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Links from GEO DataSets

Items: 20

1.

ASCL1 ChIP-seq of patient-derived-xenograft (PDX) GBM lines and RNA-seq of mouse glioma tumors

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens; Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL11002 GPL10999
14 Samples
Download data: BW
Series
Accession:
GSE152401
ID:
200152401
2.

RNA-seq of mouse glioma tumors with or without ASCL1

(Submitter supplied) Tamoxifen was administered to Glast-CreER;Nf1-flox/flox;Tp53-flox/flox or Glast-CreER;Ascl1-flox/flox;Nf1-flox/flox;Tp53-flox/flox at E14.5 to induce tumors in the brain
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11002
10 Samples
Download data: TXT
Series
Accession:
GSE152400
ID:
200152400
3.

ASCL1 ChIP-seq of patient-derived-xenograft (PDX) GBM lines

(Submitter supplied) R548 and R738 PDX-GBMs were grown orthotopically in the brains of NOD-SCID mice
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL10999
4 Samples
Download data: BW
Series
Accession:
GSE152399
ID:
200152399
4.

Identifying ASCL1-mediated chromatin changes in primary GBM stem cell cultures [ATAC-seq]

(Submitter supplied) ASCL1 mediates neuronal differentiation of GBM stem cell (GSC) cultures. We sought to identify chromatin changes upon induced ASCL1 expression in primary human GSC cultures. In this dataset, we include ATAC-seq data obtained from GSC cultures harbouring a CRISPR-deletion of ASCL1. We assessed differential ASCL1 binding between control and GSC cultures induced to overexpress ASCL1 after 14 days of doxycycline treatment.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL16791
4 Samples
Download data: NARROWPEAK
Series
Accession:
GSE90547
ID:
200090547
5.

Temporal gene expression of human-fetal and glioblastoma stem cell cultures under directed differentiation conditions

(Submitter supplied) Primary glioblastoma (GBM) cultures vary with respect to differentiation competency. We sought to identify putative transcription factors necessary for the differentiation of GBM cultures. In this dataset, we include expression data obtained from 2 human-fetal neural stem cell (HF-NS) cultures and 2 GBM stem cell (GSC) cultures. We assessed changes in gene expression from 3 timepoints during an in vitro differentiation protocol.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL5188
12 Samples
Download data: CEL
Series
Accession:
GSE87619
ID:
200087619
6.

Identifying ASCL1 target genes in primary GBM stem cell cultures [ChIP-seq]

(Submitter supplied) ASCL1 mediates neuronal differentiation of GBM stem cell (GSC) cultures. We sought to identify genomic targets of ASCL1 in primary human GSC cultures. In this dataset, we include ChIP-seq data obtained from GSC cultures harbouring a CRISPR-deletion of ASCL1. We assessed differential ASCL1 binding between control and GSC cultures induced to overexpress ASCL1 after 18 hours of doxycycline treatment.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL16791
8 Samples
Download data: NARROWPEAK
Series
Accession:
GSE87618
ID:
200087618
7.

Identifying ASCL1 target genes in primary GBM stem cell cultures [RNA-seq]

(Submitter supplied) ASCL1 mediates neuronal differentiation of GBM stem cell (GSC) cultures. We sought to identify targets of ASCL1 in primary human GSC cultures. In this dataset, we include RNA-seq data obtained from GSC cultures harbouring a CRISPR-deletion of ASCL1. We assessed differential gene expression between control and GSC cultures induced to overexpress ASCL1 after 7 days of doxycycline treatment.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
6 Samples
Download data: TXT
Series
Accession:
GSE87617
ID:
200087617
8.

ASCL1 mediates neuronal differentiation of primary GBM stem cell cultures upon Notch signalling blockade [RNA-seq]

(Submitter supplied) ASCL1 mediates neuronal differentiation of GBM stem cell (GSC) cultures upon Notch signalling inhibition. We sought to identify gene expression changes that were specific to ASCL1 function. In this dataset, we include RNA-seq data obtained from GSC cultures harbouring wildtype or CRISPR-deletion of ASCL1. We assessed differential gene expression between wildtype and ASCL1-knockout after treatment with gamma-secretase inhibitor for 7 days.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
12 Samples
Download data: TXT
Series
Accession:
GSE87615
ID:
200087615
9.

Silencing of ASCL1 in U87MG glioma cells

(Submitter supplied) ASCL1 is known to act as transcriptional activator of notch signaling pathway. We have found that ASCL1 is over expressed in secondary glioblastoma. In order to delineate its functional role in gliomagensis we have used gene silencing approach to identify genes differentially regulated upon ASCL1 down regulation in U87MG glioma cell line.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL16356
6 Samples
Download data: CEL
Series
Accession:
GSE76652
ID:
200076652
10.

ASCL1 represses a SOX9+ neural-crest-stem-like state in small cell lung cancer

(Submitter supplied) ASCL1 is a neuroendocrine-lineage-specific oncogenic driver of small cell lung cancer (SCLC), highly expressed in a significant fraction of tumors. However, ~25% of human SCLC are ASCL1-low and associated with low-neuroendocrine fate and high MYC expression. Using genetically-engineered mouse models (GEMMs), we show that alterations in Rb1/Trp53/Myc in the mouse lung induce an ASCL1+ state of SCLC in multiple cells of origin. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
4 Samples
Download data: MTX, TSV
Series
Accession:
GSE169529
ID:
200169529
11.

ASCL1 represses a latent osteogenic program in small cell lung cancer in multiple cells of origin

(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:
GPL24247 GPL17021
15 Samples
Download data: BW, MTX, TSV
Series
Accession:
GSE155692
ID:
200155692
12.

ASCL1 represses a latent osteogenic program in small cell lung cancer in multiple cells of origin [RNA-Seq]

(Submitter supplied) ASCL1 is a neuroendocrine-lineage-specific oncogenic driver of small cell lung cancer (SCLC), highly expressed in a significant fraction of tumors. However, ~25% of human SCLC are ASCL1-low and associated with low-neuroendocrine fate and high MYC expression. Using genetically-engineered mouse models (GEMMs), we show that alterations in Rb1/Trp53/Myc in the mouse lung induce an ASCL1+ state of SCLC in multiple cell types. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
7 Samples
Download data: TXT
Series
Accession:
GSE155691
ID:
200155691
13.

ASCL1 represses a latent osteogenic program in small cell lung cancer in multiple cells of origin [ChIP-Seq]

(Submitter supplied) ASCL1 is a neuroendocrine-lineage-specific oncogenic driver of small cell lung cancer (SCLC), highly expressed in a significant fraction of tumors. However, ~25% of human SCLC are ASCL1-low and associated with low-neuroendocrine fate and high MYC expression. Using genetically-engineered mouse models (GEMMs), we show that alterations in Rb1/Trp53/Myc in the mouse lung induce an ASCL1+ state of SCLC in multiple cell types. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL17021
4 Samples
Download data: BW
Series
Accession:
GSE155690
ID:
200155690
14.

MYC drives temporal evolution of small cell lung cancer subtypes by reprogramming neuroendocrine fate [Human SCLC biopsy]

(Submitter supplied) Small cell lung cancer (SCLC) is a neuroendocrine tumor treated clinically as a single disease with poor outcomes. Distinct SCLC molecular subtypes have been defined based on expression of lineage-related transcription factors: ASCL1, NEUROD1, POU2F3 or YAP1, but their origins remain unknown. We developed an in vitro model of MYC-driven SCLC tumor cell progression, and performed a time-series analysis of single-cell transcriptome profiling to reveal that MYC drives the dynamic evolution of SCLC subtypes. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
1 Sample
Download data: MTX, TSV
Series
Accession:
GSE150766
ID:
200150766
15.

MYC drives temporal evolution of small cell lung cancer subtypes by reprogramming neuroendocrine fate [WGS data]

(Submitter supplied) Distinct SCLC molecular subtypes have been defined based on expression of lineage-related transcription factors: ASCL1, NEUROD1, POU2F3 or YAP1, but their origins remain unknown. To study transcriptional dynamics of MYC-driven tumor evolution and compare transcriptional states to human SCLC tumors, we performed bulk and single-cell RNA-sequencing on various timepoints of Rb1/Trp53/MycT58A (RPM) tumor cells (from Ad-Cgrp-Cre infected mice) as they progress in culture, and on RPM bulk tumors. more...
Organism:
Mus musculus
Type:
Other
Platform:
GPL24247
3 Samples
Download data: VCF
Series
Accession:
GSE149444
ID:
200149444
16.

MYC drives temporal evolution of small cell lung cancer subtypes by reprogramming neuroendocrine fate [SuperSeries]

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus; Homo sapiens
Type:
Expression profiling by high throughput sequencing; Other
Platforms:
GPL24676 GPL24247 GPL17021
38 Samples
Download data: MTX, TSV
Series
Accession:
GSE149180
ID:
200149180
17.

MYC drives temporal evolution of small cell lung cancer subtypes by reprogramming neuroendocrine fate [Single Cell RNA seq on RPM time-series cells and 4 RPM bulk tumors]

(Submitter supplied) Small cell lung cancer (SCLC) is a neuroendocrine tumor treated clinically as a single disease with poor outcomes. Distinct SCLC molecular subtypes have been defined based on expression of lineage-related transcription factors: ASCL1, NEUROD1, POU2F3 or YAP1, but their origins remain unknown. Here, we develop an in vitro model of MYC-driven SCLC tumor cell progression and perform a time-series analysis of single-cell transcriptome profiling to reveal that MYC drives the dynamic evolution of SCLC subtypes. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
11 Samples
Download data: MTX, TSV
Series
Accession:
GSE149179
ID:
200149179
18.

MYC drives temporal evolution of small cell lung cancer subtypes by reprogramming neuroendocrine fate [Bulk RNA-seq of RPM time-series cells]

(Submitter supplied) Distinct SCLC molecular subtypes have been defined based on expression of lineage-related transcription factors: ASCL1, NEUROD1, POU2F3 or YAP1, but their origins remain unknown. To study transcriptional dynamics of MYC-driven tumor evolution and compare transcriptional states to human SCLC tumors, we performed bulk RNA-sequencing on various timepoints of Rb1/Trp53/MycT58A (RPM) tumor cells (from Ad-Cgrp-Cre infected mice) as they progress in culture. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
8 Samples
Download data: CSV, TXT
Series
Accession:
GSE149178
ID:
200149178
19.

MYC drives temporal evolution of small cell lung cancer subtypes by reprogramming neuroendocrine fate [Bulk RNA-seq of RPM and RPR2 tumors]

(Submitter supplied) Distinct SCLC molecular subtypes have been defined based on expression of lineage-related transcription factors: ASCL1, NEUROD1, POU2F3 or YAP1, but their origins remain unknown. We perform bulk RNA-sequencing on SCLC tumors from RPM and Rb1/Trp53/Rbl2 (RPR2) GEMMs, initiated by CGRP-Cre, to complement time-series analysis of single-cell transcriptome profiling and reveal that MYC drives the dynamic evolution of SCLC subtypes. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL24247 GPL17021
15 Samples
Download data: TXT, XLSX
Series
Accession:
GSE149175
ID:
200149175
20.

Inhibition of Karyopherin β1-mediated nuclear import of lineage-defining TFs in small cell lung cancer

(Submitter supplied) Extensive genomic studies support the classification of small cell lung cancer (SCLC) into subtypes based on expression of lineage-defining transcription factors including ASCL1 and NEUROD1, which together account for ~80% of this disease. ASCL1 and NEUROD1 activate SCLC oncogene expression and drive distinct transcriptional programs. ASCL1 is also required for tumorigenesis in SCLC mouse models, and both ASCL1 and NEUROD1 maintain the in vitro growth and oncogenic properties of ASCL1+ or NEUROD1+ SCLC cell lines. more...
Organism:
Mus musculus; Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL21626 GPL21697
32 Samples
Download data: TXT
Series
Accession:
GSE185187
ID:
200185187
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