Project description:Single-cell RNA-Seq was conducted on 19 pediatric high-grade glioma patient samples to study tumor heterogeneity and tumor/immune cell interaction.

2023-11-03 | GSE231859 | GEO

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

Gene expression (RNA-Seq) in pediatric high-grade glioma cell lines treated with selinexor and vehicle

Project description:Cultured pediatric high-grade glioma cell lines (SU-DIPG-IV, HSJD-DIPG-007, HSJD-GBM-001,BT 245 (RRID:CVCL_IP13)) were treated with selinexor (Karyopharm Therapeutics) at 5xIC50 for 16 hours or vehicle (0.1% DMSO) followed by bulk RNA-Seq

2020-01-06 | GSE137702 | 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

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

Project description:Comprehensive molecular characterization of pediatric radiation-induced high-grade glioma

| PRJNA732694 | ENA

miRNA expression data from pediatric high grade gliomas

Project description:miRNA expression analysis was performed on 14 cases of high grade gliomas and 4 controls obtained from age-matched epileptic patients. After this differentially miRNA analysis has been done among T53,H3F3A,normal and pediatric high grade glioma patient and try to identify the highly altered miRNA expression as well as sno expression pattern.

2016-11-01 | GSE63319 | 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

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