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Links from GEO DataSets

Items: 20

1.

Core pathway mutations induce de-differentiation of murine astrocytes into glioblastoma stem cells that are sensitive to radiation, but resistant to temozolomide

(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
Platform:
GPL19057
13 Samples
Download data: BW
Series
Accession:
GSE75592
ID:
200075592
2.

Core pathway mutations induce de-differentiation of murine astrocytes into glioblastoma stem cells that are sensitive to radiation, but resistant to temozolomide (RNA-seq)

(Submitter supplied) Introduction: Glioma stem cells isolated from human glioblastomas are resistant to radiation and cytotoxic chemotherapy and may drive tumor recurrence. Treatment efficacy may depend on the presence of glioma stem cells, expression of DNA repair enzymes such as methylguanine methyltransferase (MGMT), or transcriptome subtype. Methods: To model genetic alterations in the core signaling pathways of human glioblastoma, we induced conditional Rb knockout, Kras activation, and Pten deletion mutations in cortical murine astrocytes. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
4 Samples
Download data: TXT
Series
Accession:
GSE75589
ID:
200075589
3.

Core pathway mutations induce de-differentiation of murine astrocytes into glioblastoma stem cells that are sensitive to radiation, but resistant to temozolomide (FAIRE-seq)

(Submitter supplied) Introduction: Glioma stem cells isolated from human glioblastomas are resistant to radiation and cytotoxic chemotherapy and may drive tumor recurrence. Treatment efficacy may depend on the presence of glioma stem cells, expression of DNA repair enzymes such as methylguanine methyltransferase (MGMT), or transcriptome subtype. Methods: To model genetic alterations in the core signaling pathways of human glioblastoma, we induced conditional Rb knockout, Kras activation, and Pten deletion mutations in cortical murine astrocytes. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL19057
9 Samples
Download data: BW
Series
Accession:
GSE73262
ID:
200073262
4.

Core pathway mutations induce de-differentiation of murine astrocytes into glioblastoma stem cells that are sensitive to radiation but resistant to temozolomide.

(Submitter supplied) BACKGROUND: Glioma stem cells (GSCs) from human glioblastomas (GBMs) are resistant to radiation and chemotherapy and may drive recurrence. Treatment efficacy may depend on GSCs, expression of DNA repair enzymes such as methylguanine methyltransferase (MGMT), or transcriptome subtype. METHODS: To model genetic alterations in human GBM core signaling pathways, we induced Rb knockout, Kras activation, and Pten deletion mutations in cortical murine astrocytes. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL11202
37 Samples
Download data: TXT
Series
Accession:
GSE59116
ID:
200059116
5.

Oncogenic alterations in multiple core signaling pathways are required for glioblastoma pathogenesis in vitro and in vivo

(Submitter supplied) Here, we use a series of genetically-defined murine cortical astrocytes with conditional inactivation of Rb/Pten and activated Kras to systematically investigate the individual and combinatorial roles of these pathways during gliomagenesis. We show that genetic disruption of all three pathways, which frequently occurs in human GBM, leads to maximal in vitro growth, migration, and invasion and produces stem-like transcriptomal profiles similar to the proneural subtype of human GBM. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL7202
23 Samples
Download data: TXT
Series
Accession:
GSE40265
ID:
200040265
6.

Expression data from glioblastoma stem-like cells (GSCs) and astrocyte co-cultured GSCs

(Submitter supplied) consequences of astrocytes on GSCs, gene expression profiles generated from glioblastoma stem-like cells grown alone (mono-culture) and compared to those generated 48h after the initiation of co-culture with astrocytes We used microarrays show that astrocytes are capable to modify via a paracrine mechanism GSC gene expression and thus phenotype.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL571
12 Samples
Download data: CEL, CHP
Series
Accession:
GSE63037
ID:
200063037
7.

Quiescent glioblastoma cells shift to an epithelial-mesenchymal transition-like gene program

(Submitter supplied) Quiescent stem cells of glioblastoma (GBM), a malignant primary brain tumor, are potential sources for recurrence after therapy. However, the gene expression program underlying the physiology of GBM stem cells remains unclear. We have isolated quiescent GBM cells by engineering them with a knock-in H2B-GFP proliferation reporter and expanding them in a 3D tumor organoid model that mimics tumor heterogeneity. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
12 Samples
Download data: CSV, TXT
8.

Expression data from glioma cells exposed to interferon (IFN)-beta

(Submitter supplied) Glioma cells are sensitized to the alkylator temozolomide after exposure to IFN-beta. In glioma-initiating cells (GIC), IFN-beta alone reduces clonogenicity. We investigated differentially expressed genes with or without IFN exposure in either longterm glioma cells or GIC. We used microarrays to investigate differential gene regulation in glioma cells after exposure to either ddH20 or IFN-beta 300 IU/ml at 6 h or 24 h.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL571
12 Samples
Download data: CEL
Series
Accession:
GSE53213
ID:
200053213
9.

Glioblastoma from a homogenous cohort of patients treated within clinical trial

(Submitter supplied) Analysis of 80 glioblastoma specimen of patients treated within clinical trials and 4 samples of "normal" brain tissue (non-tumoral). The data was used to identify factors of resistance to a chemoradiation therapy protocol of radiotherapy and concomitant and adjuvant temozolomide (alkylating agent). Keywords: Disease state comparison
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
84 Samples
Download data: CEL
Series
Accession:
GSE7696
ID:
200007696
10.

Glioblastoma stem cell (GSC) clones survived 500uM Temozolomide (TMZ) treatment

(Submitter supplied) Comparison of parental GSC (GSC-parental) with treatment resistant GSC clones survived 500uM TMZ treatment (GSC-500uM TMZ) We used microarrays to identify defense profiles of GSC-500uM TMZ
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
12 Samples
Download data: CEL
Series
Accession:
GSE68029
ID:
200068029
11.

Novel KDM1A inhibitors induce differentiation and apoptosis of glioma stem cells via unfolded protein response (UPR) pathway

(Submitter supplied) We examined the transcriptional changes modulated by KDM1A inhibitor NCD-38 by performing global transcriptome analysis. Glioma Stem Cells (GSC10) were treated with either vehicle or NCD-38 for 24 h and the isolated RNA was utilized for RNA-seq analysis. Our results demonstrated that NCD-38 modulated several genes that are involved in unfolded protein response, endoplasmic reticulum stress pathway and NRF-2 mediated oxidative stress response.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
4 Samples
Download data: TXT
12.

Enriching glioma stem cells by intracranial implantation and developing clinically relevant model for therapeutic intervention

(Submitter supplied) It is becoming better understood that radiation resistance in glioblastomas (GBMs) may be secondary to a self-renewing subpopulation of cells in the bulk tumor that form neurospheres in culture. This population has been referred to as Glioma stem cells (GSCs). One of the limitations regarding the use of GSCs is that these studies require fresh tumor biopsy samples obtained from patients, and can be extremely difficult to culture, propagate, and perform treatment-response assays. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
7 Samples
Download data: CEL
Series
Accession:
GSE54660
ID:
200054660
13.

EGFR/FOXO3a/BIM signalling pathway determines chemosensitivity of BMP4-differentiated glioma stem cells to temozolomide

(Submitter supplied) Accumulating evidence suggests that glioma stem cells (GSCs), rare cells characterised by pluripotency and self-renewal, are responsible for glioblastoma (GBM) propagation, recurrence and resistance to therapy. Differentiation with bone morphogenic proteins (BMPs) is considered to be a promising approach to eliminate GSCs and sensitise glioma to chemotherapeutics. Epidermal growth factor receptor (EGFR) gene alterations are detected in more than a half of GBMs, however, the role of EGFR in chemoresistance of glioma stem cells remain elusive. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18460
12 Samples
Download data: BEDGRAPH, TSV
14.

Expression data from glioblastoma stem cell clones (GSC)

(Submitter supplied) Comparison of treatment sensitive GSC clones (TSGC) with treatment resistant GSC clones (TRGC). We used microarrays to identify molecular signatures of TRGC (upregulated genes).
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
12 Samples
Download data: CEL, DCP
Series
Accession:
GSE46531
ID:
200046531
15.

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
16.

RNA-sequencing WT vs SOCS3 knockout Glioblastoma stem-cells

(Submitter supplied) Glioblastoma stem cells were infected with lentivirus expressing a non-targeting (gRNA-LacZ) or SOCS3 targeting gRNA to assess the function of SOCS3 in the stem cell compartment of Glioblastoma
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
6 Samples
Download data: TXT
Series
Accession:
GSE122486
ID:
200122486
17.

Patient-derived glioblastoma stem cells transcriptome regulation by CD109

(Submitter supplied) Glioma stem cells (GSCs) drive propagation and therapeutic resistance of glioblastomas, the most aggressive diffuse brain tumor. However, the molecular mechanisms that maintain the stemness and promote therapy resistance remain poorly understood. Here we study CD109 – STAT3 axis as crucial for the maintenance of stemness and tumorigenicity of GSCs and as a mediator of chemoresistance. Mechanistically, CD109 physically interacts with glycoprotein 130 (GP130) to promote activation of the IL-6/STAT3 pathway in GSCs. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
20 Samples
Download data: XLSX
18.

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
19.

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
20.

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
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