Frequent Co‐Alterations of TP53, p16/CDKN2A, p14 ARF , PTEN Tumor Suppressor Genes in Human Glioma Cell Lines.

Ishii, Nobuaki; Maier, Daniel; Merlo, Adrian; Tada, Mitsuhiro; Sawamura, Yutaka; Diserens, Annie‐Claire; Van Meir, Erwin G.

doi:10.1111/j.1750-3639.1999.tb00536.x

Cited by 571Glioma Diagnosis and TreatmentCancer-related Molecular PathwaysChromatin Remodeling and Cancer

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Frequent Co‐Alterations of TP53, p16/CDKN2A, p14 ARF , PTEN Tumor Suppressor Genes in Human Glioma Cell Lines.

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Ishii, Nobuaki, Maier, Daniel, Merlo, Adrian, Tada, Mitsuhiro, Sawamura, Yutaka, Diserens, Annie‐Claire, Van Meir, Erwin G.·1999·Brain Pathology

DOI 10.1111/j.1750-3639.1999.tb00536.xPMC PMC8098486

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Abstract

In this study we established the simultaneous status of TP53, p16, p14ARF and PTEN tumor suppressor genes in 34 randomly chosen human glioma cell lines. Nine cell lines (26.4%) harbored mutations or deletions in all four tumor suppressor genes and 22 cell lines (64%) had alterations in at least three. Mutations/deletions were found at the following frequencies: TP53 (76.5%), p14ARF (64.7%), p16 (64.7%), PTEN (73.5%). Thus, there was a high incidence of alterations in the cellular pathways involving the p53 transcription factor (94.1%), the retinoblastoma protein (64.7%) and the PTEN phosphatase (73.5%) and 91% of cell lines carried mutations in two or more pathways. This provides the first clear genetic evidence that these tumor suppressors participate in biological pathways which are functioning separately/independently in glioma cells. The status of the gene alterations did not correlate with tumorigenicity in immunocompromized mice or any clinical parameters. Although the mutation rate was higher in glioma cell lines than that reported for glioma tissues, the alterations were molecularly representative of those found in adult de novo glioblastoma. This study highlights the importance of developing therapeutic approaches applicable to tumors with a broad range of genetic alterations and also provides an invaluable panel of glioma cell lines to make this possible.

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“The p53-ARF-MDM2 pathway is deregulated in 84% of glioblastoma (GBM) patients and 94% of GBM cell lines.”
From The p53 Pathway in Glioblastoma (2018) · cites this paper as [20]
U87 cells are a common model of human gliomas.
“In these experiments, we used tumorigenic U87 cells, a common model of human gliomas (23).”
From MicroRNA 21 Promotes Glioma Invasion by Targeting Matrix Metalloproteinase Regulators (2008) · cites this paper as [23]

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Authors: Ishii, N., Maier, D., Merlo, A., Tada, M., Sawamura, Y., Diserens, A., & Van Meir, E. G.
Affiliations: Centre Hospitalier Universitaire Vaudois (CH)
University Hospital of Basel (CH)
Hokkaido University (JP)
ORCID: Ishii, Nobuaki
Tada, Mitsuhiro
Venue: Brain Pathology
Publisher: Wiley
Published: 1999-07
Volume: 9
Issue: 3
Pages: 469-479
ISSN: 1015-6305 (ISSN-L)
1750-3639
DOI: 10.1111/j.1750-3639.1999.tb00536.x
PMC: PMC8098486
OpenAlex: W2155140015
Cited by: 569
References: 48
Citations by year: 2026: 9 · 2025: 10 · 2024: 24 · 2023: 20 · 2022: 21 · 2021: 23 · 2020: 13 · 2019: 25 · 2018: 14 · 2017: 16 · 2016: 14 · 2015: 27 · 2014: 33 · 2013: 25 · 2012: 34
FWCI: 11.06
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: onlinelibrary.wiley.com/termsAndConditions#vor (vor, 2470 d)
Locations: Brain Pathology (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
IRIS (submittedVersion)
SERVAL (Université de Lausanne) (submittedVersion)
Topics: Health Sciences › Medicine › Oncology › Glioma Diagnosis and Treatment
Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Chromatin Remodeling and Cancer
Keywords: glioma cell lines, TP53 mutation, CDKN2A/p16, p14ARF, PTEN, p53 pathway, glioblastoma, tumorigenicity, genetic alterations
MeSH terms: Adult, Aged, Animals, Brain Neoplasms, Child, DNA Mutational Analysis, Female, Glioma, Humans, Male, Mice, Nude, Middle Aged, Neoplasm Transplantation, Neoplastic Processes, Phosphoric Monoester Hydrolases, Proteins, Sex Factors, Tumor Cells, Cultured, Genes, Tumor Suppressor, Tumor Suppressor Protein p53, Point Mutation, Sequence Deletion, Cyclin-Dependent Kinase Inhibitor p16, Tumor Suppressor Proteins, Tumor Suppressor Protein p14ARF, PTEN Phosphohydrolase, Mice

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Frequent Co‐Alterations of TP53, p16/CDKN2A, p14 ARF , PTEN Tumor Suppressor Genes in Human Glioma Cell Lines.

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