Chromosomal abnormalities in 47 pediatric brain tumors

Agamanolis, Dimitris P.; Malone, James M.

doi:10.1016/0165-4608(94)00123-s

Cited by 57 publications

(35 citation statements)

References 16 publications

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“…In agreement with findings in previous studies (Neumann et al, 1993;Agamanolis and Malone 1995;Roberts et al, 2001;Orr et al, 2002), the PAs and (Deshmukh et al, 2008;Jones et al, 2008;Pfister et al, 2008;Jacob et al, 2009). As it was present in both infratentorial and supratentorial PAs, the gain does not seem to be specific for tumours of a given anatomic location.…”

Section: Genome-wide Array Comparative Genomic Hybridisation (Acgh)supporting

confidence: 81%

Genomic aberrations in 80 cases of primary glioblastoma multiforme: Pathogenetic heterogeneity and putative cytogenetic pathways

Dahlback

Brandal

Meling

et al. 2009

Genes Chromosomes & Cancer

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Screening the whole glioblastoma multiforme (GBM) genome for aberrations is a good starting point when looking for molecular markers that could potentially stratify patients according to prognosis and optimal treatment. We investigated 80 primary untreated GBM using both G‐banding analysis and high‐resolution comparative genomic hybridization (HR‐CGH). Abnormal karyotypes were found in 83% of the tumors. The most common numerical chromosome aberrations were +7, −10, −13, −14, −15, +20, and −22. Structural abnormalities most commonly involved chromosomes 1 and 3, and the short arm of chromosome 9. HR‐CGH verified these findings and revealed additional frequent losses at 1p34‐36, 6q22‐27, and 19q12‐13 and gains of 3q26 and 12q13‐15. Although most karyotypes and gain/loss patterns were complex, there was also a distinct subset of tumors displaying simple karyotypic changes only. There was a statistically significant association between trisomy 7 and monosomy 10, and also between +7/−10 as putative primary aberrations and secondary losses of 1p, 9p, 13q, and 22q. The low number of tumors in the rarer histological tumor subgroups precludes definite conclusions, but there did not seem to be any clear‐cut cytogenetic‐pathological correlations, perhaps with the exception of ring chromosomes in giant cell glioblastomas. Our findings demonstrate that although GBM is a pathogenetically very heterogeneous group of diseases, distinct genomic aberration patterns exist. © 2009 Wiley‐Liss, Inc.

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Section: Genome-wide Array Comparative Genomic Hybridisation (Acgh)supporting

confidence: 81%

Genomic aberrations in 80 cases of primary glioblastoma multiforme: Pathogenetic heterogeneity and putative cytogenetic pathways

Dahlback

Brandal

Meling

et al. 2009

Genes Chromosomes & Cancer

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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%

High-resolution, dual-platform aCGH analysis reveals frequent HIPK2 amplification and increased expression in pilocytic astrocytomas

Deshmukh

Yeh

et al. 2008

Oncogene

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“…Whereas ependymomas occur in both children and adults, subependymomas and myxopapillary ependymomas are more common in adults. 267 The CGAP website identifies 106 ependymoma karyotypes 1,22,50,62,64,83,92,117,161,175,207,209,225,227,257,270,278,281,293,294 (also reviewed by Mazewski,et al 161 ). The karyotypes described are predominantly normal, and when abnormal are near-diploid, and are characterized by gains and losses of entire chromosomes.…”

Section: Neurosurg Focus / Volume 19 / November 2005mentioning

confidence: 99%

“…The choroid plexus carcinoma is the malignant form of this tumor. The CGAP database describes 15 cases 1,22,50,69,71,147,165,175,196,202,203,228 of choroid plexus papilloma or carcinoma. The karyotypes are predominantly near-diploid, hypodiploid, or hypotriploid, and are characterized by whole chromosomal gains and losses; these include gains of chromosomes 5,6,7,8,9,12,15,18, and 20 and losses of chromosomes 1, 3, 10, 16, 17, 21, and 22.…”

Section: Nonglial Tumorsmentioning

confidence: 99%

“…In 410 cases of astrocytomas Grades II and IV found at the CGAP site (large studies 1,22,26,27,29,30,50,62,117,141,149,154,159,175,201,207,211,249,270,295,298 ), karyotypes similar to those among the lowgrade astrocytomas persist, namely normal karyotypes or those only missing a sex chromosome, as well as karyotypes with copy number changes from chromosomes 7, 9, 10, 19, and 22, as described earlier. As with the low-grade tumors, these karyotypes typically possess gains and losses of the entire chromosome.…”

mentioning

confidence: 99%

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Molecular cytogenetic analysis in the study of brain tumors: findings and applications

Bayani¹,

Pandita²,

Squire³

2005

FOC

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Classic cytogenetics has evolved from black and white to technicolor images of chromosomes as a result of advances in fluorescence in situ hybridization (FISH) techniques, and is now called molecular cytogenetics. Improvements in the quality and diversity of probes suitable for FISH, coupled with advances in computerized image analysis, now permit the genome or tissue of interest to be analyzed in detail on a glass slide. It is evident that the growing list of options for cytogenetic analysis has improved the understanding of chromosomal changes in disease initiation, progression, and response to treatment. The contributions of classic and molecular cytogenetics to the study of brain tumors have provided scientists and clinicians alike with new avenues for investigation. In this review the authors summarize the contributions of molecular cytogenetics to the study of brain tumors, encompassing the findings of classic cytogenetics, interphase- and metaphase-based FISH studies, spectral karyotyping, and metaphase- and array-based comparative genomic hybridization. In addition, this review also details the role of molecular cytogenetic techniques in other aspects of understanding the pathogenesis of brain tumors, including xenograft, cancer stem cell, and telomere length studies.

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Chromosomal abnormalities in 47 pediatric brain tumors

Cited by 57 publications

References 16 publications

Genomic aberrations in 80 cases of primary glioblastoma multiforme: Pathogenetic heterogeneity and putative cytogenetic pathways

Genomic aberrations in 80 cases of primary glioblastoma multiforme: Pathogenetic heterogeneity and putative cytogenetic pathways

High-resolution, dual-platform aCGH analysis reveals frequent HIPK2 amplification and increased expression in pilocytic astrocytomas

Molecular cytogenetic analysis in the study of brain tumors: findings and applications

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