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Links from GEO DataSets

Items: 20

1.

Cancer avatars derived from genetically engineered pluripotent stem cells allow for longitudinal assessment of tumor development

(Submitter supplied) Many current cellular models aimed to elucidate cancer biology do not recapitulate pathobiology including tumor heterogeneity, an inherent feature of cancer that underlies treatment resistance. Here we introduce a new cancer modeling paradigm using genetically engineered human pluripotent stem cells (hiPSCs) that capture authentic cancer pathobiology. Orthotopic engraftment of the neural progenitor cells derived from hiPSCs introduced with tumor-associated genetic driver mutations revealed by The Cancer Genome Atlas project for glioblastoma (GBM) results in formation of brain tumors. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20301
6 Samples
Download data: TSV
Series
Accession:
GSE133479
ID:
200133479
2.

Cancer avatars derived from genetically engineered pluripotent stem cells allow for longitudinal assessment of tumor development

(Submitter supplied) Many current cellular models aimed to elucidate cancer biology do not recapitulate pathobiology including tumor heterogeneity, an inherent feature of cancer that underlies treatment resistance. Here we introduce a new cancer modeling paradigm using genetically engineered human pluripotent stem cells (hiPSCs) that capture authentic cancer pathobiology. Orthotopic engraftment of the neural progenitor cells derived from hiPSCs introduced with tumor-associated genetic driver mutations revealed by The Cancer Genome Atlas project for glioblastoma (GBM) results in formation of brain tumors. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
14 Samples
Download data: H5, HTML
3.

Cooperative actions of p53 and Pten in normal and neoplastic progenitor cell renewal and differentiation

(Submitter supplied) Glioblastoma (GBM) is a highly lethal brain tumor presenting as one of two subtypes with distinct clinical histories and molecular profiles. The primary GBM subtype presents acutely as high-grade disease that typically harbors EGFR, PTEN and Ink4a/Arf mutations, and the secondary GBM subtype evolves from the slow progression of low-grade disease that classically possesses PDGF and p53 events1. Here, we show that concomitant CNS-specific deletion of p53 and Pten in the mouse CNS generates a penetrant acute-onset high-grade malignant glioma phenotype with striking clinical, pathological and molecular resemblance to primary GBM in humans. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
5 Samples
Download data: CEL
Series
Accession:
GSE12694
ID:
200012694
4.

Gene Expression Profile of high grade glioma in Nestin-creERT2 and NG2-creERTM driven tumor suppressors knockout mouse model

(Submitter supplied) Mouse model with P53f/f;Nf1f/+;Ptenf/+ configuration driven by Nestin-creERT2 and NG2-creERTM induced at 1 month postnatal forms high grade glioma in the brain. Tumors were harvested and total RNA were extracted for gene expression profile.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6887
13 Samples
Download data: TXT
Series
Accession:
GSE57038
ID:
200057038
5.

Particulate radiation-induced gliomas

(Submitter supplied) Trangenic mice with brain-targeted deletion of one allele of p53 and one allele ot Pten were irradiated with particulate radiation. Radiation induced gliomas were analyzed to identify copy number variations
Organism:
Mus musculus
Type:
Genome variation profiling by array
Platform:
GPL21714
7 Samples
Download data: TXT
Series
Accession:
GSE130677
ID:
200130677
6.

Olig1/2-expressing intermediate lineage progenitors are predisposed to PTEN/p53-loss-induced gliomagenesis and harbor specific therapeutic vulnerabilities

(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; Other
4 related Platforms
30 Samples
Download data: BED, BIGWIG
Series
Accession:
GSE200892
ID:
200200892
7.

Transit-amplifying lineage states convey the susceptibility of PTEN and P53 loss to gliomagenesis [CUT&RUN]

(Submitter supplied) To investigate the glioma mouse model by knocking out Pten and Trp53 in embryonal Olig2 and Olig1 positive cells in glioma pathogenesis. Chromatin immunoprecipitation DNA-sequencing (ChIP-seq) for H3K27Ac in PPO1 and PPO2 mouse glioma cell lines and compare the active enhancers with oligodendrocyte progenitor cells.
Organism:
Mus musculus
Type:
Other
Platform:
GPL24247
4 Samples
Download data: BED, BIGWIG
Series
Accession:
GSE200891
ID:
200200891
8.

Transit-amplifying lineage states convey the susceptibility of PTEN and P53 loss to gliomagenesis [ATAC-seq]

(Submitter supplied) To investigate the glioma mouse model by knocking out Pten and Trp53 in embryonal Olig2 and Olig1 positive cells in glioma pathogenesis. ATAC-seq
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL17021
2 Samples
Download data: BED, BIGWIG
Series
Accession:
GSE200890
ID:
200200890
9.

Transit-amplifying lineage states convey the susceptibility of PTEN and P53 loss to gliomagenesis [PPO1_and PPO1_Cells_RNA-seq]

(Submitter supplied) To investigate the glioma mouse model by knocking out Pten and Trp53 in embryonal Olig2 and Olig1 positive cells in glioma pathogenesis. We then performed gene expression profiling analysis using data obtained from RNA-seq of 4 PPO2, 4 PPO1 and 2 OPN cell lines.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL23479
10 Samples
Download data: TXT
Series
Accession:
GSE200889
ID:
200200889
10.

Transit-amplifying lineage states convey the susceptibility of PTEN and P53 loss to gliomagenesis [PPO2_Bulk_RNA-seq]

(Submitter supplied) To investigate the glioma mouse model by knocking out Pten and Trp53 in embryonal Olig2 positive cells in glioma pathogenesis. We then performed gene expression profiling analysis using data obtained from RNA-seq of 4 PPO2 tumor tissue with 2 Control cortex tissue.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL23479
6 Samples
Download data: TXT
Series
Accession:
GSE200888
ID:
200200888
11.

Transit-amplifying lineage states convey the susceptibility of PTEN and P53 loss to gliomagenesis [PPO1_Bulk_RNA-seq]

(Submitter supplied) To investigate the glioma mouse model by knocking out Pten and Trp53 in embryonal Olig1 positive cells in glioma pathogenesis and track its evolution over multiple time-points. We then performed gene expression profiling analysis using data obtained from RNA-seq of 5 PPO1 tumor tissue with 3 Control cortex tissue.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
8 Samples
Download data: TXT
Series
Accession:
GSE200887
ID:
200200887
12.

Identification and molecular characterization of distinct glioblastoma cancer stem cell populations

(Submitter supplied) Malignant glioblastoma (GBM) is a highly aggressive brain tumor with a dismal prognosis and limited therapeutic options. Genomic profiling of GBM samples in the TCGA database has identified four molecular subtypes (Proneural, Neural, Classical and Mesenchymal), which may arise from different glioblastoma stem-like cell (GSC) populations. In the present study, we identify two GSC populations that produce GBM tumors by subcutaneous and intracranial injection with identical histological features. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL10558
12 Samples
Download data: IDAT
Series
Accession:
GSE65576
ID:
200065576
13.

Progression from low- to high-grade astrocytoma is characterized by transcriptomal heterogeneity and genomic number copy alterations

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by array; Genome variation profiling by genome tiling array
Platforms:
GPL11202 GPL15076 GPL7202
172 Samples
Download data: TXT
Series
Accession:
GSE49269
ID:
200049269
14.

Progression from low- to high-grade astrocytoma is characterized by transcriptomal heterogeneity and genomic number copy alterations (part 4)

(Submitter supplied) We used genetically-engineered mice (GEM) to target constitutive RTK effector pathway (KrasG12D and/or Pten deletion) mutations in G1/S checkpoint-defective adult mouse astrocytes. Genetic lineage tracing showed that these mutations potentiated tumor initiation in cortical, diencephalic, brainstem, and olfactory bulb astrocytes, producing low-grade astrocytomas (LGA). LGA lacked copy number abnormalities (CNA), but showed oncogenic driver- and astrocyte location-specific transcriptome profiles, suggesting that both driver mutations and cellular origin contribute to LGA genomic heterogeneity. more...
Organism:
Mus musculus
Type:
Genome variation profiling by genome tiling array
Platform:
GPL15076
41 Samples
Download data: TXT
Series
Accession:
GSE49268
ID:
200049268
15.

Progression from low- to high-grade astrocytoma is characterized by transcriptomal heterogeneity and genomic number copy alterations (part 3)

(Submitter supplied) We used genetically-engineered mice (GEM) to target constitutive RTK effector pathway (KrasG12D and/or Pten deletion) mutations in G1/S checkpoint-defective adult mouse astrocytes. Genetic lineage tracing showed that these mutations potentiated tumor initiation in cortical, diencephalic, brainstem, and olfactory bulb astrocytes, producing low-grade astrocytomas (LGA). LGA lacked copy number abnormalities (CNA), but showed oncogenic driver- and astrocyte location-specific transcriptome profiles, suggesting that both driver mutations and cellular origin contribute to LGA genomic heterogeneity. more...
Organism:
Mus musculus
Type:
Genome variation profiling by genome tiling array
Platform:
GPL15076
10 Samples
Download data: TXT
Series
Accession:
GSE49267
ID:
200049267
16.

Progression from low- to high-grade astrocytoma is characterized by transcriptomal heterogeneity and genomic number copy alterations (part 2)

(Submitter supplied) We used genetically-engineered mice (GEM) to target constitutive RTK effector pathway (KrasG12D and/or Pten deletion) mutations in G1/S checkpoint-defective adult mouse astrocytes. Genetic lineage tracing showed that these mutations potentiated tumor initiation in cortical, diencephalic, brainstem, and olfactory bulb astrocytes, producing low-grade astrocytomas (LGA). LGA lacked copy number abnormalities (CNA), but showed oncogenic driver- and astrocyte location-specific transcriptome profiles, suggesting that both driver mutations and cellular origin contribute to LGA genomic heterogeneity. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL11202
43 Samples
Download data: TXT
Series
Accession:
GSE49266
ID:
200049266
17.

Progression from low- to high-grade astrocytoma is characterized by transcriptomal heterogeneity and genomic number copy alterations (part 1)

(Submitter supplied) We used genetically-engineered mice (GEM) to target constitutive RTK effector pathway (KrasG12D and/or Pten deletion) mutations in G1/S checkpoint-defective adult mouse astrocytes. Genetic lineage tracing showed that these mutations potentiated tumor initiation in cortical, diencephalic, brainstem, and olfactory bulb astrocytes, producing low-grade astrocytomas (LGA). LGA lacked copy number abnormalities (CNA), but showed oncogenic driver- and astrocyte location-specific transcriptome profiles, suggesting that both driver mutations and cellular origin contribute to LGA genomic heterogeneity. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL7202
78 Samples
Download data: TXT
Series
Accession:
GSE49265
ID:
200049265
18.

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
19.

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
20.

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
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