Targeted gene expression panel for meningiomas
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ABSTRACT:
PROVIDER: PRJNA917520 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:A custom Nanostring nCounter panel of 100 or 75 meningioma related genes and reference genes was developed, and performed on human frozen and FFPE meningioma samples. This was done as part of a study developing and validating a targeted gene expression biomarker for meningioma outcomes after surgey and benefit from raditherapy.
2023-09-06 | GSE222054 | GEO
Project description:Primary outcome(s): Gene expression of targeted genes
| 2625389 | ecrin-mdr-crc
Project description:Meningiomas are one of the most common adult brain tumors. For most patients, surgical excision is curative. However, up to 20% recur. Currently, the molecular determinants predicting recurrence and malignant transformation are lacking. We performed global genetic and genomic analysis of 85 meningioma samples of various grades. Copy number alterations were assessed by 100K SNP arrays and correlated with gene expression, proliferation indices, and clinical outcome. In addition to chromosome 22q loss, which was detected in the majority of clinical samples, chromosome 18q and 6q loss significantly predicted recurrence and was associated with anaplastic histology. Five classes of meningiomas were detected by gene expression analysis that correlated with copy number alterations, recurrence risk, and malignant histology. These classes more accurately predicted tumor recurrence than Ki-67 index, the gold standard for determining risk of recurrence, and highlight substantial expression heterogeneity between meningiomas. These data offer the most complete description of the genomic landscape of meningiomas and provide a set of tools that could be used to more accurately stratify meningioma patients into prognostic risk groups.
2010-11-30 | GSE16581 | GEO
Project description:Meningiomas, named for their cell of origin, are the most common intracranial tumors in adults, representing 39% of all primary adult central nervous system tumors. These tumors originate in the meninges, which are the outer three layers of tissue between the skull and the brain that cover and protect the brain just under the skull. Most meningioma tumors (85-90 percent) are categorized as benign, with the remaining 10-15 percent being atypical meningioma or malignant meningioma (cancerous). The word “benign” can be misleading for meningiomas. Depending on location and growth rate, a benign meningioma brain tumor may impinge on vital nerves or compress the brain, causing disability. They may even become life threatening. We describe transcriptional signatures of four most common groups of benign meningiomas. Each subgroup of meningiomas displayed a unique gene expression program identifying signaling pathways potentially implicated in the tumorigenesis. These findings will improve our understanding of meningioma tumorigenesis. Objective: To define gene expression signatures of the most common subtypes of meningiomas to better understand cellular processes and signaling pathways specific for each tumor genotype.
2023-03-10 | GSE221429 | GEO
Project description:Specific gene expression signatures of low grade meningiomas
| PRJNA914288 | ENA
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
Project description:Meningiomas are one of the most common adult brain tumors. For most patients, surgical excision is curative. However, up to 20% recur. Currently, the molecular determinants predicting recurrence and malignant transformation are lacking. We performed global genetic and genomic analysis of 85 meningioma samples of various grades. Copy number alterations were assessed by 100K SNP arrays and correlated with gene expression, proliferation indices, and clinical outcome. In addition to chromosome 22q loss, which was detected in the majority of clinical samples, chromosome 18q and 6q loss significantly predicted recurrence and was associated with anaplastic histology. Five classes of meningiomas were detected by gene expression analysis that correlated with copy number alterations, recurrence risk, and malignant histology. These classes more accurately predicted tumor recurrence than Ki-67 index, the gold standard for determining risk of recurrence, and highlight substantial expression heterogeneity between meningiomas. These data offer the most complete description of the genomic landscape of meningiomas and provide a set of tools that could be used to more accurately stratify meningioma patients into prognostic risk groups. Tumor biopsies from 43 female and 25 male subjects with sporadic meningioma were identified from the UCLA Neuro-oncology Program Tissue Bank through institutional review board approved protocols. 43 tumors were designated "benign" WHO I, 19 tumors were "atypical" WHO II, and 6 were "anaplastic" WHO III. Gene expression analysis was performed on the 68 tumor biopsies.
2010-11-30 | E-GEOD-16581 | biostudies-arrayexpress
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. 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.
2013-01-05 | E-GEOD-43290 | biostudies-arrayexpress
Project description:We report genomic analysis of 300 meningiomas, the most common primary brain tumors, leading to the discovery of mutations in TRAF7, a proapoptotic E3 ubiquitin ligase, in nearly one-fourth of all meningiomas. Mutations in TRAF7 commonly occurred with a recurrent mutation (K409Q) in KLF4, a transcription factor known for its role in inducing pluripotency, or with AKT1(E17K), a mutation known to activate the PI3K pathway. SMO mutations, which activate Hedgehog signaling, were identified in ~5% of non-NF2 mutant meningiomas. These non-NF2 meningiomas were clinically distinctive-nearly always benign, with chromosomal stability, and originating from the medial skull base. In contrast, meningiomas with mutant NF2 and/or chromosome 22 loss were more likely to be atypical, showing genomic instability, and localizing to the cerebral and cerebellar hemispheres. Collectively, these findings identify distinct meningioma subtypes, suggesting avenues for targeted therapeutics. Analysis of meningioma gene expression data for each mutation subtype. Includes gene expression data from 75 unique meningiomas and 39 replicates.
2014-05-29 | E-GEOD-58037 | biostudies-arrayexpress
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