Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Effect of disulfiram treatment on pediatric high grade glioma

ABSTRACT: RNA-seq analysis was performed to compare gene expression between glioma cells treated with disulfiram and untreated glioma cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE138863 | GEO | 2019/10/16

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Effect of disulfiram treatment on pediatric high grade glioma

Project description:Effect of disulfiram treatment on pediatric high grade glioma

| PRJNA577636 | ENA

Alcohol-abuse drug disulfiram targets pediatric glioma via MLL degradation

Project description:Alcohol-abuse drug disulfiram targets pediatric glioma via MLL degradation

| PRJNA578095 | ENA

G207 and PVSRIPO treatment of medulloblastoma and pediatric high grade glioma

Project description:HSV G207 and polio:rhinovirus PVSRIPO are two different viral immunotherapies used to treat malignant brain tumors in children. While some patients experience durable survival with these viral immunotherapies, many children have no response. The purpose of this work is to explore these viral immunotherapies in pediatric high grade glioma (pHGG) and medulloblastoma in order to elucidate how tumor response to treatment and to identify putative biomarkers of response and therapeutic targets.

2024-01-31 | GSE233949 | GEO

Alcohol-abuse drug disulfiram targets pediatric glioma via MLL degradation

Project description:RNA-seq analysis was performed to compare gene expression of glioma cells with MLL1 and MLL2 knockdown, and control glioma cells.

2019-12-20 | GSE139016 | GEO

Comprehensive molecular characterization of pediatric radiation-induced high-grade glioma

Project description:Radiation-induced high-grade gliomas (RIGs) are an incurable late complication of cranial radiation therapy. We performed DNA methylation profiling, RNA-seq, and DNA sequencing on 32 RIG tumors and an in vitro drug screen in two RIG cell lines. We report that based on DNA methylation, RIGs cluster primarily with the pediatric receptor tyrosine kinase I high-grade glioma subtype. Common copy-number alterations include Chromosome (Ch.) 1p loss/1q gain, and Ch. 13q and Ch. 14q loss; focal alterations include PDGFRA and CDK4 gain and CDKN2A and BCOR loss. Transcriptomically, RIGs comprise a stem-like subgroup with lesser mutation burden and Ch. 1p loss and a pro-inflammatory subgroup with greater mutation burden and depleted DNA repair gene expression. Chromothripsis in several RIG samples is associated with extrachromosomal circular DNA-mediated amplification of PDGFRA and CDK4. Drug screening suggests microtubule inhibitors/stabilizers, DNA-damaging agents, MEK inhibition, and, in the inflammatory subgroup, proteasome inhibitors as potentially effective therapies.

2021-05-27 | GSE175543 | GEO

Single-cell ATAC-Seq of pediatric high-grade glioma

Project description:Single-cell ATAC-Seq of pediatric high-grade glioma

| PRJNA687013 | ENA

High grade glioma methylation analysis using bisulfite and oxidative bisulfite-treatment

Project description:Bisulfite and oxidative bisulfite treated sample methylation analysis of IDH1 mutant and wild-type high grade human gliomas, to profile 5-methylcytosine (5mC) and 5-hydroxymethylcytosine (5hmC). Genomic DNA isolated directly from fresh-frozen human high grade glioma specimens.

2020-10-06 | GSE104723 | GEO

Epigenomic Landscape and 3D Genome Structure in Pediatric High-Grade Glioma

Project description:Pediatric high-grade gliomas (pHGGs), including glioblastoma multiforme (GBM) and diffuse intrinsic pontine glioma (DIPG), are highly morbid childhood brain tumors. Even with treatment, overall survival is poor, making pHGG the number one cause of cancer death in children. Up to 80% of DIPGs harbor a somatic missense mutation in genes encoding Histone H3 proteins. To investigate whether this H3K27M mutation is associated with distinct chromatin structure that alters transcription regulation, we generated the first high-resolution Hi-C maps of pHGG cell lines and tumor tissue. By integrating transcriptome (RNA-Seq), enhancer landscape (ChIP-Seq), genome structure (Hi-C), and chromatin accessibility (ATAC-Seq) datasets from H3K27M mutant and wild-type specimens, we identified tumor specific enhancers and regulatory networks for known oncogenes. In addition, we identified distinct genomic structural variations that lead to enhancer hijacking and gene co-amplification, including A2M, JAG2, FLRT1.

2021-06-03 | GSE162976 | GEO

Tumor and immune cell types interact to produce heterogeneous phenotypes of pediatric high grade glioma [bulkRNA-seq]

Project description:Bulk RNA-Seq of pediatric high-grade glioma patient samples

2023-11-03 | GSE231858 | GEO

CircGLIS3 promotes high-grade glioma invasion via modulating Ezrin phosphorylation

Project description:High-grade glioma is highly aggressive and malignant, resistant to combined therapies and easy to relapse. A better understanding of circRNA biological function in high-grade glioma might contribute to the therapeutic efficacy. Here, a circRNA merely up-regulated in high-grade glioma, circGLIS3 (hsa_circ_0002874, originating from exon 2 of GLIS3), was validated by microarray and qRT-PCR. Functional experiments uncovered that up-regulation of circGLIS3 promoted glioma cell migration and invasion, and showed aggressive characteristics in tumor-bearing mice. Fluorescence in situ hybridization, RNA pull-down, RNA immunoprecipitation and immunohistochemical staining showed that circGLIS3 could promoted Ezrin T567 phosphorylation. Further investigation showed that circGLIS3 could be excreted by glioma through exosomes and induced endothelial cells angiogenesis. This study indicates that circGLIS3 is up-regulated in high-grade glioma and contributes to the invasion and angiogenesis of glioma via promoting Ezrin T567 phosphorylation.

2021-09-22 | GSE165859 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data