Intratumoral Patterns of Genomic Imbalance in Glioblastomas

Nobusawa, Sumihito; Lachuer, Joel; Wierinckx, Anne; Kim, Young Ho; Huang, Jian; Legras, Catherine; Kleihues, Paul; Ohgaki, Hiroko

doi:10.1111/j.1750-3639.2010.00395.x

Cited by 76Glioma Diagnosis and TreatmentGenomic variations and chromosomal abnormalitiesCancer Genomics and Diagnostics

Intratumoral Patterns of Genomic Imbalance in Glioblastomas

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Nobusawa, Sumihito, Lachuer, Joel, Wierinckx, Anne, Kim, Young Ho, Huang, Jian, Legras, Catherine, Kleihues, Paul, Ohgaki, Hiroko·2010·Brain Pathology

DOI 10.1111/j.1750-3639.2010.00395.xPMC PMC8094667

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Abstract

Glioblastomas are morphologically and genetically heterogeneous, but little is known about the regional patterns of genomic imbalance within glioblastomas. We recently established a reliable whole genome amplification (WGA) method to randomly amplify DNA from paraffin‐embedded histological sections with minimum amplification bias [Huang et al (J Mol Diagn 11: 109–116, 2009)]. In this study, chromosomal imbalance was assessed by array comparative genomic hybridization (CGH; Agilent 105K, Agilent Technologies, Santa Clara, CA, USA), using WGA‐DNA from two to five separate tumor areas of 14 primary glioblastomas (total, 41 tumor areas). Chromosomal imbalances significantly differed among glioblastomas; the only alterations that were observed in ≥6 cases were loss of chromosome 10q, gain at 7p and loss of 10p. Genetic alterations common to all areas analyzed within a single tumor included gains at 1q32.1 (PIK3C2B, MDM4), 4q11–q12 (KIT, PDGFRA), 7p12.1–11.2 (EGFR), 12q13.3–12q14.1 (GLI1, CDK4) and 12q15 (MDM2), and loss at 9p21.1–24.3 (p16 INK4a/p14 ARF), 10p15.3–q26.3 (PTEN, etc.) and 13q12.11–q34 (SPRY2, RB1). These are likely to be causative in the pathogenesis of glioblastomas (driver mutations). In addition, there were numerous tumor area‐specific genomic imbalances, which may be either nonfunctional (passenger mutations) or functional, but constitute secondary events reflecting progressive genomic instability, a hallmark of glioblastomas.

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Array comparative genome hybridization and WGA-DNA from two to five separate tumor areas of 14 glioblastomas demonstrated common genetic alterations including amplifications in 1q32.1 and 12q15, which contain MDM4 and MDM2.
“An assessment of chromosomal imbalance using array comparative genome hybridization and WGA-DNA from two to five separate tumor areas of 14 GBMs demonstrated that there was a list of genetic alterations that were common to all tumor areas, including amplifications in 1q32.1 and 12q15, which contain MDM4 and MDM2 [42].”
From The p53 Pathway in Glioblastoma (2018) · cites this paper as [42]

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Authors: Nobusawa, S., Lachuer, J., Wierinckx, A., Kim, Y. H., Huang, J., Legras, C., Kleihues, P., & Ohgaki, H.
Affiliations: Centre international de recherche sur le cancer (FR)
University Hospital Zurich (CH)
ORCID: Nobusawa, Sumihito
Wierinckx, Anne
Kim, Young Ho
Huang, Jian
Venue: Brain Pathology
Publisher: Wiley
Published: 2010-08-02
Volume: 20
Issue: 5
Pages: 936-944
ISSN: 1015-6305 (ISSN-L)
1750-3639
DOI: 10.1111/j.1750-3639.2010.00395.x
PMC: PMC8094667
OpenAlex: W1953848330
Cited by: 75
References: 35
Citations by year: 2025: 1 · 2024: 1 · 2023: 6 · 2022: 4 · 2021: 3 · 2020: 5 · 2019: 8 · 2018: 4 · 2017: 4 · 2016: 4 · 2015: 6 · 2014: 7 · 2013: 5 · 2012: 8
FWCI: 3.00
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Locations: Brain Pathology (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Topics: Health Sciences › Medicine › Genetics › Glioma Diagnosis and Treatment
Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genomic variations and chromosomal abnormalities
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
Keywords: glioblastoma, intratumoral heterogeneity, chromosomal imbalances, genomic instability, driver mutations, passenger mutations, whole genome amplification, paraffin-embedded tissue, 10q loss, EGFR, PTEN, p16INK4a, KIT, PDGFRA, Gli1, CDK4, MDM2, MDM4
MeSH terms: Adult, Aged, Aged, 80 and over, Brain Neoplasms, Chromosome Aberrations, Female, Glioblastoma, Humans, Male, Middle Aged, Reproducibility of Results, Genome, Human, Loss of Heterozygosity, Receptor, Platelet-Derived Growth Factor alpha, Proto-Oncogene Proteins c-akt, Comparative Genomic Hybridization

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Intratumoral Patterns of Genomic Imbalance in Glioblastomas

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