear mutually exclusive in human glioblastoma, suggesting that they may be functionally redundant in glioma tumorigenesis. The P53 pathway is, therefore, disrupted in 81.8% of malignant gliomas (WHO grades III and IV), either by mutation of the p53 gene (31.8%) or by p14arf deletion (54.5%). These tumors further showed MDM2 overexpression (9.1%), egfr oncogene amplification/egfr overexpression (50%), pten mutations (27.3%) and loss of heterozygosity (LOH) at the chromosomal regions 10q23.3 (86.4%) and 10q25-26 (100%). These alterations did not segregate with p53 mutations or p14arf deletions, while p14arf and cdkn2a were always deleted.
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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.