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Links from GEO DataSets

Items: 20

1.

H3.3 K27M depletion increases differentiation and extends latency of diffuse intrinsic pontine glioma growth in vivo

(Submitter supplied) Xenografts from human pediatric brainstem gliomas bearing K27M in H3F3A were transduced with non silencing or H3F3A shRNA to assess the impact of the K27M on tumor growth, gene expression and epigenetics
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL16791 GPL20301
130 Samples
Download data: BED, BW, NARROWPEAK
Series
Accession:
GSE115875
ID:
200115875
2.

H3.3 K27M depletion increases differentiation and extends latency of diffuse intrinsic pontine glioma growth in vivo [RNA-Seq]

(Submitter supplied) xenografts from human pediatric brainstem gliomas bearing K27M in H3F3A were transduced with non silencing or H3F3A shRNA to assess the impact of the K27M on tumor growth, gene expression and epigenetics
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL20301 GPL16791
50 Samples
Download data: TXT
3.

H3.3 K27M depletion increases differentiation and extends latency of diffuse intrinsic pontine glioma growth in vivo [ChIP-Seq]

(Submitter supplied) Xenografts from human pediatric brainstem gliomas bearing K27M in H3F3A were transduced with non silencing or H3F3A shRNA to assess the impact of the K27M on tumor growth, gene expression and epigenetics
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL20301 GPL16791
80 Samples
Download data: BED, BW, NARROWPEAK
Series
Accession:
GSE115872
ID:
200115872
4.

Spontaneous DIPG Modeling Reveals Novel H3.3 K27M-Mediated Oncogenic Mechanisms Acting Through Epigenetic Effects

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL21103 GPL17021
100 Samples
Download data: BED, BW, NARROWPEAK
Series
Accession:
GSE108364
ID:
200108364
5.

Spontaneous DIPG Modeling Reveals Novel H3.3 K27M-Mediated Oncogenic Mechanisms Acting Through Epigenetic Effects [RNA-seq]

(Submitter supplied) A mouse knock-in model engineered for Cre recombinase-activated expression of the endogenous mouse H3f3a allele generating an epitope-tagged H3.3 equipped with or without a K27M mutation to investigate H3.3 K27M effects on brain cell and tumor growth, gene expression and epigenetics.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL17021 GPL21103
41 Samples
Download data: TXT
Series
Accession:
GSE108362
ID:
200108362
6.

Spontaneous DIPG Modeling Reveals Novel H3.3 K27M-Mediated Oncogenic Mechanisms Acting Through Epigenetic Effects [ChIP-seq]

(Submitter supplied) A mouse knock-in model engineered for Cre recombinase-activated expression of the endogenous mouse H3f3a allele generating an epitope-tagged H3.3 equipped with or without a K27M mutation to investigate H3.3 K27M effects on brain cell and tumor growth, gene expression and epigenetics.
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL17021
59 Samples
Download data: BED, BW, NARROWPEAK
Series
Accession:
GSE108344
ID:
200108344
7.

Re-programing chromatin with a bifunctional LSD1/HDAC inhibitor induces therapeutic differentiation in DIPG

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL16791
30 Samples
Download data: BED, BIGWIG, TXT
Series
Accession:
GSE110572
ID:
200110572
8.

Re-programing chromatin with a bifunctional LSD1/HDAC inhibitor induces therapeutic differentiation in DIPG [RNA-seq]

(Submitter supplied) Histone H3 lysine 27 to methionine mutations (H3K27M) resulting in aberrant chromatin regulation are frequently observed in Diffuse Intrinsic Pontine Glioma (DIPG), a pediatric brain tumor with no cure. We conducted a CRISPR screen to determine if various chromatin regulators might be targeted to treat DIPG. Excitingly, this genetic screen reveals that co-targeting lysine specific demethylase 1 (LSD1) and histone deacetylases (HDACs) results in an enhanced growth suppressive effect in patient DIPG cells. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
12 Samples
Download data: TXT
Series
Accession:
GSE110571
ID:
200110571
9.

Re-programing chromatin with a bifunctional LSD1/HDAC inhibitor induces therapeutic differentiation in DIPG [ChIP-seq]

(Submitter supplied) Histone H3 lysine 27 to methionine mutations (H3K27M) resulting in aberrant chromatin regulation are frequently observed in Diffuse Intrinsic Pontine Glioma (DIPG), a pediatric brain tumor with no cure. We conducted a CRISPR screen to determine if various chromatin regulators might be targeted to treat DIPG. Excitingly, this genetic screen reveals that co-targeting lysine specific demethylase 1 (LSD1) and histone deacetylases (HDACs) results in an enhanced growth suppressive effect in patient DIPG cells. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL16791
18 Samples
Download data: BED, BIGWIG
Series
Accession:
GSE110570
ID:
200110570
10.

Potent anti-tumor efficacy of palbociclib in H3K27M-mutant diffuse intrinsic pontine glioma

(Submitter supplied) Diffuse intrinsic pontine glioma (DIPG) is a rare and fatal pediatric brain cancer without cure. DIPG has high percentage histone mutation at K27M on histone H3 locus, which is believed to be one of the drivers of the tumorigenesis. Dysregulation of G1/S cell cycle checkpoint is more enriched in the H3.3K27M mutant subgroup. In this study, we reported that palbociclib (PD0332991), a specific and cytostatic inhibitor of CDK4/6, effectively suppresses the growth of DIPG cells in vitro and in vivo. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20795
4 Samples
Download data: FPKM_TRACKING
11.

RNAseq analysis of murine brainstem gliomas with and without H3.3K27M

(Submitter supplied) Using the RCAS/tv-a system, we induced murine brainstem gliomas (PDGF-B; p53 loss using RCAS-Cre with and without H3.3K27M) in Nestin tv-a; p53 floxed mice
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL9185
6 Samples
Download data: XLSX
Series
Accession:
GSE98765
ID:
200098765
12.

Analyzing the Effect of the K27M Mutation in Histone H3.3 on Gene Expression in Pluripotent Stem Cells and Neural Stem Cells.

(Submitter supplied) Diffuse intrinsic pontine glioma (DIPG) is an aggressive childhood tumor of the brainstem with currently no curative treatment available. The vast majority of DIPGs carry a mutation in histone H3 leading to a lysine 27-to-methionine exchange (H3K27M). The H3K27M mutation has been shown to inhibit EZH2, the catalytic subunit of the polycomb repressive complex 2, which presumably leads to global reduction of H3K27 trimethylation and upregulation of tumor-driving genes. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
14 Samples
Download data: CEL
Series
Accession:
GSE133153
ID:
200133153
13.

Analyzing the Effect of the K27M Mutation in Histone H3.3 on Chromatin Regulation in Pluripotent Stem Cells, Neural Stem Cells, and Oligodendroglial Progenitor Cells

(Submitter supplied) Diffuse intrinsic pontine glioma (DIPG) is an aggressive childhood tumor of the brainstem with currently no curative treatment available. The vast majority of DIPGs carry a mutation in histone H3 leading to a lysine 27-to-methionine exchange (H3K27M). The H3K27M mutation has been shown to inhibit EZH2, the catalytic subunit of the polycomb repressive complex 2, which presumably leads to global reduction of H3K27 trimethylation and upregulation of tumor-driving genes. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
16 Samples
Download data: BW, XLSX
Series
Accession:
GSE132605
ID:
200132605
14.

Histone H3.3 K27M chromatin functions implicate a network of neurodevelopmental factors including ASCL1 and NEUROD1 in DIPG

(Submitter supplied) Background: The histone variant H3.3 K27M mutation is a defining characteristic of diffuse intrinsic pontine glioma (DIPG)/diffuse midline glioma (DMG). This histone mutation is responsible for major alterations to histone H3 post-translational modification (PTMs) and subsequent aberrant gene expression. However, much less is known about the effect this mutation has on chromatin structure and function, including open versus closed chromatin regions as well as their transcriptomic consequences. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
8 Samples
Download data: BED
Series
Accession:
GSE201265
ID:
200201265
15.

Heterotypic nucleosomes and PRC2 drive DIPG oncogenesis

(Submitter supplied) Diffuse intrinsic pontine gliomas (DIPG) are characterized by a heterozygous lysine-to-methionine mutation of histone H3 (H3K27M) that potently reduces Polycomb Repressive Complex 2 (PRC2) methylation of wild-type histone H3K27 (H3K27wt). The role of H3K27M and reduced H3K27wt methylation in DIPG pathogenesis has yet to be determined. Here, we have performed epigenomic profiling of patient-derived H3K27M mutant DIPG cells and demonstrate that H3K27M resides in nucleosomes with H3K27wt acetylation (H3K27ac), and H3K27M-H3K27ac containing nucleosomes co-localize with bromodomain proteins at actively transcribed genes and that PRC2 is excluded from H3K27M occupied regions. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
100 Samples
Download data: BW
16.

Epigenetic changes in mouse neuronal stem cells and human DIPG cells with histone H3K27M mutations

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens; Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL19057 GPL18573
16 Samples
Download data
Series
Accession:
GSE135419
ID:
200135419
17.

Epigenetic changes in human DIPG cells with histone H3K27M mutations [ATAC-seq]

(Submitter supplied) We assessed changes in chromatin accessibility in H3.3K27M DIPG cell lines on knockdown of metabolic enzymes including HK2, GDH and IDH1
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
8 Samples
Download data: CSV
Series
Accession:
GSE135418
ID:
200135418
18.

Epigenetic changes in mouse neuronal stem cells with histone H3K27M mutations [ChIP-seq]

(Submitter supplied) H3.3K27M mutations or H3.3 WT were expressed in in neuronal stem cells (Nsc) derived from p16Ink4a/p14Arf knockout (KO) animal. Genomic changes in H3K27me3, H3K27ac and H3K4me3 were assessed between H3.3K27M and H3.3WT cells.
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL19057
8 Samples
Download data: XLSX
Series
Accession:
GSE135417
ID:
200135417
19.

Effect of CBL0137 on DIPG cells

(Submitter supplied) Diffuse intrinsic pontine glioma (DIPG) is an aggressive and incurable childhood brain tumor for which new treatments are needed. A high throughput drug screen of 3600 pharmaceutical compounds found that anti-malarials, including quinacrine had potent activity against DIPG neurospheres. CBL0137 is a novel anti-cancer compound developed from quinacrine, which targets Facilitates Chromatin Transcription (FACT), a chromatin remodelling complex involved in transcription, replication, and DNA repair. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL28835
6 Samples
Download data: CEL
Series
Accession:
GSE153883
ID:
200153883
20.

Combination of CBL0137 and Panobinostat in DIPG

(Submitter supplied) Diffuse intrinsic pontine glioma (DIPG) is an aggressive and incurable childhood brain tumor for which new treatments are needed. A high throughput drug screen of 3600 pharmaceutical compounds found that anti-malarials, including quinacrine had potent activity against DIPG neurospheres. CBL0137 is a novel anti-cancer compound developed from quinacrine, which targets Facilitates Chromatin Transcription (FACT), a chromatin remodelling complex involved in transcription, replication, and DNA repair. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL28782
12 Samples
Download data: CEL
Series
Accession:
GSE153441
ID:
200153441
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