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Links from GEO DataSets

Items: 20

1.

TWIST2-Mediated Chromatin Remodeling Promotes Fusion-Negative Rhabdomyosarcoma [RNA-seq Xenograft]

(Submitter supplied) Sarcomas are derailed in pathways that specify mesenchymal lineages during embryogenesis, causing tumor cells to stall at early stages of differentiation. Among them, rhabdomyosarcoma (RMS) is a pediatric soft tissue sarcoma of skeletal muscle origin. A key feature of RMS is their inability to terminally differentiate despite the high expression of master myogenic regulator MYOD. The bHLH transcription factor TWIST2, which governs mesenchymal stem cell identity and restricts myogenesis, is overexpressed in patient fusion-negative RMS (FN-RMS) tumors. more...
Organism:
Mus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL23693
6 Samples
Download data: TXT
Series
Accession:
GSE207168
ID:
200207168
2.

TWIST2-Mediated Chromatin Remodeling Promotes Fusion-Negative Rhabdomyosarcoma.

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus; Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing
Platforms:
GPL16791 GPL23693 GPL18573
42 Samples
Download data: BED, BIGWIG, TXT
Series
Accession:
GSE207170
ID:
200207170
3.

TWIST2-Mediated Chromatin Remodeling Promotes Fusion-Negative Rhabdomyosarcoma [RNA-seq FN-RMS Cells]

(Submitter supplied) Sarcomas are derailed in pathways that specify mesenchymal lineages during embryogenesis, causing tumor cells to stall at early stages of differentiation. Among them, rhabdomyosarcoma (RMS) is a pediatric soft tissue sarcoma of skeletal muscle origin. A key feature of RMS is their inability to terminally differentiate despite the high expression of master myogenic regulator MYOD. The bHLH transcription factor TWIST2, which governs mesenchymal stem cell identity and restricts myogenesis, is overexpressed in patient fusion-negative RMS (FN-RMS) tumors. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL18573 GPL16791
12 Samples
Download data: TXT
Series
Accession:
GSE207167
ID:
200207167
4.

TWIST2-Mediated Chromatin Remodeling Promotes Fusion-Negative Rhabdomyosarcoma [ChIP-seq]

(Submitter supplied) Sarcomas are derailed in pathways that specify mesenchymal lineages during embryogenesis, causing tumor cells to stall at early stages of differentiation. Among them, rhabdomyosarcoma (RMS) is a pediatric soft tissue sarcoma of skeletal muscle origin. A key feature of RMS is their inability to terminally differentiate despite the high expression of master myogenic regulator MYOD. The bHLH transcription factor TWIST2, which governs mesenchymal stem cell identity and restricts myogenesis, is overexpressed in patient fusion-negative RMS (FN-RMS) tumors. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
24 Samples
Download data: BED, BIGWIG, TXT
Series
Accession:
GSE207165
ID:
200207165
5.

Genome-wide maps of Twist2-binding, MyoD-binding and chromatin state in Twist2-overexpressing Twist2+ cells

(Submitter supplied) Integrated analysis of genome-wide ChIP-Seq and RNA-Seq data revealed the first dynamic chromatin and transcriptional landscape of Twist2 binding during myogenic differentiation. During differentiation, Twist2 competes with MyoD at shared DNA motifs to direct global gene transcription and repression of the myogenic program. Additionally, TWIST2 shapes the epigenetic landscape to drive chromatin opening at oncogenic loci and chromatin closing at myogenic loci. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL19057
34 Samples
Download data: BIGWIG
Series
Accession:
GSE127998
ID:
200127998
6.

Liaison between SNAI2 and MYOD enhances oncogenesis and suppresses differentiation in Fusion-Negative Rhabdomyosarcoma

(Submitter supplied) Rhabdomyosarcoma (RMS) is a pediatric malignancy of mesenchymal origin. Fusion Negative-RMS (FN-RMS) tumors are associated with RAS-pathway activation. RMS tumors express pro-differentiation myogenic transcription factors MYOD and MYOG, yet why they are unable to differentiate is poorly understood. Here we show that SNAI2 is highly expressed in FN-RMS, is regulated by MYOD and blocks myogenic differentiation promoting growth. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing; Other
Platform:
GPL18573
22 Samples
Download data: HIC, NARROWPEAK, TXT
7.

PAX7 is a required target for microRNA-206-induced differentiation of fusion-negative rhabdomyosarcoma

(Submitter supplied) Genes regulated by miR-206 were identified by microarray analysis in RD cells transfected with a Negative Control (NC) or miR-206 Mimic
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL16686
8 Samples
Download data: CEL
Series
Accession:
GSE82129
ID:
200082129
8.

The BAF complex blocks Myogenesis in rhabdomyosarcoma 

(Submitter supplied) Rhabdomyosarcoma (RMS) is a highly malignant pediatric cancer of skeletal muscle lineage. The aggressive alveolar subtype is commonly characterized by t(2;13) or t(1;13) translocations with the expression of PAX3- or PAX7-FOXO1 fusion transcription factors respectively and is known as fusion positive RMS (FP-RMS). FP-RMS tumors rely on the fusion gene to maintain their proliferative state while avoiding terminal differentiation program. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL20301 GPL24676 GPL18573
52 Samples
Download data: BED, TXT
9.

Selective Disruption of Core Regulatory Transcription

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus; Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing
Platforms:
GPL19415 GPL18573
109 Samples
Download data: BED, HIC, TXT
Series
Accession:
GSE120771
ID:
200120771
10.

Selective Disruption of Core Regulatory Transcription [ChIP-seq]

(Submitter supplied) Activation of identity determining transcription factors (TFs), or core regulatory TFs, is governed by cell-type specific enhancers, an important subset of these being super enhancers (SEs). This mechanism is distinct from constitutive expression of housekeeping genes. The characterization of drug-like small molecules to selectively inhibit core regulatory circuitry is of high interest for treatment of cancers, which are addicted to core regulatory TF function at SEs. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
48 Samples
Download data: BED
Series
Accession:
GSE116344
ID:
200116344
11.

Epigenetic Lanscape and BRD4 Transcriptional Dependency of PAX3-FOXO1 Driven Rhabdomyosarcoma

(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; Other
Platforms:
GPL11154 GPL18573
80 Samples
Download data: BED, BEDGRAPH, FPKM_TRACKING
Series
Accession:
GSE83728
ID:
200083728
12.

PAX3-FOXO1 establishes myogenic super enhancers and recruits BRD4 de novo [7250 ChIP-seq]

(Submitter supplied) The fusion transcription factor PAX3-FOXO1 drives oncogenesis in a subset of rhabdomyosarcomas, however the mechanisms by which it remodels chromatin are unknown. We find PAX3-FOXO1 reprograms the cis-regulatory landscape by inducing super enhancers (SEs), in collaboration with master transcription factors MYOG, MYOD and MYCN. This myogenic SE circuitry is consistent across cell lines and primary tumors. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL18573 GPL11154
14 Samples
Download data: BED
Series
Accession:
GSE83725
ID:
200083725
13.

CD73 contributes to the pathogenesis of Fusion-Negative Rhabdomyosarcoma through the purinergic signaling pathway

(Submitter supplied) We performed RNA-seq to evaluated the transcriptional changes of CD73 knockdown in RD cells, a Fusion Negative Rhabdomyosarcoma cell line. We used a Dox-inducible shRNA targetting the 3'UTR of CD73 to knockdown this gene. Cells with No-Dox were used as control.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21697
12 Samples
Download data: TXT
Series
Accession:
GSE240722
ID:
200240722
14.

RNA-Seq and ChIP-Seq in SIX1 deficient Rhabdomyosarcoma cells

(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
Platforms:
GPL24676 GPL18573
21 Samples
Download data: TDF
Series
Accession:
GSE173155
ID:
200173155
15.

Chromatin states and transcription factor binding in SIX1 deficient Rhabdomyosarcoma cells

(Submitter supplied) Genetic and shRNA-mediated inhibition of SIX1 expression in RMS cells induces myogenic differentiation and impedes RMS tumor growth. To elucidate the mechanism by which SIX1 loss activates a differentiation program, we performed SIX1, MYOD1, and H3K27ac ChIPseq in two SIX1 knockdown SMS-CTR cell lines and one control SMS-CTR cell line to profile changes in transcriptional activity and myogenic transcription factor binding in fusion-negative Rhabdomyosarcoma.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
12 Samples
Download data: TDF
Series
Accession:
GSE173151
ID:
200173151
16.

Transcriptomes of SIX1 deficient and control Rhabdomyosarcoma cells

(Submitter supplied) Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to compare NGS-derived retinal transcriptome profiling (RNA-seq) to microarray and quantitative reverse transcription polymerase chain reaction (qRT–PCR) methods and to evaluate protocols for optimal high-throughput data analysis Genetic and shRNA-mediated inhibition of SIX1 expression in RMS cells induces myogenic differentiation and impedes RMS tumor growth. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
9 Samples
Download data: TXT
17.

A MYOD-SKP2 axis boosts tumorigenesis in fusion negative rhabdomyosarcoma by preventing differentiation through p57Kip2 targeting [Hi-ChIP]

(Submitter supplied) Rhabdomyosarcoma (RMS) is a pediatric mesenchymal-derived malignancy encompassing Fusion Positive (FP)-RMS expressing PAX3/7-FOXO1 and Fusion Negative (FN)-RMS often mutated in the RAS pathway. RMS expresses the master myogenic transcription factor MYOD that, paradoxically, is unable to support differentiation while essential for tumor cell survival. We identify here SKP2, an oncogenic E3-ubiquitin ligase, as a critical driver of tumorigenesis in FN-RMS. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing; Other
Platform:
GPL24676
2 Samples
Download data: HIC
Series
Accession:
GSE245495
ID:
200245495
18.

A MYOD-SKP2 axis boosts tumorigenesis in fusion negative rhabdomyosarcoma by preventing differentiation through p57Kip2 targeting

(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:
GPL24676
10 Samples
Download data: BED, HIC, TXT
Series
Accession:
GSE241283
ID:
200241283
19.

A MYOD-SKP2 axis boosts tumorigenesis in fusion negative rhabdomyosarcoma by preventing differentiation through p57Kip2 targeting [RNA-seq]

(Submitter supplied) Rhabdomyosarcoma (RMS) is a pediatric mesenchymal-derived malignancy encompassing Fusion Positive (FP)-RMS expressing PAX3/7-FOXO1 and Fusion Negative (FN)-RMS often mutated in the RAS pathway. RMS expresses the master myogenic transcription factor MYOD that, paradoxically, is unable to support differentiation while essential for tumor cell survival. We identify here SKP2, an oncogenic E3-ubiquitin ligase, as a critical driver of tumorigenesis in FN-RMS. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
4 Samples
Download data: TXT
Series
Accession:
GSE241282
ID:
200241282
20.

A MYOD-SKP2 axis boosts tumorigenesis in fusion negative rhabdomyosarcoma by preventing differentiation through p57Kip2 targeting [ChIP-seq]

(Submitter supplied) Rhabdomyosarcoma (RMS) is a pediatric mesenchymal-derived malignancy encompassing Fusion Positive (FP)-RMS expressing PAX3/7-FOXO1 and Fusion Negative (FN)-RMS often mutated in the RAS pathway. RMS expresses the master myogenic transcription factor MYOD that, paradoxically, is unable to support differentiation while essential for tumor cell survival. We identify here SKP2, an oncogenic E3-ubiquitin ligase, as a critical driver of tumorigenesis in FN-RMS. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL24676
4 Samples
Download data: BED
Series
Accession:
GSE241279
ID:
200241279
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