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
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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“TP53 mutations have been reported both in primary and secondary grade lesions (30% and 65%, respectively) [86,87].”
From The p53 Pathway in Glioblastoma (2018) · cites this paper as [86]
Citations
Cites
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The Biology of Cancer: Metabolic Reprogramming Fuels Cell Growth and Proliferation
DeBerardinis, R. J., Lum, J. J., Hatzivassiliou, G., & Thompson, C. B. (2008) · Cell Metabolism · doi:10.1016/j.cmet.2007.10.002 · Cited by 4,088
Glioblastoma multiforme: a review of where we have been and where we are going
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The p53 Pathway in Glioblastoma
Zhang, Y., Dube, C., Gibert, M., Cruickshanks, N., Wang, B., Coughlan, M., Yang, Y., Setiady, I., Deveau, C., Saoud, K., et al. (2018) · Cancers · doi:10.3390/cancers10090297 · Cited by 440
Reardon, D. A., & Wen, P. Y. (2006) · The Oncologist · doi:10.1634/theoncologist.11-2-152 · Cited by 233
Rho/ROCK and MAPK signaling pathways are involved in glioblastoma cell migration and proliferation.
Zohrabian, V. M., Forzani, B., Chau, Z., Murali, R., & Jhanwar‐Uniyal, M. (2009) · PubMed · Cited by 177
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
- 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
- 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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