Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcription profiling of human Ewing sarcoma primary tumors of patients to determine molecular predictors of outcome.

ABSTRACT: The improvement of Ewing's sarcoma (EWS) therapy is currently linked to find strategies to select patients with poor and good prognosis at diagnosis and to generate modified treatment regimens. In this study, we analyze the molecular factors governing EWS response to chemotherapy in order to identify genetic signatures that may be used for risk-adapted therapy. Experiment Overall Design: Affimetrix platform was used for profiling 30 primary tumors of patients that were classified according to event-free survival and 7 metastasis. NED: no evidence of diseaase (event-free); REL: relapse; MET: metastasis. For selected genes, Real-Time PCR was applied in 42 EWS primary tumors as validation assay. MTT test was used to evaluate in vitro drug sensitivity.

ORGANISM(S): Homo sapiens

SUBMITTER: Daniel Remondini

PROVIDER: E-GEOD-12102 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Overcoming resistance to conventional drugs in Ewing’s sarcoma and identification of molecular predictors of outcome.

Project description:The improvement of Ewing's sarcoma (EWS) therapy is currently linked to find strategies to select patients with poor and good prognosis at diagnosis and to generate modified treatment regimens. In this study, we analyze the molecular factors governing EWS response to chemotherapy in order to identify genetic signatures that may be used for risk-adapted therapy. Keywords: Gene Expression Analysis.

2008-07-15 | GSE12102 | GEO

The human Ewing's Sarcoma oncoprotein EWS-FLI1 causes Ewing's-type tumors in zebrafish

Project description:The fusion oncoprotein EWS-FLI1 arises from a t(11;22)(q24;q12) chromosomal translocation and causes Ewing's Sarcoma, a malignant bone tumor. The mechanism whereby EWS-FLI1 transforms cells is unknown. Somatic, mosaic expression of human EWS-FLI1 in zebrafish from the heat shock promoter [Tg(HSP:EWS-FLI1)] caused small round blue cell tumors (SRBCTs) similar to human Ewing's sarcoma. We performed microarray studies comparing zebrafish SRBCTs to another tumor type, zebrafish malignant peripheral nerve sheath tumors (MPNSTs). The results identify a conserved set of EWS-FLI1-regulated genes,and provide insight into the pathogenesis of Ewing's Sarcoma tumors.

2011-11-01 | GSE31186 | GEO

A zebrafish transgenic model of Ewing's Sarcoma reveals conserved mediators of EWS-FLI1 tumorigenesis

Project description:This SuperSeries is composed of the following subset Series: GSE31185: The human Ewing's Sarcoma oncoprotein EWS-FLI1 causes developmental defects in zebrafish embryos GSE31186: The human Ewing's Sarcoma oncoprotein EWS-FLI1 causes Ewing's-type tumors in zebrafish Refer to individual Series

2011-11-01 | E-GEOD-31217 | biostudies-arrayexpress

The human Ewing's Sarcoma oncoprotein EWS-FLI1 causes developmental defects in zebrafish embryos

2011-11-01 | GSE31185 | GEO

The human Ewing's Sarcoma oncoprotein EWS-FLI1 causes Ewing's-type tumors in zebrafish

2011-11-01 | E-GEOD-31186 | biostudies-arrayexpress

Re-activation of EWS-FLI1 suppressed FOXO1 expression as a novel therapeutic strategy for Ewing´s sarcoma

Project description:Transient transfection of a Ewing's Sarcoma cell line expressing type I EWS-FLI1 fusion and doxycycline-inducible short hairpin RNA against EWS-FLI1 (A673sh)

2013-07-01 | GSE37409 | GEO

pediatric sarcoma: rhabdomyosarcoma & Ewing's sarcoma

Project description:Affymetrx U95Av2 GeneChip hybridizations, RNA extracted from primary human pediatric alveolar (aRMS) and embryonal (eRMS) rhabdomyosarcoma, plus primary pediatric Ewing's sarcoma (EWS) Keywords = pediatric sarcoma Keywords = Ewing's sarcoma Keywords = rhabdomyosarcoma Keywords: other

2004-03-13 | GSE967 | GEO

The human Ewing's Sarcoma oncoprotein EWS-FLI1 causes developmental defects in zebrafish embryos

Project description:The fusion oncoprotein EWS-FLI1 arises from a t(11;22)(q24;q12) chromosomal translocation and causes Ewing's Sarcoma, a malignant bone tumor. The mechanism whereby EWS-FLI1 transforms cells is unknown. We made germline transgenic zebrafish expressing human EWS-FLI1 under the control of the heat shock promoter. Induction of EWS-FLI1 expression causes multiple defects in embryonic development. We compared gene expression in control and transgenic EWS-FLI1 zebrafish. The results identify a conserved set of EWS-FLI1-regulated genes, and provide insight into the pathogenesis of Ewing's Sarcoma tumors. We performed heat shock and isolated total RNA for microarray studies comparing wildtype AB strain zebrafish with transgenic zebrafish expressing human EWS-FLI1 [Tg(HSP:EWS-FLI1)]. RNA was biotin-lableled and hybridized to zebrafish-specific Affymetrix arrays.

2011-11-01 | E-GEOD-31185 | biostudies-arrayexpress

Role of epigenetic therapy in the modulation of tumor growth and migration in human castration resistance prostate cancer cells with neuroendocrine differentiation

Project description:Neuroendocrine transdifferentiation (NED) of prostate cancer cells and aberrant activation of survival pathways involved in tumorigenesis are among the events that lead to the development of resistance to anti-androgen therapy and are associated with poor prognosis in patients with castration resistance prostate cancer (CRPC). Most of these molecular events appear to be mediated by epigenetic mechanisms, in particular DNA methylation. In this study, we evaluated the antitumor activity and epigenetic modulation of two epigenetic drugs, 5-aza-2’-deoxycytidine (AZA) and S-adenosylmethionine (SAM) in two human CRPC cell lines with NED (NED-CRPC), DU-145 and PC-3. The effects of AZA and SAM on the cell growth proliferation, cell cycle, apoptosis, migration and genome-wide DNA methylation profiling have been evaluated through MTT assay, DNA flow cytometry with propidium iodide, and Annexin V-FITC/propidium iodide staining, wound-healing assay and Infinium450k microarray, respectively. Both epigenetic drugs showed a prominent antitumor activity in NED-CRPC cell line exerted through perturbation of cell cycle progression, induction of apoptosis and migration arrest. AZA and SAM reversed NED in DU-145 and PC-3, respectively. Moreover, AZA treatment profoundly modified DNA methylation pattern, sustaining a pervasive hypomethylation of the genome, with a relevant effect on several pathways involved in regulation of cell migration, cell proliferation and apoptosis. Among these, the Wnt/beta-catenin signaling appeared to be the most directly involved. In conclusion, both AZA and SAM showed a relevant antitumor activity on NED-CRPC cell lines. This opens a new scenario in the therapy of this lethal variant of prostate cancer.

2023-01-13 | GSE164249 | GEO

A673 Stable-Knockdown

Project description:A673 Ewing's sarcoma cells containing either control RNAi retroviral constructs (luc-RNAi), or RNAi retroviral constructs targeting the endogenous EWS/FLI fusion transcript (either EF-2-RNAi or EF-4-RNAi). Keywords: Expression analysis of RNAi knockdown of endogenous EWS/FLI

2006-05-15 | GSE4560 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

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