Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| ERR14102254_1.fastq.gz | Fastqsanger.gz | |||
| ERR14102254_2.fastq.gz | Fastqsanger.gz | |||
| ERR14102255_1.fastq.gz | Fastqsanger.gz | |||
| ERR14102255_2.fastq.gz | Fastqsanger.gz |
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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:To examine fosB regulation of neurogenesis, depression and epilepsy, we compared the gene expression profiles of wild type, fosBd/d and fosB-null mice by microarray analysis. Microarray analysis revealed that genes related to neurogenesis, depression and epilepsy are altered in the hippocampus of fosB-null mice.
2013-01-01 | GSE37056 | GEO
Project description:To examine fosB regulation of neurogenesis, depression and epilepsy, we compared the gene expression profiles of wild type, fosBd/d and fosB-null mice by microarray analysis. Microarray analysis revealed that genes related to neurogenesis, depression and epilepsy are altered in the hippocampus of fosB-null mice. Total RNA from the hippocampus of wild-type, fosBd/d and fosB-null mice was prepared using ISOGEN and RNeasy Mini kits. For DNA microarray experiments, total RNA (100ng) was added to poly-A control and treated with WT Expression Kit. cDNA was labeled using WT terminal labeling kit and hybridized with Affymetrix GeneChip Mouse Gene 1.0 ST platform (GPL6246).
2013-01-01 | E-GEOD-37056 | biostudies-arrayexpress
Project description:The aim of this study was to determine the relationship between gene expression profiles and new metabolic subgroups of benign meningioma with potential clinical relevance. 19 human meningiomas biopsies were obtained at the Department of Neurosurgery of the Clinical University Hospital of Valencia. This study was reviewed and approved by the local ethics committee. During surgery, most of the resected tissue was sent for routine histological analysis and the remainder was immediately put in cryogenic vials and snap-frozen in liquid nitrogen. All snap-frozen samples were stored in a freezer at -80 C until further analysis. Tumors were classified according to the 2007 WHO Histological Classification 1. Grade II meningioma were classified according to previously published criteria, including high mitotic index and three out of five markers of atypia.In summary, this work demonstrates gene expression differences in a new subgroup of histological benign meningiomas that exhibit aggressive metabolism and tumor recurrence.
2012-08-31 | E-MEXP-3586 | biostudies-arrayexpress
Project description:Meningiomas are frequent central nervous system tumors. Although most meningiomas are benign (WHO grade I) and curable by surgery, WHO grade II and III tumors remain therapeutically challenging due to frequent recurrence. Interestingly, relapse also occurs in some WHO grade I meningiomas. Hence, we investigated the transcriptional features defining aggressive (recurrent, malignantly progressing or WHO grade III) meningiomas in 144 cases. Meningiomas were categorized into non-recurrent (NR), recurrent (R), and tumors undergoing malignant progression (M) in addition to their WHO grade. Unsupervised transcriptomic analysis in 62 meningiomas revealed transcriptional profiles lining up according to WHO grade and clinical subgroup. Notably aggressive subgroups (R+M tumors and WHO grade III) shared a large set of differentially expressed genes (n=332; p<0.01, FC>1.25). In an independent multicenter validation set (n=82), differential expression of 10 genes between WHO grades was confirmed. Additionally, among WHO grade I tumors differential expression between NR and aggressive R+M tumors was af rmed for PTTG1, AURKB, ECT2, UBE2C and PRC1, while MN1 and LEPR discriminated between NR and R+M WHO grade II tumors. Univariate survival analysis revealed a significant association with progression-free survival for PTTG1, LEPR, MN1, ECT2, PRC1, COX10, UBE2C expression, while multivariate analysis identified a prediction for PTTG1 and LEPR mRNA expression independent of gender, WHO grade and extent of resection. Finally, stainings of PTTG1 and LEPR confirmed malignancy-associated protein expression changes. In conclusion, based on the so far largest study sample of WHO grade III and recurrent meningiomas we report a comprehensive transcriptional landscape and two prognostic markers. Comparative transcriptomic analysis of 62 low- and high-grade meningiomas
2016-02-15 | E-GEOD-74385 | biostudies-arrayexpress
Project description:To identify genes whose expression is regulated by Fosb gene products in microglia, we performed microarray analysis using RNA prepared from wild-type and fosB-null microglial cells. Microarray analysis revealed that expression levels of 6 genes are altered in primary cultured microglial cells prepared from fosB-null mice compared with wild type. fosB+/G mice with a null-mutant allele, fosBG, were established and maintained by backcrossing to C57BL/6J. To yield homozygous mutant mice, fosB+/G (N20 generation) mice were intercrossed. C57BL/6J mice were used as wild-type control.
2014-04-18 | E-GEOD-40714 | 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
Project description:Proteomics data of endothelial meningiomas, fibrous meningiomas and anaplastic meningiomas
2022-03-17 | PXD032342 |
Project description:Meningiomas are frequent central nervous system tumors. Although most meningiomas are benign (WHO grade I) and curable by surgery, WHO grade II and III tumors remain therapeutically challenging due to frequent recurrence. Interestingly, relapse also occurs in some WHO grade I meningiomas. Hence, we investigated the transcriptional features defining aggressive (recurrent, malignantly progressing or WHO grade III) meningiomas in 144 cases. Meningiomas were categorized into non-recurrent (NR), recurrent (R), and tumors undergoing malignant progression (M) in addition to their WHO grade. Unsupervised transcriptomic analysis in 62 meningiomas revealed transcriptional profiles lining up according to WHO grade and clinical subgroup. Notably aggressive subgroups (R+M tumors and WHO grade III) shared a large set of differentially expressed genes (n=332; p<0.01, FC>1.25). In an independent multicenter validation set (n=82), differential expression of 10 genes between WHO grades was confirmed. Additionally, among WHO grade I tumors differential expression between NR and aggressive R+M tumors was af rmed for PTTG1, AURKB, ECT2, UBE2C and PRC1, while MN1 and LEPR discriminated between NR and R+M WHO grade II tumors. Univariate survival analysis revealed a significant association with progression-free survival for PTTG1, LEPR, MN1, ECT2, PRC1, COX10, UBE2C expression, while multivariate analysis identified a prediction for PTTG1 and LEPR mRNA expression independent of gender, WHO grade and extent of resection. Finally, stainings of PTTG1 and LEPR confirmed malignancy-associated protein expression changes. In conclusion, based on the so far largest study sample of WHO grade III and recurrent meningiomas we report a comprehensive transcriptional landscape and two prognostic markers.
2016-02-15 | GSE74385 | GEO
Project description:Among fos family genes modulating the cell fates such as cell proliferation, differentiation and cell death, only the fosB gene produces two forms of mature mRNA for FosB and deltaFosB proteins by alternative splicing of an exonic intron in the exon 4. FosB dramatically enhances the transcription regulation of AP-1 dependent promoters by Jun, while deltaFosB, a truncated form of FosB lacking its C-terminal transactivation domain, suppresses the function of Jun. We and other have shown that FosB and deltaFosB have a distinct function to control the cell fate as well as neuronal functions based on their exogenous expression. To elucidate the authentic function of each protein, it is essential to control each expression separately. We established a mutant mouse embryonic stem (ES) cell line carrying homozygous fosBd/d alleles which encode exclusively deltaFosB, and compared its gene expression profile and phenotypes with fosB-null and wild-type ES cell lines. Both mutant ES cells are devoid of FosB, therefore the common phenotypes between the two mutant ES cells in comparison to wild type depict the effects of FosB deficiency. Opposite phenotypes between the two are considered to be determined by deltaFosB itself. We analyzed the gene expression and cellular function among these two mutant and wild-type ES cells. Experiment Overall Design: Total RNA was purified from ES cells grown in the absence of feeder cells using the Isogen kit (Nippon Gene), according to the manufacturerâs instructions. For DNA microarray experiments, Total RNA (10 microg) were labeled using the Agilent Linear Amplification/Labeling Kit (Agilent Technologies) according to the manufacturer's instructions. One microgram of each Cy3-labeled wild-type and Cy5-labeled mutant cDNA or each Cy3-labeled mutant and Cy5-labeled wild-type cDNA, respectively, were mixed, then hybridized to Agilent Mouse cDNA Microarrays (G4104A, design file number: 000522R000679, Agilent Technologies) with 8500 unique clones from Incyteâs mouse UniGene 1 clone set, according to the manufacturer's hybridization protocol. After the washing step, the microarray slides were analyzed with an Agilent G2565AA microarray scanner system. These experiments were carried out in duplicate using exchanged dye-labeled cDNA probes (i.e., Cy3 and Cy5 dye-swapping experiments).
2008-06-14 | E-GEOD-5963 | biostudies-arrayexpress