ArticleJournal of neuro-oncology2003
Deregulation of the p14ARF/Mdm2/p53 pathway and G1/S transition in two glioblastoma sets.
Article in Journal of neuro-oncology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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.
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Who cites it
10 citing papers in PubMed, 21 citations in OpenAlex.
- Cystic glioblastoma IDH-wildtype: genetic alterations and outcomes.Journal of neuro-oncology · 2025Article
- New phase therapeutic pursuits for targeted drug delivery in glioblastoma multiforme.Exploration of targeted anti-tumor therapy · 2022Review
- The p53 Pathway in Glioblastoma.Cancers · 2018Review
- Article
- Connective tissue growth factor associated with oncogenic activities and drug resistance in glioblastoma multiforme.International journal of cancer · 2010Article
- Cerebral glioblastoma with oligodendrogliomal component: analysis of 36 cases.Journal of neuro-oncology · 2009Article
- Therapeutic targets in the ARF tumor suppressor pathway.Current medicinal chemistry · 2007Review
- Search for germline alterations in CDKN2A/ARF and CDK4 of 42 Jewish melanoma families with or without neural system tumours.British journal of cancer · 2005Article
- Mutant, wild type, or overall p53 expression: freedom from clinical progression in tumours of astrocytic lineage.British journal of cancer · 2004Article
- Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sixty-one glioblastomas have been studied, subdivided into the categories of classic glioblastomas (GBM) and glioblastomas with astrocytic (GBA) and oligodendroglial (GBO) differentiated areas. On surgical samples, TP53, Mdm2, CDKN2A/p16-p14 alterations were studied by molecular biology techniques and by immunohistochemistry. It has been found that Mdm2 amplification was more frequent in GBM than in GBA and GBO, that p14ARF was inactivated in a high percentage of cases in the three tumor categories. Both these and other alterations did not reach a statistical significance, with the exception of CDKN2A/p16 homozygous deletion which showed the highest frequency in GBO. The latter finding could be in line with the observation that CDKN2A/p16 inactivation is a step in the molecular pathway to tumor progression in oligodendrogliomas. TP53 mutations and Mdm2 amplifications were mutually exclusive, whereas TP53 mutations and CDKN2A/p14 inactivation coexisted in 5 cases. The alterations of the p53/Mdm2/p14ARF pathway occurred in 73% of cases and in 80% of cases if CDKN2A homozygous deletions were associated. All glioblastomas with gemistocytic areas showed p14ARF inactivation. Immunohistochemistry showed higher percentages of positivity in comparison with molecular genetics, but with similar variations.
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Registered trials
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