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Cited by 235Glioma Diagnosis and TreatmentCancer Genomics and DiagnosticsCancer-related Molecular Pathways

The DOI matches its Crossref record; 64 of the 64 references it cites were found in a registry or an index.

Genetic pathways to glioblastomas

Ohgaki, Hiroko·2005·Neuropathology
DOI 10.1111/j.1440-1789.2004.00600.x
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Abstract

Glioblastomas, the most frequent and malignant human brain tumors, may develop de novo (primary glioblastoma) or by progression from low-grade or anaplastic astrocytoma (secondary glioblastoma). These glioblastoma subtypes constitute distinct disease entities that affect patients of different ages and develop through different genetic pathways. Our recent population-based study in the Canton of Zürich, Switzerland, shows that primary glioblastomas develop in older patients (mean age, 62 years) and typically show LOH on chromosome 10q (69%) and other genetic alterations (EGFR amplification, TP53 mutations, p16INK4a deletion, and PTEN mutations) at frequencies of 24-34%. Secondary glioblastomas develop in younger patients (mean, 45 years) and frequently show TP53 mutations (65%) and LOH 10q (63%). Common to both primary and secondary glioblastoma is LOH on 10q, distal to the PTEN locus; a putative suppressor gene at 10q25-qter may be responsible for the glioblastoma phenotype. Of the TP53 point mutations in secondary glioblastomas, 57% were located in hotspot codons 248 and 273, while in primary glioblastomas, mutations were more widely distributed. Furthermore, G:C-->A:T mutations at CpG sites were more frequent in secondary than in primary glioblastomas (56% vs 30%). These data suggest that the TP53 mutations in these glioblastoma subtypes arise through different mechanisms. There is evidence that G:C-->A:T transition mutations at CpG sites in the TP53 gene are significantly more frequent in low-grade astrocytomas with promoter methylation of the O6-methylguanine-DNA methyltransferase (MGMT) gene than in those without methylation. This suggests that, in addition to deamination of 5-methylcytosine (the best known mechanism of formation of G:C-->A:T transitions at CpG sites), involvement of alkylating agents that produce O6-methylguanine or related adducts recognized by MGMT cannot be excluded in the pathway leading to secondary glioblastomas.

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Crossref · 10.1111/j.1440-1789.2004.00600.x

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Research works printed but not linked: 1

  1. Kleihues P, 2000, WHO Classification of Tumours. Pathology and Genetics of Tumours of the Nervous System.

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Metadata

Authors
Ohgaki, H.
Affiliations
Centre international de recherche sur le cancer (FR)
Corresponding author
Ohgaki, Hiroko
Venue
Neuropathology
Publisher
Wiley
Published
2005-02-28
Volume
25
Issue
1
Pages
1-7
ISSN
  • 0919-6544 (ISSN-L)
  • 1440-1789
DOI
10.1111/j.1440-1789.2004.00600.x
OpenAlex
W2097876071
Cited by
235
References
64
Citations by year
2026: 4 · 2025: 2 · 2024: 6 · 2023: 5 · 2022: 3 · 2021: 4 · 2020: 8 · 2019: 8 · 2018: 7 · 2017: 6 · 2016: 14 · 2015: 8 · 2014: 12 · 2013: 11 · 2012: 11
FWCI
3.08
Type
journal article
Language
en
Open access
closed
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Locations
  • Neuropathology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Oncology › Glioma Diagnosis and Treatment
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
  • Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
Keywords
glioblastoma, primary glioblastoma, secondary glioblastoma, low-grade astrocytoma, anaplastic astrocytoma, tumor progression, TP53 mutation, promoter methylation, MGMT, alkylating agents, EGFR amplification, PTEN mutation, suppressor genes, gene pathways
MeSH terms
Age Factors, Brain Neoplasms, Glioblastoma, Humans, Middle Aged

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