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Links from GEO DataSets

Items: 20

1.

Expression data from stem like glioblastoma cells treated with vehicle, or BRD protein inhibitor, or HDAC inhibitor or the combination

(Submitter supplied) Inhibition of BRD proteins by OTX015, and inhibition of HDAC by Panobinostat and the combination alters the gene expression of the glioblastoma cells. To compare the drug effect and find out the resonal of the synergisty of the bombination, we performed microarray experiments.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL17930
8 Samples
Download data: CEL
Series
Accession:
GSE108958
ID:
200108958
2.

Epigenetic Targeting of the Warburg Effect by Inhibition of Histone-Deacetylases Leads to Activation of Oxidative Metabolism

(Submitter supplied) FDA-approved global (panobinostat, vorinostat) and selective (romidepsin) histone-deacetylase (HDAC) inhibitors elicit metabolic reprogramming in concert with disruption of several Warburg-effect related super-enhancers
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
8 Samples
Download data: BIGWIG
Series
Accession:
GSE144399
ID:
200144399
3.

Gene expression of patient derived xenograft glioblastoma treated with DMSO control or Panobinostat.

(Submitter supplied) Panobinostat is a non-selective histone deactylase inhibitor which has been approved by FDA for treatment of mutiple myeloma. Whether and how the drug works on glioblastoma remains unclear. Here we treated mice implanted with patient derived xenograft glioblastoma G43 with DMSO or Panobinostat and harvest the tumors for microarray analysis for gene expression results.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL17930
2 Samples
Download data: CEL
Series
Accession:
GSE108957
ID:
200108957
4.

Expression data of U87 MG glioblastoma cells with vehicle or with 30nM Panobinostat treatment for 3 weeks

(Submitter supplied) Low dose of HDAC inhibitor (Panobinostat) treatment causes U87 cells to become resistant to the drug. Gene expression of the resistant cell line is altered comparing to the vehicle control.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL17930
2 Samples
Download data: CEL
Series
Accession:
GSE103961
ID:
200103961
5.

MET Inhibition Elicits PGC1α Dependent Metabolic Reprogramming in Glioblastoma

(Submitter supplied) By utilizing proteomic and transcriptomic analysis coupled with untargeted polar and non-polar metabolite analysis by liquid chromatography/mass spectrometry, we identified a specific metabolic program elicited by c-MET inhibition. Interference with c-MET drives oxidative metabolism by increasing fatty acid oxidation (FAO) and glucose anaplerosis, which was orchestrated by the master-regulator, PGC1α. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL26944
4 Samples
Download data: CEL
Series
Accession:
GSE134676
ID:
200134676
6.

Expression data of glioblastoma cells with Crizotinib acute and chronic treatment vs its own vehicle control

(Submitter supplied) Gene expression of chronically or acutely Crizotinib treated glioblastoma cells vs vehicle controls
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL17930
4 Samples
Download data: CEL
Series
Accession:
GSE113961
ID:
200113961
7.

Effect of ONC201 and its derivatives (ONC206 and ONC212) on glioma cells

(Submitter supplied) We performed microarray analysis in order to evaluate the effect of ONC201 and its derivatives (ONC206 and ONC212) on gene expression in U87 glioma cells.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL17930
4 Samples
Download data: CEL
Series
Accession:
GSE104273
ID:
200104273
8.

Effect of TIC10/ONC201 on glioma cells

(Submitter supplied) We performed microarray analysis in order to evaluate the effect of ONC201 on gene expression in glioma cells (U87).
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL17930
2 Samples
Download data: CEL
Series
Accession:
GSE103963
ID:
200103963
9.

Inhibition of HDAC1/2 along with TRAP1 causes Synthetic Lethality in Glioblastoma Model Systems

(Submitter supplied) Pan and selective HDAC inhibition is synthetically lethal with TRAP1 inhibition in various model systems of glioblastoma, including patient derived xenograft (PDX) cells. Mechanistically, this occurs through several mechanisms, including the induction of metabolic stress by interference with tumor cell energy metabolism accompanied by modulation of pro- and anti-apoptotic Bcl-2 family proteins and the induction of a cell death with apoptotic features.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL20301
2 Samples
Download data: BIGWIG
Series
Accession:
GSE150395
ID:
200150395
10.

Activation of the Mitochondrial ClpP protease is Synthetically Lethal with HDAC1/2 Inhibition in Glioblastoma Model Systems

(Submitter supplied) By integration of transcriptome and metabolite analyses, we showed that pharmacological activation of the mitochondrial ClpP protease through utilization of enhanced imipridone compounds (ONC206 and ONC212) in combination with global (Panobinostat) and selective (romidepsin) HDAC – inhibitors caused synergistic reduction of viability in established and patient-derived xenograft (PDX) cultures of human GBM. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL27949
8 Samples
Download data: CEL
Series
Accession:
GSE166111
ID:
200166111
11.

Aurora A kinase Inhibition Reprograms Metabolism dependent on PGC1α to Drive Synthetic Lethality with Fatty Acid Oxidation Inhibition in Glioblastoma

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
6 Samples
Download data: BIGWIG
Series
Accession:
GSE161574
ID:
200161574
12.

Aurora A kinase Inhibition Reprograms Metabolism dependent on PGC1α to Drive Synthetic Lethality with Fatty Acid Oxidation Inhibition in Glioblastoma [ChIP-Seq]

(Submitter supplied) By integration of transcriptome, CHIP-seq, ATAC-seq, proteomic and metabolite screening followed by carbon tracing (U-13C-Glucose, U-13C-Glutamine and U-13C-Palmitic acid) and extracellular flux analysis we provided evidence that genetic (shRNA and CRISPR/Cas9) and pharmacological (Alisertib) AURKA inhibition elicited substantial metabolic reprogramming supported in part by inhibition of MYC targets and concomitant activation of PPARA signaling. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
2 Samples
Download data: BIGWIG
Series
Accession:
GSE161573
ID:
200161573
13.

Aurora A kinase Inhibition Reprograms Metabolism dependent on PGC1α to Drive Synthetic Lethality with Fatty Acid Oxidation Inhibition in Glioblastoma [ATAC-Seq]

(Submitter supplied) By integration of transcriptome, CHIP-seq, ATAC-seq, proteomic and metabolite screening followed by carbon tracing (U-13C-Glucose, U-13C-Glutamine and U-13C-Palmitic acid) and extracellular flux analysis we provided evidence that genetic (shRNA and CRISPR/Cas9) and pharmacological (Alisertib) AURKA inhibition elicited substantial metabolic reprogramming supported in part by inhibition of MYC targets and concomitant activation of PPARA signaling. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
4 Samples
Download data: BIGWIG
Series
Accession:
GSE161572
ID:
200161572
14.

AURKA Inhibition Reprograms Metabolism dependent on PGC1α to Drive Synthetic Lethality with Fatty Acid Oxidation Inhibition in Glioblastoma

(Submitter supplied) We described the metabolic alterations in glioblastoma model systems elicited by AURKA inhibition. By utilizing proteomic and transcriptomic analyses coupled with untargeted polar and nonpolar metabolite analysis by LC/MC, we found that AURKA inhibition leads to a profound reprogramming of tumor metabolism, which suppresses c-Myc protein levels and increases pro-survival PGC1α which in concert mediate a suppression of glycolysis and a concomitant activation of oxidative phosphorylation (OXPHOS) that is fueled by enhanced fatty acid oxidation (FAO). more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL17930
4 Samples
Download data: CEL
Series
Accession:
GSE152612
ID:
200152612
15.

Anti-Warburg effect elicited by mitochondrial biogenesis drives differentiation of glioblastoma cells into astroglial cells

(Submitter supplied) Glioblastoma (GBM) is among the most aggressive of human cancers. Although differentiation therapy has been proposed to be potential approach to treat GBM, the mechanisms of induced differentiation remain poorly defined. Here, we established the induced differentiation model of GBM by using cAMP activators, which specifically directed GBM into astroglia. Next, transcriptomic and proteomic analyses uncovered oxidative phosphorylation and mitochondrial biogenesis were involved in induced differentiation of GBM. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
5 Samples
Download data: TXT
16.

Differential gene expression in neuroblastoma cells after treatment with vehicle control, JQ1, panobinostat, or combination of JQ1 and panobinostat

(Submitter supplied) The bromodomain inhibitor JQ1 and the histone deacetylase inhibitor panobinostat induce synergistic anticancer effects We analyzed whether JQ1 and panobinostat synergistically modulate gene expression
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL16686
12 Samples
Download data: CEL
Series
Accession:
GSE68690
ID:
200068690
17.

Disulfiram when combined with copper enhances the therapeutic effects of temozolomide for the treatment of Glioblastoma

(Submitter supplied) Dilsulfiram together with Copper shows efficacy against patient derived Brain Tumor Initiating Cells (BTICs) in vitro and sensitizes BTICs to the DNA damaging agent TMZ. In addition, preclinical assessment found that DSF/Cu potentiaties the efficicacy of TMZ in vivo and prolongs survival. We used microarrays to detail the global profile of gene expression underlying DSF/Cu treatment in vitro and in vivo in BTICs.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL15207
10 Samples
Download data: CEL
Series
Accession:
GSE76146
ID:
200076146
18.

Gene expression analysis of IDH1 wild type and IDH1 R132H mutated U87 cells

(Submitter supplied) U87 cells were transduced with IDH1 WT or IDH1 R132H and stable clones were selected.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL17930
2 Samples
Download data: CEL
Series
Accession:
GSE101291
ID:
200101291
19.

Synergistic Immunostimulatory Effects and Therapeutic Benefit of Combined Histone Deacetylase and Bromodomain Inhibition in Non-small Cell Lung Cancer.

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by array; Expression profiling by high throughput sequencing
Platforms:
GPL19057 GPL22364
204 Samples
Download data: RCC
Series
Accession:
GSE98049
ID:
200098049
20.

Single-cell profiling of tumor infiltrating T cells and macrophages [RNA-Seq]

(Submitter supplied) Effective therapies for non-small cell lung cancer (NSCLC) remain challenging despite an increasingly comprehensive understanding of somatically altered oncogenic pathways. It is now clear that therapeutic agents with potential to impact the tumor immune microenvironment potentiate immune-orchestrated therapeutic benefit. Herein we evaluated the immunoregulatory properties of histone deacetylase (HDAC) and bromodomain inhibitors, two classes of drugs that modulate the epigenome, with a focus on key cell subsets that are engaged in an immune response. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
192 Samples
Download data: TXT
Series
Accession:
GSE98048
ID:
200098048
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