Copy number analysis of human glioblastoma multiforme
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE13021 | GEO | 2009/01/05
SECONDARY ACCESSION(S): PRJNA112561
REPOSITORIES: GEO
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Project description:Copy number analysis of human GBM samples were performed, and a high frequency of deletions of the PTPRD gene on chromosome 9p23-24.1 were identified. Keywords: SNP microarray, glioblastoma multiforme, copy number, amplification, deletion Genomic DNA from 58 GBM tumor samples were hybridized to Affymetrix 250K NspI Gene Chip Arrays and analyzed by dChip using the hg17 genome assembly.
2009-01-04 | E-GEOD-13021 | biostudies-arrayexpress
Project description:Glioblastoma multiforme (GBM) is a highly heterogeneous disease that shows an wide range of genetic abnormalities in comparison to other astrocytic tumors. We have extracted between 4 and 8 tumor subsamples from different areas of the malignant tissue that were at least 1cm apart. Our aim to asses the intra-tumoral heterogeneity by comparing copy number aberrations in different tumor areas to uncover important dynamics underlying GBM progression.
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Project description:Genomic copy number number characterisation of glioblastoma (GBM) cell lines.
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Project description:Glioblastoma multiforme (GBM) is a lethal malignancy whose clinical intransigence has been linked to extensive intra-clonal genetic and phenotypic diversity and therapeutic resistance of cancer stem cells (CSCs). This interpretation embodies an implicit assumption that CSCs are themselves genetically diverse. To test this, we screened neurosphere cultures by SNP arrays to identify copy number alterations (CNA) (minimum of three) that could be visualised in single cells by multi-colour FISH. Interrogation of neurosphere-derived cells (from four patients) and cells derived from secondary transplants of these same cells in Nod/Scid mice allowed us to infer clonal phylogenic architecture and the likely derivation of functional CSCs. This proof-of-principle experiment revealed that more than one sub-clone (but not all) in each GBM had functionally defined, genetically distinct stem cells.
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Project description:The purpose of this study is to determine whether the combination of two agents, INC280 and bevacizumab, is safe and effective when administered to patients with Glioblastoma Multiforme (GBM) who have progressed after receiving prior therapy or who have unresectable GBM.
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Project description:Renal tumors with complex morphology require extensive workup for accurate classification. Chromosomal aberrations that define subtypes of renal epithelial neoplasms have been reported. We explored if whole-genome chromosome copy number and loss-of-heterozygosity analysis with single nucleotide polymorphism (SNP) arrays can be used to identify these aberrations. Keywords: Chromosome copy number and LOH analysis with SNP Genotyping Arrays
2008-01-24 | GSE9469 | GEO
Project description:We used high-resolution SNP genotyping to identify regions of genomic gain and loss in the genome of 212 medulloblastomas, a malignant pediatric brain tumor. Focal amplifications of fifteen known oncogenes and focal deletions of twenty known tumor suppressor genes (TSG) were revealed, most not previously implicated in medulloblastoma. Importantly, we identified novel amplifications and homozygous deletions, including recurrent, mutually exclusive, highly focal genetic events in genes targeting histone lysine methylation, particularly histone 3, lysine 9 (H3K9). Post-translational modification of histone proteins is critical for regulation of gene expression, can participate in determining stem cell fates, and has been implicated in carcinogenesis. Consistent with our genetic data, restoration of expression of genes controlling H3K9 methylation greatly diminishes proliferation of medulloblastoma in vitro. Copy number aberrations of genes with critical roles in writing, reading, removing, and blocking the state of histone lysine methylation, particularly H3K9, suggest that defective control of the histone code contributes to the pathogenesis of medulloblastoma. Keywords: Affymetrix SNP array Genomic DNA isolated from fresh frozen primary human medulloblastomas and medulloblastoma cell lines were subjected to SNP genotyping using either Affymetrix 100K or 500K GeneChip Mapping array sets for the purpose of obtaining genome-wide copy number and LOH profiles.
2010-04-06 | E-GEOD-14437 | biostudies-arrayexpress
Project description:We used high-resolution SNP genotyping to identify regions of genomic gain and loss in the genome of 212 medulloblastomas, a malignant pediatric brain tumor. Focal amplifications of fifteen known oncogenes and focal deletions of twenty known tumor suppressor genes (TSG) were revealed, most not previously implicated in medulloblastoma. Importantly, we identified novel amplifications and homozygous deletions, including recurrent, mutually exclusive, highly focal genetic events in genes targeting histone lysine methylation, particularly histone 3, lysine 9 (H3K9). Post-translational modification of histone proteins is critical for regulation of gene expression, can participate in determining stem cell fates, and has been implicated in carcinogenesis. Consistent with our genetic data, restoration of expression of genes controlling H3K9 methylation greatly diminishes proliferation of medulloblastoma in vitro. Copy number aberrations of genes with critical roles in writing, reading, removing, and blocking the state of histone lysine methylation, particularly H3K9, suggest that defective control of the histone code contributes to the pathogenesis of medulloblastoma. Keywords: Affymetrix SNP array
2009-04-15 | GSE14437 | GEO
Project description:In order to benchmark the reproducibility of Affymetrix Genome-Wide Human SNP Array 6.0 for detecting copy-number alterations, we performed replicate hybridizations of 3 tumor cell lines and 2 paired normal cell lines obtained from the American Type Culture Collection (ATCC). We calculated copy numbers at each SNP probeset by a custom copy-number pipeline (PMID: 18772890). For each cell line, copy number data from replicate arrays are supplied in the accompanying matrix files. For each SNP probeset, we calculated the median copy number across replicate arrays. We compared the copy-number alterations detected by Circular Binary Segmentation segmentation of these arrays with statistical analyses of short sequence reads obtained from the Illumina/Solexa 1G GenomeAnalyzer. Shotgun sequencing results can be found in the NCBI Short Read Archive, accession number SRP000246 Keywords: disease state analysis
2008-11-14 | GSE13372 | GEO
Project description:Copy-number variants (CNVs) are large-scale amplifications or deletions of DNA that can drive rapid adaptive evolution and result in large-scale changes in gene expression. Whereas alterations in the copy number of one or more genes within a CNV can confer a selective advantage, other genes within a CNV can decrease fitness when their dosage is changed. Dosage compensation - in which the gene expression output from multiple gene copies is less than expected - is one means by which an organism can mitigate the fitness costs of deleterious gene amplification. Previous research has shown evidence for dosage compensation at both the transcriptional level and at the level of protein expression; however, the extent of compensation differs substantially between genes, strains, and studies. Here, we investigated sources of dosage compensation at multiple levels of gene expression regulation by defining the transcriptome, translatome and proteome of experimentally evolved yeast (Saccharomyces cerevisiae) strains containing adaptive CNVs.
2023-11-01 | PXD046587 | Pride