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Expression data from meningiomas and normal meninges

ABSTRACT: Correlate the gene expression profiles with the most relevant patterns of chromosome abnormalities (cytogenetic subgroups of meningiomas) and the gene expression profiles could help to explain the differences in clinical behaviour of meningiomas. The impact of tumor cytogenetics on the gene expression analyzed in meningiomas. Here, we analyzed the gene expression profiles (GEP) of 47 tumors and correlated them with the most clinical relevant cytogenetic subgroups of meningiomas, including diploid tumors, isolated -22/22q-, del(1p36) alone and complex karyotypes associated with del(1p36) and/or -14q. In addition, 4 samples containing purified RNA extracted from normal meningeal cells (BioChain Institute, Hayward, CA and US Biological, Swampscott, MA, USA) were also processed.

ORGANISM(S): Homo sapiens

SUBMITTER: MariaDolores Tabernero

PROVIDER: E-GEOD-43290 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Expression data from meningiomas and normal meninges

Project description:Correlate the gene expression profiles with the most relevant patterns of chromosome abnormalities (cytogenetic subgroups of meningiomas) and the gene expression profiles could help to explain the differences in clinical behaviour of meningiomas.

2013-01-05 | GSE43290 | GEO

Recurrent somatic mutations in POLR2A define a distinct subset of meningiomas [RNA-seq]

Project description:RNA polymerase II mediates the transcription of all protein-coding genes in eukaryotic cells, a process that is fundamental to life. Genomic mutations in this enzyme have not been previously linked to any pathology in humans, a testament to its indispensable role in cell biology. Based on a combination of next-generation genomic analyses of 775 meningiomas, we report that recurrent somatic p.Gln403Lys or p.Leu438_His439del mutations in POLR2A, which encodes the catalytic subunit of RNA polymerase II, are sufficient to hijack this essential enzyme and drive neoplasia. POLR2A mutant tumors reveal dysregulation of key meningeal identity genes, including WNT6 and ZIC1/ZIC4. In addition to POLR2A, NF2, SMARCB1, TRAF7, KLF4, AKT1, PIK3CA and SMO, we also report somatic mutations in AKT3, PIK3R1, PRKAR1A, and SUFU in meningiomas. Our results identify a role for essential transcriptional machinery in driving tumorigenesis and define mutually exclusive meningioma subgroups with distinct clinical and pathological features. RNAseq data from 19 meningioma tumors representing major mutation groups (NF2/chr22 loss, POLR2A, KLF4/TRAF7, PI3K mutant)

2016-08-21 | E-GEOD-85133 | biostudies-arrayexpress

Recurrent somatic mutations in POLR2A define a distinct subset of meningiomas [array]

Project description:RNA polymerase II mediates the transcription of all protein-coding genes in eukaryotic cells, a process that is fundamental to life. Genomic mutations in this enzyme have not been previously linked to any pathology in humans, a testament to its indispensable role in cell biology. Based on a combination of next-generation genomic analyses of 775 meningiomas, we report that recurrent somatic p.Gln403Lys or p.Leu438_His439del mutations in POLR2A, which encodes the catalytic subunit of RNA polymerase II, are sufficient to hijack this essential enzyme and drive neoplasia. POLR2A mutant tumors reveal dysregulation of key meningeal identity genes, including WNT6 and ZIC1/ZIC4. In addition to POLR2A, NF2, SMARCB1, TRAF7, KLF4, AKT1, PIK3CA and SMO, we also report somatic mutations in AKT3, PIK3R1, PRKAR1A, and SUFU in meningiomas. Our results identify a role for essential transcriptional machinery in driving tumorigenesis and define mutually exclusive meningioma subgroups with distinct clinical and pathological features. Expression microarray data from 121 total samples, including 96 tumors representing the major meningioma mutation groups (NF2/chr22 loss, POLR2A, KLF4/TRAF7, PI3K mutant, Sonic Hedgehog mutant) and 25 control samples (3 dura, 13 adult meninges, and 9 embryonic meninges).

2016-08-21 | E-GEOD-84263 | biostudies-arrayexpress

GeneChip Mapping 500K set and Genome-Wide Human SNP 6.0 Array in meningioma tumors

Project description:Cytogenetic profiles of 50 meningiomas using high-density GeneChip Mapping 500K set and Genome-Wide Human SNP 6.0 Array in the tumor tissues and in the peripheral blood of the same patients. A total of two hundred 500k arrays (100 tumor samples and 100 blood samples) and 14 SNP6.0 arrays (7 tumour samples and 7 peripheral blood samples) were studied to explore the most common recurrent chromosomal abnormalities (gains and losses) in meningiomas. Our results confirm that del(22q) (52%) and del(1p) (16%) (common deleted regions: 22q11.21-22q13.3. and 1p31.2-p36.33) are the most frequent abnormalities. Additionally, recurrent monosomy 14 (8%), del(6p) (10%), del(7p) (10%) and del(19p) (6%) were also observed, while copy number variation (CNV) patterns consistent with recurrent chromosome gains, gene amplification was absent or rare. Based on their overall SNP profiles meningiomas could be classified into: i) diploid cases, ii) meningiomas with a single chromosome change (e.g. monosomy 22/del(22q) and iii) tumours with ≥2 altered chromosomes.

2012-11-30 | GSE42624 | GEO

Global expression profile in a combined study in low grade meningiomas and schwannomas shows upregulation in PDGF, CDH1, SLIT2 and MET.

Project description:Background: Schwannomas and grade I meningiomas are non-metastatic neoplasms that shares the common mutation of gene NF2. They usually appear in Neurofibromatosis type 2 patients. Currently, there is no drug treatment available for both tumors, so the use of wide expression technologies is crucial to find those therapeutic targets. Methodology: Affymetrix Human Gene 1.0 ST was used to test global gene expression in 22 meningiomas, 31 schwannomas and, as non-tumoral controls, 3 healthy meningeal tissues, 8 non-tumoral nerves and 1 primary Schwann cells culture. A non-stringent P-cutoff and fold change were used to establish deregulated genes. Results and discussion: We found a subset of genes that were upregulated in meningiomas and schwannomas when compared to their respectively healthy tissue, including PDGFD, CDH1, SLIT2 and MET. Thus, those genes could be more thoroughly studied as targets in a possible combined treatment. Methodology: Affymetrix Human Gene 1.0 ST was used to test global gene expression in 22 meningiomas, 31 schwannomas and, as non-tumoral controls, 3 healthy meningeal tissues, 8 non-tumoral nerves and 1 primary Schwann cells culture. A non-stringent P-cutoff and fold change were used to establish deregulated genes.

2015-08-30 | E-GEOD-54934 | biostudies-arrayexpress

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2016-08-21 | GSE84263 | GEO

Recurrent somatic mutations in POLR2A define a distinct subset of meningiomas [ChIP-seq]

2016-08-21 | GSE85132 | GEO

Recurrent somatic mutations in POLR2A define a distinct subset of meningiomas [RNA-seq]

2016-08-21 | GSE85133 | GEO

GeneChip Mapping 500K set and Genome-Wide Human SNP 6.0 Array in meningioma tumors

2012-11-30 | E-GEOD-42624 | biostudies-arrayexpress

Genomic landscape of meningiomas

Project description:This SuperSeries is composed of the following subset Series: GSE16581: Genomic landscape of meningiomas: gene expression GSE16583: Genomic landscape of meningiomas: genotyping Refer to individual Series

2010-12-01 | E-GEOD-16584 | biostudies-arrayexpress

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