Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression Profiling of human Fusion-Positive and Fusion-Negative Rhabdomyosarcoma

ABSTRACT: Genome-wide gene expression in 33 fusion-positive and 25 fusion-negative rhabdomyosarcoma cases was studied using GeneChip Human Genome U133 Plus2 (Affymetrix)

ORGANISM(S): Homo sapiens

PROVIDER: GSE66533 | GEO | 2016/06/01

SECONDARY ACCESSION(S): PRJNA277218

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Expression Profiling of human Fusion-Positive and Fusion-Negative Rhabdomyosarcoma

Project description:Genome-wide gene expression in 33 fusion-positive and 25 fusion-negative rhabdomyosarcoma cases was studied using GeneChip Human Genome U133 Plus2 (Affymetrix) Fusion-positive versus fusion-negative rhabdomyosarcoma tumors

2016-06-01 | E-GEOD-66533 | biostudies-arrayexpress

Fusion Negative Rhabdomyosarcoma Cell Lines

Project description:Fusion Negative Rhabdomyosarcoma Cell Lines

| PRJNA330685 | ENA

Clinical Application of Prognostic Gene Expression Signature in Fusion Gene-Negative Rhabdomyosarcoma

Project description:To date, there are no known prognostic markers identified in patients with fusion gene-negative rhabdomyosarcoma. This study validates the 5-gene (MG5) signature as a prognostic marker in patients with fusion negative intermediate-risk rhabdomyosarcoma clearly stratifying this otherwise clinically homogenous population of patients into two risk groups based on outcome. In addition, this analysis was performed using nCounter assay on paraffin embedded tissues and the results were concordant to previously published results using frozen tissues in a different patient cohort. Therefore, this work holds tremendous translational relevance as the MG5 signature can be reliably assessed in readily available paraffin embedded tissues of fusion gene-negative rhabdomyosarcoma patients in prospective clinical trials to stratify them into prognostic risk groups as well as to potentially tailor future therapy based on these risk groups.

2015-07-31 | E-MTAB-3580 | biostudies-arrayexpress

Gene Expression Profiling of Fusion Negative Rhabdomyosarcoma Cell Lines

Project description:We analyzed the expression of two fusion-negative established Rhabdomyosarcoma cell lines. Together with Chip-seq, we were able to identify transcribed loci bound by myogenic regulatory transcription factors (MYF5 and MYOD) that pertain to embryonic muscle development and cell cycle regulation pathways. Keywords: rhabdomyosarcoma, gene expression profiling, RD, Rh18

2016-12-20 | GSE84629 | GEO

Defining the interactome of CHD4 in fusion-positive rhabdomyosarcoma

Project description:The goal of this study was to explore in detail how the chromatin remodeler and NuRD subunit CHD4 controls the oncogenic signature of the tumor driver and fusion protein PAX3-FOXO1 in fusion-positive rhabdomyosarcoma. To this aim, we defined the interactome of CHD4 by LC-MS, identified its location in the genome by ChIP-seq, assessed its influence on DNA accessibility by DNase I hypersensitivity assays, and determined its target genes by RNA-seq.

2020-08-11 | PXD015231 | Pride

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

Project description: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.

2024-02-07 | GSE240722 | GEO

Expression Profiling of Rhabdomyosarcoma patients and normal muscle samples

Project description:Genome-wide gene expression in 66 Rhabdomyosarcoma patients and 16 normal muscle samples were studied using Affymetrix Human Genome U133 Plus 2.0 Array.

2019-12-10 | GSE141690 | GEO

Transcriptome analysis of genetically engineered murine fusion-negative rhabdomyosarcoma model-derived cell lines

Project description:Fusion-negative rhabdomyosarcoma (FN-RMS) is the most common soft tissue sarcoma of childhood arising from undifferentiated skeletal muscle cells. Tumor cells derived from genetically engineered murine models are a valid tool to study cancer biology. In order to investigate the poor myogenic commitment of FN-RMS, we performed RNA sequencing of two cell lines derived from a previously described genetically engineered murine model of FN-RMS. We then performed bioinformatics analysis to compare the transcriptome with murine satellite cells, and identify the key factors that distinguish FN-RMS from skeletal muscle cells.

2021-05-31 | GSE175816 | GEO

Expression data from the Finnish Nodular Lymphocyte Predominant Hodgkin Lymphoma (NLPHL) family and ten controls

Project description:Gene expression was studied from the blood derived RNAs of the Finnish family members as well as from 10 controls using GeneChip Human Genome U133 Plus2 (Affymetrix). Eight out of 10 family members in the expression analysis are heterozygous for the NPAT c.2437-2438delAG, three of which are NLPHL cases.

2011-04-14 | GSE28536 | GEO

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

Project description: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. We show that knockdown of TWIST2 enables FN-RMS cells to exit the cell cycle and undergo myogenic differentiation, thereby reducing the growth of FN-RMS xenograft tumors. ChIP-seq analysis revealed that most TWIST2-mediated gene regulation occurs independent of changes in MYOD binding in FN-RMS cells. Instead, TWIST2 controls the deposition of H3K27 acetylation at distal enhancers by interacting with the chromatin remodelers, SMARCA4 and CHD3, to activate growth-related and repress myogenesis-related TWIST2 target genes. Our findings provide new insights into the role of TWIST2 in maintaining an undifferentiated and tumorigenic state of FN-RMS and highlight the clinical potential of reversing the TWIST2-regulated phenotype.

2023-03-20 | GSE207165 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data