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Items: 12

1.
Full record GDS4470

Glioblastoma brain tumors

Analysis of glioblastoma (GBM) tumors from different regions of the brain from patients of various ages. Mutations in H3F3A and IDH1 define distinct epigenetic and biological subgroups of GBM. Results provide insight into heterogeneity of GBM and oncogenic pathways leading to gliomagenesis.
Organism:
Homo sapiens
Type:
Expression profiling by array, count, 27 age, 7 disease state, 5 genotype/variation, 3 other, 13 tissue sets
Platform:
GPL570
Series:
GSE36245
46 Samples
Download data: CEL
DataSet
Accession:
GDS4470
ID:
4470
2.

Methylation data from glioblastoma tumor samples

(Submitter supplied) Glioblastoma (GBM) is an incurable brain tumor carrying a dismal prognosis, which displays considerable heterogeneity. We have recently identified recurrent H3F3A mutations affecting two critical positions of histone H3.3 (K27, G34) in one-third of pediatric GBM. Here we show that each of these H3F3A mutations defines an epigenetic subgroup of GBM with a distinct global methylation pattern, and are mutually exclusive with IDH1 mutations (characterizing a CpG-Island Methylator Phenotype (CIMP) subgroup). more...
Organism:
Homo sapiens
Type:
Methylation profiling by genome tiling array
Platform:
GPL13534
142 Samples
Download data: TXT
Series
Accession:
GSE36278
ID:
200036278
3.

Gene expression data from glioblastoma tumor samples

(Submitter supplied) Glioblastoma (GBM) is an incurable brain tumor carrying a dismal prognosis, which displays considerable heterogeneity. We have recently identified recurrent H3F3A mutations affecting two critical positions of histone H3.3 (K27, G34) in one-third of pediatric GBM. Here we show that each of these H3F3A mutations defines an epigenetic subgroup of GBM with a distinct global methylation pattern, and are mutually exclusive with IDH1 mutation (characterizing a CpG-Island Methylator Phenotype (CIMP) subgroup). more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Dataset:
GDS4470
Platform:
GPL570
46 Samples
Download data: CEL
Series
Accession:
GSE36245
ID:
200036245
4.

Isocitrate dehydrogenase 1 (IDH1) mutant gliomas demonstrate a distinct global CpG island methylation profile compared to IDH1 wildtype gliomas using MRSE

(Submitter supplied) In order to identify other molecular aberrations that may cooperate with IDH1R132MUT in gliomagenesis, we performed CpG-island methylation profiling analysis using MSRE (Tran et al. Front. Neurosci. 3:57. Doi: 10.3389/neuro.15.005.2009) on a subset of IDH1R132MUT and IDH1R132WT GBMs and found a distinct pattern of CpG island hypermethylation that was detected in all GBMs and lower grade gliomas with IDH1R132MUT. more...
Organism:
Homo sapiens
Type:
Methylation profiling by genome tiling array
Platform:
GPL13349
40 Samples
Download data: TXT
Series
Accession:
GSE28271
ID:
200028271
5.

Epigenetic determinants of self-renewal in glioblastoma [ATAC-seq]

(Submitter supplied) We over-expressed an epigenetic regulator in a glioblastoma (GBM) primary culture from an adult patient. These GBM cells have cancer stem cell phenotypes, as they have self-renewal properties and tumor initiation potential when transplanted in immunocompromised mice. ATAC-seq was performed on cells over-expressing the epigenetic regulator and control cells expressing EGFP.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing; Other
Platform:
GPL16791
12 Samples
Download data: NARROWPEAK
Series
Accession:
GSE67633
ID:
200067633
6.

MLL5 Orchestrates a Cancer Self-Renewal State by Repressing the Histone Variant H3.3 and Globally Reorganizing Chromatin [expression]

(Submitter supplied) Mutations in the histone 3 variant H3.3 have been identified in one-third of pediatric glioblastomas (GBMs), but not in adult tumors. Here we show that H3.3 is a dynamic determinant of functional properties in adult GBM. H3.3 is repressed by mixed lineage leukemia 5 (MLL5) in self-renewing GBM cells. MLL5 is a global epigenetic repressor that orchestrates reorganization of chromatin structure by punctuating chromosomes with foci of compacted chromatin, favoring tumorigenic and self-renewing properties. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL17586
6 Samples
Download data: CEL, TXT
Series
Accession:
GSE63296
ID:
200063296
7.

MLL5 orchestrates a cancer self-renewal state by repressing the histone variant H3.3 and globally reorganizing chromatin [methylation]

(Submitter supplied) Genome wide DNA methylation profiling of fourteen adult GBM primary cultures and their comparison to pediatric GBMs [GSE36278; GSE55712]
Organism:
Homo sapiens
Type:
Methylation profiling by genome tiling array
Platform:
GPL13534
14 Samples
Download data: IDAT, TXT
Series
Accession:
GSE63267
ID:
200063267
8.

Gene expression data of pHGG tumor samples

(Submitter supplied) Pediatric high-grade gliomas (pHGGs) harboring the K27M mutation of H3F3A (histone H3.3) are characterized by global reduction of the repressive histone mark H3K27me3 and DNA hypomethylation. Analysis of K27M-induced changes on H3K27me3 occupancy and DNA methylation at differentially expresed genes (K27M vs. wild-type H3.3) in primary pHGG tumor samples.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
22 Samples
Download data: CEL
Series
Accession:
GSE49822
ID:
200049822
9.

Frequent driver mutations in histone H3.3 and chromatin remodeling genes in paediatric glioblastoma

(Submitter supplied) Whole exome sequencing identified frequent driver mutations in a series of paediatric glioblastomas We used microarray-based profiling to investigate differences in gene expression according to mutational status of driver genes
Organism:
Homo sapiens
Type:
Expression profiling by array
Dataset:
GDS4477
Platform:
GPL570
27 Samples
Download data: CEL
Series
Accession:
GSE34824
ID:
200034824
10.
Full record GDS4477

Pediatric glioblastoma brain tumors: histone H3.3 mutations

Analysis of pediatric glioblastoma (GBM) tumors with mutations in H3F3A gene. Mutation of key residues in histone H3.3 are specific to GBM and highly prevalent in children and young adults. Results indicate that defects in chromatin architecture underlie pediatric GBM pathogenesis.
Organism:
Homo sapiens
Type:
Expression profiling by array, count, 4 genotype/variation sets
Platform:
GPL570
Series:
GSE34824
27 Samples
Download data: CEL
DataSet
Accession:
GDS4477
ID:
4477
11.

EGFR Mutation Promotes Glioblastoma Through Epigenome and Transcription Factor Network Remodeling

(Submitter supplied) Epidermal Growth Factor Receptor (EGFR) gene amplification and mutations are the most common oncogenic events in Glioblastoma (GBM), but the mechanisms by which they promote aggressive tumor growth are not well understood. Here, through integrated epigenome and transcriptome analyses of cell lines, genotyped clinical samples and TCGA data, we show that EGFR mutations remodel the activated enhancer landscape of GBM, promoting tumorigenesis through a SOX9 and FOXG1-dependent transcriptional regulatory network in vitro and in vivo. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing; Other
Platform:
GPL11154
87 Samples
Download data: BIGWIG, BW
12.

Mosaic Amplification of Multiple Receptor Tyrosine Kinase Genes in Glioblastoma

(Submitter supplied) Here we present a novel example of genetic heterogeneity in human malignant brain tumors, in which multiple closely-related driver genes are amplified and activated simultaneously in adjacent intermingled cells. We have observed up to 3 different receptor tyrosine kinases (EGFR, MET, PDGFRA) amplified in single tumors in different cells in a mutually exclusive fashion. However, these subpopulations cannot be always observed with a genome wide studies such as aCGH. more...
Organism:
Homo sapiens
Type:
Genome variation profiling by genome tiling array; Genome variation profiling by SNP array; SNP genotyping by SNP array
Platform:
GPL11358
3 Samples
Download data: TXT
Series
Accession:
GSE33483
ID:
200033483
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