Karyotypes in 90 human gliomas

Thiel, Gundula; Losanowa, T.; Kintzel, Dieter; Nisch, Gunter; Martin, H; Vorpahl, K; Witkowski, Regine

doi:10.1016/0165-4608(92)90095-p

Cited by 132 publications

(71 citation statements)

References 26 publications

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“…9,10 Molecular studies demonstrated the amplification of several genes in these tumors, especially of the EGFR gene; the amplified sequences were found located on dmin, analyzed in a small number of cases by in situ hybridization of tumor metaphases. 15,16 However, studies by FISH in interphase nuclei are more frequent, displaying a considerable heterogeneity of EGFR copy number.…”

Section: Discussionmentioning

confidence: 99%

“…8 The first evidence of gene amplification in glioblastoma was provided by cytogenetic analyses that exhibited the presence of dmin. 9,10 Molecular screening for gene amplification revealed frequent amplification of the EGFR, observed in about 35-70% of glioblastomas. 8,11,12 Differences in the frequency of EGFR amplification are most probably due to different methods used, such as Southern blot, polymerase chain reaction (PCR), and fluorescent in situ hybridization (FISH).…”

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New pattern of EGFR amplification in glioblastoma and the relationship of gene copy number with gene expression profile

et al. 2010

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Gene amplification is a process that is characterized by an increase in the copy number of a restricted region in a chromosome arm, and is frequently associated with an overexpression of the corresponding amplified gene. Amplified DNA can be organized either as extrachromosomal elements, repeated units at a single locus or scattered throughout the genome. The amplification of the gene for epidermal growth factor receptor (EGFR) is a common finding in glioblastomas and the amplified gene copies appears as double minutes. The aim of this study was to investigate the different patterns of EGFR amplification in 40 cases of glioblastoma using FISH analysis in metaphases and paraffin sections, and to investigate the relationship of gene copy number with gene expression profile. The analysis of copy number alterations of EGFR was validated by quantitative PCR and SNP microarrays. We observed that in 42% of the cases, the type of amplification of EGFR was as double minute chromosomes. In addition, we detected another type of amplification, with extra copies of EGFR inserted in different loci of chromosome 7, present in 28% of cases. In this form of amplification, the number of copies is small, and the percentage of cells with EGFR amplification is rarely more than 15%. This model of amplification could correspond to a variant of the insertion mechanism, or a consequence of a process of duplication. Our results suggest that this mechanism could represent an early stage of amplification in glioblastomas. Overall, we found a close correlation between EGFR gene copy-number alterations and the level of EGFR protein expression. However, all cases with a high level of mRNA exhibited strong expression for the EGFR protein, and most cases with a low level of mRNA showed no overexpression of EGFR protein.

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Section: Discussionmentioning

confidence: 99%

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New pattern of EGFR amplification in glioblastoma and the relationship of gene copy number with gene expression profile

et al. 2010

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“…Several studies have linked the morphological features of anaplasia to a poor outcome or suggested ependymoma grade affects survival postradiotherapy (1,5,13,14,(27)(28)(29)(30)(31)51). However other studies refuted this or failed to establish an association between anaplasia and prognosis, including those adopting a WHO classification system (reviewed in refs.…”

Section: Histology Tumor Morphology and Prognosismentioning

confidence: 99%

Pediatric Ependymoma: Biological Perspectives

Kilday

Rahman

Dyer

et al. 2009

Molecular Cancer Research

168

204

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Pediatric ependymomas are enigmatic tumors that continue to present a clinical management challenge despite advances in neurosurgery, neuroimaging techniques, and radiation therapy. Difficulty in predicting tumor behavior from clinical and histological factors has shifted the focus to the molecular and cellular biology of ependymoma in order to identify new correlates of disease outcome and novel therapeutic targets. This article reviews our current understanding of pediatric ependymoma biology and includes a meta-analysis of all comparative genomic hybridization (CGH) studies done on primary ependymomas to date, examining more than 300 tumors. From this meta-analysis and a review of the literature, we show that ependymomas in children exhibit a different genomic profile to those in adults and reinforce the evidence that ependymomas from different locations within the central nervous system (CNS) are distinguishable at a genomic level. Potential biological markers of prognosis in pediatric ependymoma are assessed and the ependymoma cancer stem cell hypothesis is highlighted with respect to tumor resistance and recurrence. We also discuss the shifting paradigm for treatment modalities in ependymoma that target molecular alterations in tumor-initiating cell populations. (Mol Cancer Res 2009;7(6):765-86)

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“…Similarly, although chromosomal aberrations or amplification/deletion of specific genes related to cell cycle control, growth factor receptors and signal transduction pathways are commonly identified in other glioma subtypes (Koschny et al, 2002;Schmidt et al, 2002;Ohgaki et al, 2004;Ohgaki, 2005), most cytogenetic studies have shown that the majority of PAs have normal karyotypes. Structural aberrations involving chromosomes 6, 7, 8, 11, 17 and 19 have been reported in a few cases (Jenkins et al, 1989;Thiel et al, 1992;Agamanolis and Malone, 1995), and the most consistently identified cytogenetic changes involve gains on chromosomes 7 and 8 (White et al, 1995;Zattara-Cannoni et al, 1998;Sanoudou et al, 2000;Jones et al, 2006). We have previously identified a transcript on chromosome 8 whose expression is increased in PA (Sharma et al, 2006); however, no specific genes have been implicated on chromosome 7.…”

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confidence: 99%