Trial reportBrain pathology (Zurich, Switzerland)1997
Association of EGFR gene amplification and CDKN2 (p16/MTS1) gene deletion in glioblastoma multiforme.
Trial report in Brain pathology (Zurich, Switzerland), 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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
44 citing papers in PubMed, 129 citations in OpenAlex.
- Survival of patients with glioblastoma multiforme is not influenced by altered expression of p16, p53, EGFR, MDM2 or Bcl-2 genes.Brain pathology (Zurich, Switzerland) · 1998Trial
- Glioblastoma multiforme: insights into pathogenesis, key signaling pathways, and therapeutic strategies.Molecular cancer · 2025Review
- EGFR suppresses p53 function by promoting p53 binding to DNA-PKcs: a noncanonical regulatory axis between EGFR and wild-type p53 in glioblastoma.Neuro-oncology · 2022Article
- CiberAMP: AnBiology · 2022Article
- Current understanding of gliomagenesis: from model to mechanism.International journal of medical sciences · 2022Review
- Clonal Evolution of a High-Grade Pediatric Glioma With Distant Metastatic Spread.Neurology. Genetics · 2021Article
- Comprehensive genetic alteration profiling in primary and recurrent glioblastoma.Journal of neuro-oncology · 2019Article
- Toward precision medicine in glioblastoma: the promise and the challenges.Neuro-oncology · 2015Review
- Arsenic trioxide sensitizes glioblastoma to a myc inhibitor.PloS one · 2015Article
- EGFR-dependent mechanisms in glioblastoma: towards a better therapeutic strategy.Cellular and molecular life sciences : CMLS · 2014Review
- Testing of SNS-032 in a Panel of Human Neuroblastoma Cell Lines with Acquired Resistance to a Broad Range of Drugs.Translational oncology · 2013Article
- Radiation-induced upregulation of telomerase activity escapes PI3-kinase inhibition in two malignant glioma cell lines.International journal of oncology · 2013Article
- Curcumin and its derivatives: their application in neuropharmacology and neuroscience in the 21st century.Current neuropharmacology · 2013Article
- 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
- Human neuroblastoma cells with acquired resistance to the p53 activator RITA retain functional p53 and sensitivity to other p53 activating agents.Cell death & disease · 2012Article
- Review
- Adaptation of cancer cells from different entities to the MDM2 inhibitor nutlin-3 results in the emergence of p53-mutated multi-drug-resistant cancer cells.Cell death & disease · 2011Article
- Aberrant signaling pathways in glioma.Cancers · 2011Article
- The nature and timing of specific copy number changes in the course of molecular progression in diffuse gliomas: further elucidation of their genetic "life story".Brain pathology (Zurich, Switzerland) · 2011Article
- Update and developments in the treatment of glioblastoma multiforme - focus on bevacizumab.Pharmacogenomics and personalized medicine · 2010Article
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 2 institutions in 2 countries.
Funding
Abstract
Glioblastoma multiforme (GBM) can be divided into genetic subsets: approximately one-third of GBM, primarily in older adults, have EGFR amplification; another one-third, primarily in younger adults, have TP53 mutation. The majority of GBM also have homozygous deletions of the CDKN2 (p16/MTS1) gene, resulting in cell cycle deregulation and elevated proliferation indices. We evaluated the relationship between CDKN2 deletions and the GBM subsets as defined by EGFR amplification or TP53 mutation in 70 GBM. Twenty-eight cases (40%) had EGFR amplification, 21 (30%) had TP53 mutation, and 21 (30%) had neither change. CDKN2 deletions were present in 36 (51%) GBM. Of the 28 GBM with EGFR amplification, 20 (71%) had CDKN2 deletion (p = 0.0078). The remaining 16 cases with CDKN2 loss were divided between GBM with TP53 mutations (6 cases) and GBM with neither EGFR amplification nor TP53 mutation (10 cases). Thus, CDKN2 deletions occur twice as commonly in GBM with EGFR amplification (71%) than in GBM with TP53 mutation (29%). CDKN2 deletions occurred in GBM from patients somewhat older than those patients with GBM lacking CDKN2 deletion (mean age 53 vs. 48 years). Specifically among GBM with EGFR amplification, those with CDKN2 deletions also occurred in patients slightly older than those few GBM without CDKN2 deletions (mean age 55 vs. 51 years). The presence of CDKN2 deletions in most GBM with EGFR amplification and in generally older patients may provide one explanation for the potentially more aggressive nature of such tumors.
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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.