Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression data from Down syndrome and non-Down syndrome pediatric acute lymphoblastic leukemia cases

ABSTRACT: Gene expression profiling (GEP) can reveal characteristic signatures associated with distinct biologic subtypes of acute lymphoblastic leukemia (ALL). We performed GEP on Down syndrome (DS) and comparison non-Down syndrome (NDS) ALL cases to identify biologic differences between these groups.

ORGANISM(S): Homo sapiens

PROVIDER: GSE20910 | GEO | 2011/07/12

SECONDARY ACCESSION(S): PRJNA129649

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Expression data from Down syndrome and non-Down syndrome pediatric acute lymphoblastic leukemia cases

Project description:Gene expression profiling (GEP) can reveal characteristic signatures associated with distinct biologic subtypes of acute lymphoblastic leukemia (ALL). We performed GEP on Down syndrome (DS) and comparison non-Down syndrome (NDS) ALL cases to identify biologic differences between these groups. Ficoll-enriched, cryopreserved diagnostic bone marrow samples were obtained from patients with newly diagnosed B-precursor acute lymphoblastic leukemia.

2011-07-12 | E-GEOD-20910 | biostudies-arrayexpress

Genomic profiling in Down syndrome pediatric acute lymphoblastic leukemia

Project description:Patients with Down syndrome (DS) and acute lymphoblastic leukemia (ALL) have distinct clinical and biological features. Whereas most DS-ALL cases lack the sentinel cytogenetic lesions that guide risk assignment in childhood ALL, JAK2 mutations and CRLF2 overexpression are highly enriched. To further characterize the unique biology of DS-ALL, we performed genome-wide profiling of 58 DS-ALL and 35 non-Down syndrome (NDS) ALL cases by DNA copy number, loss of heterozygosity, gene expression, and methylation analyses. We report novel deletions within the 6p22 histone gene cluster as significantly more frequent in DS-ALL, occurring in 12 DS (24%) and only a single NDS case (3%) (Fisher’s exact p = 0.013). Homozygous deletions yielded significantly lower histone expression levels, and were associated with higher methylation levels, distinct spatial localization of methylated promoters, and enrichment of highly methylated genes for specific pathways and transcription factor binding motifs. Gene expression profiling identified CRLF2 overexpression in nearly half DS-ALL cases, and supervised analysis identified an associated 39-gene signature. However, no expression signature was identified for DS-ALL overall, nor for histone status, suggesting that DS-ALL constitutes several, heterogeneous molecular entities. Characterization of pathways associated with histone deletions and high CRLF2 expression may identify opportunities for novel targeted interventions. This SuperSeries is composed of the SubSeries listed below.

2011-07-12 | GSE21094 | GEO

Methylation data from Down syndrome and non-Down syndrome pediatric acute lymphoblastic leukemia cases and controls

2011-12-01 | GSE20872 | GEO

SNP data from Down syndrome and non-Down syndrome pediatric acute lymphoblastic leukemia cases and controls

2011-07-12 | GSE21091 | GEO

Methylation data from Down syndrome and non-Down syndrome pediatric acute lymphoblastic leukemia cases and controls

Project description:Methylation profiling can reveal patterns of hypermethlation and hypomethylation associated with distinct biologic subtypes of acute lymphoblastic leukemia (ALL). We performed methylation profiling of Down syndrome ALL cases and controls to identify unique biologic features of this ALL subgroup. Ficoll-enriched, cryopreserved bone marrow aspirate samples were obtained from patients with B-precursor ALL at diagnosis and in remission

2011-12-01 | E-GEOD-20872 | biostudies-arrayexpress

SNP data from Down syndrome and non-Down syndrome pediatric acute lymphoblastic leukemia cases and controls

Project description:SNP profiling can reveal copy number abnormalities and loss of heterozygosity associated with distinct biologic subtypes of acute lymphoblastic leukemia (ALL). We performed SNP profiling of Down syndrome ALL cases and controls to identify unique biologic features of this ALL subgroup. Ficoll-enriched, cryopreserved bone marrow aspirate samples were obtained from patients with B-precursor ALL at diagnosis and in remission; and from control patients without leukemia.

2011-07-12 | E-GEOD-21091 | biostudies-arrayexpress

Down syndrome

Project description:Endothelial progenitor cells were isolated from euploid and Down syndrome (DS) affected individuals. Gene expression was analyzed on total RNA extracted before or after infection with a human pathogen Bartonella hensaele. For euploid uninfected and infected cells, 2 biological replicates were performed. For DS isolated progenitors both infected and uninfected, a single microarray hybridization was performed. All hybridizations consists of three pooled samples each.

2010-01-12 | E-MTAB-312 | biostudies-arrayexpress

Epigenetic changes in Down syndrome leukemogenesis

Project description:Acute megakaryoblastic leukemia (AMKL) is more frequently seen in Down syndrome patients, where it is often preceded by a transient myeloproliferative disorder (DS-TMD). The development of DS-TMD and DS-AMKL require not only the presence of the trisomy 21 but also that of GATA1 mutations. However, despite extensive studies into the genetics of DS-AMKL, not much is known about the epigenetic deregulation associated with this disease. In order to understand how epigenetic changes at the DNA methylation level contribute to DS leukemogenesis we performed DNA methylation profiling at different stages of development of this disease and analyzed the dynamics of epigenetic reprogramming. Early genome-wide epigenetic changes can be detected in trisomy 21 fetal liver mononuclear cells, even prior to the development of hematological abnormalities. These early changes are characterized by marked loss of DNA methylation at genes associated with regulation of key developmental processes. This first wave of aberrant DNA hypomethylation is followed by a second wave of epigenetic reprogramming detected in blast cells from DS-TMD and DS-AMKL, characterized by gains of methylation. This second wave of hypermethylation targets a distinct set of genes, preferentially affecting genes involved in hematopoiesis and regulation of cell growth and proliferation. DNA methylation profiles obtained at different stages of the development of Down syndrome AMKL and from CD41+ cells from partial trisomic mice

2013-08-19 | E-GEOD-46167 | biostudies-arrayexpress

Expression profiling of human adult postmortem brain tissue from Down syndrome and healthy control subjects

Project description:Down syndrome (DS) is the result of trisomy chromosome 21 but the mechanisms by which the genotype leads to the characteristic disease phenotype are unclear. We performed a microarray study using human adult brain tissue (dorsolateral prefrontal cortex) from DS subjects and healthy controls to characterise for the first time the human adult Down syndrome brain Keywords: disease state analysis

2007-07-27 | GSE5390 | GEO

Genome wide expression profiles in Down syndrome

Project description:Down syndrome (DS) (MIM 190685) is a complex disorder caused by the trisomy of either the entire, or a critical region of chromosome 21 (21q22.1-22.3). Despite representing the first genetic cause of mental retardation, the molecular bases of the syndrome are still largely unknown. We analyzed the genome-wide transcription profiles of lymphoblastoid cell lines (LCLs) from six DS and six euploid individuals and investigated differential gene expression and pathway deregulation associated with trisomy 21. RNA from six DS and six control LCLs was independently hybridized on the Affymetrix HU133 plus 2.0 oligonucleotide array (Affymetrix, Santa Clara, CA).The experimental design was a diseased versus control comparison. In a second approach, variability of gene expression among the DS and control group, respectively, was assessed by the analysis of the coefficient of variation (CV), calculated as the ratio between standard deviation and mean expression level for each gene among samples.

2012-12-06 | E-MTAB-1238 | biostudies-arrayexpress

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