E-MEXP-567
Ontology highlight
ABSTRACT:
PROVIDER: E-MEXP-567 | ExpressionAtlas | 2025-01-22
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-MEXP-567-analysis-methods.tsv | Tabular | |||
| E-MEXP-567-atlasExperimentSummary.Rdata | Rdata | |||
| E-MEXP-567-configuration.xml | Xml | |||
| E-MEXP-567-percentile-ranks.tsv | Tabular | |||
| E-MEXP-567.condensed-sdrf.tsv | Tabular |
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2007-03-01 | E-MEXP-567 | biostudies-arrayexpress
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Project description:Summary: Astrocytomas can be categorized as either low grade or high grade (glioblastoma). Low grade astrocytomas are not generally aggressive tumors whereas glioblastomas are and in turn have a high mortality rate. The purpose of this experiment is to identify genetic differences between the two types. Hypothesis: There will be a difference in RNA expression between high grade and low grade tumors. Specific Aim: To identify genes which make a tumor high grade or low grade Experiment Overall Design: Comparison of 8 high grade and 12 low grade tumors
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Project description:Genomewide DNA methylation array profiling of 23 previously unpublished CNS tumors resolved into a new entity, high-grade glioma with pleomorphic and pseudopapillary features (HPAP). Tumors demonstrate a variety of histologic diagnoses including glioblastoma (GBM), pleomorphic xanthoastrocytoma (PXA), anaplastic ependymoma, and polymorphous low-grade neuroepithelial tumor of the young (PLNTY). The Illumina Infinium EPIC 850k Human DNA Methylation Beadchip was used to obtain DNA methylation profiles across approximately 850,000 CpG sites of genomic DNA extracted from formalin-fixed, paraffin-embedded tumor tissue.
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Project description:Summary: Astrocytomas can be categorized as either low grade or high grade (glioblastoma). Low grade astrocytomas are not generally aggressive tumors whereas glioblastomas are and in turn have a high mortality rate. The purpose of this experiment is to identify genetic differences between the two types. Hypothesis: There will be a difference in RNA expression between high grade and low grade tumors. Specific Aim: To identify genes which make a tumor high grade or low grade Keywords: disease, cancer grade
2005-08-24 | GSE3185 | GEO
Project description:To investigate the regulatory mechanisms governing the malignant signature of different gliomas we analyzed microRNA expression profiles in human tumor samples of world health organization (WHO) grade I (benign tumors), II (low grade tumors) and IV (high grade tumors) and from primary cultures obtained from tumor samples of grade II and IV. Patients This study included tumor samples histologically verified as astrocytic gliomas obtained from patients who had undergone craniotomy for microsurgical tumor removal. According to the revised WHO classification, tumors were diagnosed as: grade I or pilocytic astrocytomas; grade II or diffuse fibrillary astrocytomas; grade IV or glioblastoma multiforme. Primary cell cultures from grade II and grade IV gliomas were also obtained and miRNA expression in these cultures were analyzed RNA extraction Total RNA, including small RNA, was isolated from tissue samples using the mirVanaTM miRNA Isolation Kit (Ambion) following the standard protocol. The quantity and quality of the purified RNA was evaluated by spectrophotometric analysis and electrophoresis on denaturing gel of acrylamide. Multiplex Real-Time Quantitative Reverse-Transcriptase Polymerase Chain Reaction (RT-PCR) The miRNAs were first converted to cDNA using Multiplex RT for TaqMan Array Human MicroRNA Panel. The RT Master mix included 100 mM each of dNTPs , 50 U/ml MultiScrabe reverse transcriptase (Applied Biosystems), 20 U/M-BM-5l RNase inhibitor (Applied Biosystems) and 10X RT Buffer. The 10 M-BM-5l reactions, including 7 M-BM-5l of RT master mix, 2 M-BM-5l of purified microRNA and 1 M-BM-5l of Multiplex RT Human primer pool (Applied Biosystem), were incubated in ice for 5 min and then in a thermal cycler for 30 min at 16M-BM-0C, 30 min at 42M-BM-0C, 5 min at 85M-BM-0C, and then hold at 4M-BM-0C. miRNA levels were normalized to the expression of small nucleolar RNAs, RNU44, RNU48 and RNU6B. All reverse transcriptase reactions, including no-template controls and RT controls, were run in duplicate. Real-time PCR was performed using a standard TaqMan PCR kit procedure on an M-bM-^@M-^\Real Time Fast 7900 HTM-bM-^@M-^] PCR System (Applied Biosystems). The 100 M-BM-5l PCR included 50 M-BM-5l RT product (before diluited 1:60) and 50 M-BM-5l TaqMan Universal PCR Master Mix (2X) (Applied Biosystems). The total volume were loaded into Card TaqMan Low Density Array Human MicroRNA Panel (Applied Biosystem) including a total of 384 human microRNAs publicated on databases www.sanger.ac.uk. The reaction cards was runned at 50M-BM-0C for 2 min and 95M-BM-0C for 10 min, followed by 40 cycles of 97M-BM-0C for 30s and 59,7M-BM-0C for 1 min. All reactions were run in triplicate. Analysis of data was performed using the SDS 2.3 software using the 2-M-bM-^HM-^FM-bM-^HM-^FCt (relative quantitative) method . The M-bM-^HM-^FCt of every miRNA was determined in relation to the endogenous control RNA U6 that was invariably expressed in all samples. The M-bM-^HM-^FM-bM-^HM-^FCt value was determined in relation to the calibrator, namely the normal brain tissue. Resulting data were grouped according to the tumor grading e selectioned using a cut-off value of 3. Results were expressed as M-bM-^@M-^\fold changeM-bM-^@M-^] over normal brain tissue. We analyzed two samples of grade I, two samples of grade II, two samples of grade IV gliomas. Four samples form norma brain were used as norma control. Primary cell cultures form grade II and grade IV samples were used for the analysis. All reverse transcriptase reactions, including no-template controls and RT controls, were run in triplicate.
2013-09-18 | E-GEOD-50924 | biostudies-arrayexpress
Project description:Glioblastoma ranks as one of the most lethal human cancers, with no effective therapies. To discover novel therapeutic targets, here we performed parallel in vivo and in vitro RNA interference screens of epigenetic regulators and show that transcription elongation factors are essential for human glioblastoma cell survival in vivo, but not in vitro. Context-specific dependency in vivo is driven by microenvironment-induced global changes in the cancer epigenome. JMJD6, a top in vivo-specific hit, binds at enhancers and correlates with increased transcription of known pause-controlled genes. JMJD6 knockdown in patient-derived glioblastoma cells enhances survival of mice bearing orthotopic tumors. Moreover, elevated levels of JMJD6 alone, as well as transcription elongation factors collectively, informs tumor grade and predicts poor prognosis for patients. Our work provides a rationale for targeting transcription elongation as a therapeutic strategy in glioblastoma and, more broadly, the power of in vivo phenotypic screening to identify therapeutically relevant targets in cancer.
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