Glioma MYC gene signature
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE206873 | GEO | 2022/09/12
REPOSITORIES: GEO
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Project description:Characterization of MYC amplification in a glioma by SNParray
2013-05-31 | E-MEXP-3285 | biostudies-arrayexpress
Project description:Ferroptosis-related Gene Signature Predicts Glioma Cell Death and Glioma Patient Progression
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Project description:Glioma-derived stem-like cells (GSCs) are hypothesized to provide a repository of cells in tumors that can self-replicate and be resistant to radiation and chemotherapeutic agents developed for the treatment of tumors. The potential lack of response of GSCs to traditional cytotoxic and radiation therapies has significant implications for tumor biology and therapeutics. At M.D. Anderson Cancer Center, a large number of GSC lines representing several glioma sub-types have been isolated and characterized with respect to gene expression. In order to identify potential therapeutic targets relating to GSC phenotype, we examined protein expression in 35 GSC lines relative to an external protein standard using label-free quantitative proteomics. Samples were analyzed in triplicate by nanoLC-MS/MS (Orbitrap Elite, Thermo) in block-randomized groups of three GSCs plus the external standard. The resulting .raw files were aligned by group in Progenesis LC-MS (Nonlinear Dynamics). Database searching was performed with PEAKS 6 software (BSI) against a UniprotKB/SwissProt Human database appended with the cRAP contaminant database. Peptide intensities were exported for analysis in DanteR. The resulting relative fold changes were used to drive unsupervised hierarchical clustering of the cell lines for the purpose of classifying cell lines, and Ingenuity Pathway Analysis (IPA) and the DAVID webtool were used to determine the biochemical pathways and biological processes impacted by protein changes in each cell line. Within IPA, Upstream Analysis was used to predict biological functions and transcriptional regulators whose increased or decreased activity was consistent with the observed fold changes, and the resulting upstream regulators with significant z-scores were exported for unsupervised hierarchical clustering. In addition to showing upstream regulators known to be associated with glioma, including Myc, tumor protein 53 (TP53), N-myc proto-oncogene protein (MYCN), two novel upstream regulators, synoviolin 1 (SYVN1) and interleukin 5 (IL5) were identified. A cluster of proteins found to be decreased relative to mixed control in mesenchymal cell lines was subjected to further bioinformatics analysis, identifying SRSF2 as a potential upstream regulator.
2015-07-07 | PXD001890 | Pride
Project description:The goal of this experiment was to compare the gene expression of glioma cells migrating on substrates of different topographies and to determine a migration-associated gene profile. Human malignant glioma U251MG cells were cultured on highly-aligned versus randomly-oriented electrospun nanofibers of poly-caprolactone. Cells migrated actively on aligned nanofibers but motility was very restricted on randomly-oriented fibers. Results of gene expression profiling indicated upregulation of a JAK/STAT signature in actively migrating glioma cells. Total RNA was extracted from 3 independent cultures of U251 glioma cells cultured on aligned versus random nanofibers and applied to Affymetrix HG-U133 plus 2 chips. Analysis of gene expression was used to determine a gene-signature correlated with different substrate topography
2011-03-24 | E-GEOD-28167 | biostudies-arrayexpress
Project description:Whole transcriptome profiling of glioma tissue with PDX model
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Project description:Diffuse midline gliomas (DMGs) are uniformly fatal pediatric central nervous system cancers, refractory to standard of care therapeutic modalities. The primary genetic drivers are a set of recurrent amino acid substitutions in genes encoding histone H3 (H3.3 and H3.1, K27M), which are currently undruggable. These H3K27M oncohistones perturb normal chromatin architecture, resulting in an aberrant epigenetic landscape, which we interrogated here for epigenetic dependencies using a CRISPR screen in patient-derived H3K27M-glioma neurospheres. We show that H3K27M-glioma cells are dependent on core components of the mammalian SWI/SNF (BAF) chromatin remodeling complex for maintaining glioma stem cells in a cycling, oligodendrocyte precursor cell (OPC)-like state. Genetic perturbation of the BAF catalytic subunit SMARCA4 (BRG1), as well as pharmacological suppression opposes proliferation, promotes differentiation, and improves overall survival of patient-derived xenograft (PDX) models. In summary, we demonstrate that therapeutic inhibition of BAF complex has translational potential for children with H3K27M-gliomas.
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Project description:Diffuse midline gliomas (DMGs) are uniformly fatal pediatric central nervous system cancers, refractory to standard of care therapeutic modalities. The primary genetic drivers are a set of recurrent amino acid substitutions in genes encoding histone H3 (H3.3 and H3.1, K27M), which are currently undruggable. These H3K27M oncohistones perturb normal chromatin architecture, resulting in an aberrant epigenetic landscape, which we interrogated here for epigenetic dependencies using a CRISPR screen in patient-derived H3K27M-glioma neurospheres. We show that H3K27M-glioma cells are dependent on core components of the mammalian SWI/SNF (BAF) chromatin remodeling complex for maintaining glioma stem cells in a cycling, oligodendrocyte precursor cell (OPC)-like state. Genetic perturbation of the BAF catalytic subunit SMARCA4 (BRG1), as well as pharmacological suppression opposes proliferation, promotes differentiation, and improves overall survival of patient-derived xenograft (PDX) models. In summary, we demonstrate that therapeutic inhibition of BAF complex has translational potential for children with H3K27M-gliomas.
2022-09-15 | GSE212718 | GEO
Project description:Diffuse midline gliomas (DMGs) are uniformly fatal pediatric central nervous system cancers, refractory to standard of care therapeutic modalities. The primary genetic drivers are a set of recurrent amino acid substitutions in genes encoding histone H3 (H3.3 and H3.1, K27M), which are currently undruggable. These H3K27M oncohistones perturb normal chromatin architecture, resulting in an aberrant epigenetic landscape, which we interrogated here for epigenetic dependencies using a CRISPR screen in patient-derived H3K27M-glioma neurospheres. We show that H3K27M-glioma cells are dependent on core components of the mammalian SWI/SNF (BAF) chromatin remodeling complex for maintaining glioma stem cells in a cycling, oligodendrocyte precursor cell (OPC)-like state. Genetic perturbation of the BAF catalytic subunit SMARCA4 (BRG1), as well as pharmacological suppression opposes proliferation, promotes differentiation, and improves overall survival of patient-derived xenograft (PDX) models. In summary, we demonstrate that therapeutic inhibition of BAF complex has translational potential for children with H3K27M-gliomas.
2022-09-15 | GSE212700 | GEO
Project description:Diffuse midline gliomas (DMGs) are uniformly fatal pediatric central nervous system cancers, refractory to standard of care therapeutic modalities. The primary genetic drivers are a set of recurrent amino acid substitutions in genes encoding histone H3 (H3.3 and H3.1, K27M), which are currently undruggable. These H3K27M oncohistones perturb normal chromatin architecture, resulting in an aberrant epigenetic landscape, which we interrogated here for epigenetic dependencies using a CRISPR screen in patient-derived H3K27M-glioma neurospheres. We show that H3K27M-glioma cells are dependent on core components of the mammalian SWI/SNF (BAF) chromatin remodeling complex for maintaining glioma stem cells in a cycling, oligodendrocyte precursor cell (OPC)-like state. Genetic perturbation of the BAF catalytic subunit SMARCA4 (BRG1), as well as pharmacological suppression opposes proliferation, promotes differentiation, and improves overall survival of patient-derived xenograft (PDX) models. In summary, we demonstrate that therapeutic inhibition of BAF complex has translational potential for children with H3K27M-gliomas.
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