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accession-icon GSE28462
Integrated Genomic Analysis of Relapsed Childhood Acute Lymphoblastic Leukemia reveals therapeutic strategies
  • organism-icon Homo sapiens
  • sample-icon 98 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Integrated genomic analysis of relapsed childhood acute lymphoblastic leukemia reveals therapeutic strategies.

Sample Metadata Fields

Specimen part, Disease

View Samples
accession-icon GSE28460
Expression data from ALL diagnosis and relapse pediatric acute lymphoblastic leukemia cases
  • organism-icon Homo sapiens
  • sample-icon 98 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

There is a distinct signature of differentially expressed probes from diagnosis to relapse

Publication Title

Integrated genomic analysis of relapsed childhood acute lymphoblastic leukemia reveals therapeutic strategies.

Sample Metadata Fields

Specimen part, Disease

View Samples
accession-icon GSE20910
Expression data from Down syndrome and non-Down syndrome pediatric acute lymphoblastic leukemia cases
  • organism-icon Homo sapiens
  • sample-icon 47 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Gene expression profiling (GEP) can reveal characteristic signatures associated with distinct biologic subtypes of acute lymphoblastic leukemia (ALL).

Publication Title

Genomic profiling in Down syndrome acute lymphoblastic leukemia identifies histone gene deletions associated with altered methylation profiles.

Sample Metadata Fields

Specimen part, Disease

View Samples
accession-icon GSE21094
Genomic profiling in Down syndrome pediatric acute lymphoblastic leukemia
  • organism-icon Homo sapiens
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon

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%) (Fishers 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.

Publication Title

Genomic profiling in Down syndrome acute lymphoblastic leukemia identifies histone gene deletions associated with altered methylation profiles.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE93754
The genomic distribution and gene expression profiling of cardiomyocyte-enriched populations
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Histone Methyltransferase G9a Is Required for Cardiomyocyte Homeostasis and Hypertrophy.

Sample Metadata Fields

Treatment

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accession-icon GSE42088
Expression data from Leishmania major infected human dendritic cells
  • organism-icon Homo sapiens
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Leishmania major infected human dendritic cells (DCs) exhibit a marked induction of IL-12 ultimately promoting a robust Th1-mediated response associated with parasite killing and protective immunity. In this study, we utilized Affymetrix Genechips to globally assess the host cell genes and pathways associated with L. major infection during early infection (2, 4, 8, and 24 hrs) in human myeloid-derived DCs. Bioinformatic analyses of the hybridized microarray chips identified 728 genes, represented by 848 unique probe sets, which, when compared to uninfected samples were observed to be significantly differentially expressed by one-way ANOVA. Altogether, the data provide a genome-wide perspective on the transcriptional influences Leishmania species exert within human DCs during early infection, and provides a platform for further investigations toward functionally characterizing candidate genes of importance to the IL-12 based immune response to infections.

Publication Title

Human dendritic cells exhibit a pronounced type I IFN signature following Leishmania major infection that is required for IL-12 induction.

Sample Metadata Fields

Specimen part, Time

View Samples
accession-icon GSE93691
Gene expression profiling of cardiomyocyte-enriched populations isolated from mice subject to transverse aortic constriction (TAC) and treated with BIX-01294 for 1 week
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

The role of the histone mehyltrasferase G9a (also known as Ehmt2) in cardiac hypertrophy has not been studied extensively. To address how G9a promotes cardiac hypertrophy, we assessed the gene expression signature defined by G9a in cardiomyocytes (CM) of mice subject to transverse aortic constriction (TAC) for 1 wk, a surgical procedure that causes cardiac hypertrophy following the induction of pressure overload. To this end, we compared the expression profiles of CMs isolated from mice treated with the G9a inhibitor BIX-01294 and control groups (untreated and DMSO-treated mice at baseline and after TAC). The expression profiles were defined by Illumina arrays .

Publication Title

Histone Methyltransferase G9a Is Required for Cardiomyocyte Homeostasis and Hypertrophy.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP096944
Gene expression profiling of cardiomyocyte-enriched populations isolated from G9a-KO and Cre mice
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

The role of the histone mehyltrasferase G9a (also known as Ehmt2) in heart has not been extensively studied. To identify the genes regulated by G9a in the normal heart, we first generated a conditional, cardiac-specific KO mouse for this gene using the Cre-Lox approach, crossing G9a flox/flox mice with aMHC-MerCreMer mice (Cre mice were used as controls). Then, we sequenced total RNA (Total-RNA-seq) from cardiomyocyte-enriched populations isolated from G9a-KO and Cre mice, and compared the two expression profiles. Overall design: Profiling of the transcriptome of cardiomyocyte-enriched populations isolated from G9a-KO and Cre mice. Two biological replicates were profiled for each cell type.

Publication Title

Histone Methyltransferase G9a Is Required for Cardiomyocyte Homeostasis and Hypertrophy.

Sample Metadata Fields

Cell line, Subject

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accession-icon SRP098738
An autofluorescence-based method for the isolation of highly purified ventricular cardiomyocytes
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

Profiling of the transcriptome of FITChigh/FSCdim and FITCdim/FSChigh sub-populations. Three biological replicates were profiled for each cell type. Overall design: Profiling of the transcriptome of FITChigh/FSCdim and FITCdim/FSChigh sub-populations. Three biological replicates were profiled for each cell type.

Publication Title

An autofluorescence-based method for the isolation of highly purified ventricular cardiomyocytes.

Sample Metadata Fields

Specimen part, Cell line, Subject

View Samples
accession-icon SRP072881
Gene expression profiling during cardiac maturation, hypertrophy and after KD of TET2
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000, NextSeq 500

Description

Methylation at 5-cytosine (5-mC) is a fundamental epigenetic DNA modification associated recently with cardiac disease. In contrast, the role of 5-hydroxymethylcytosine (5-hmC) – 5-mC's oxidation product – is unknown in the context of the heart. Here, we assess the hydroxymethylome in embryonic, neonatal, adult and hypertrophic mouse cardiomyocytes, showing that dynamic modulation of hydroxymethylated DNA is associated with specific transcriptional networks during heart development and failure. DNA hydroxymethylation marks gene bodies of highly expressed genes and distal regulatory regions with enhanced activity. Pathological hypertrophy is characterized by a partial shift towards a fetal-like distribution pattern. We further demonstrate a regulatory function of TET2 and provide evidence that the expression of key cardiac genes, such as Myh7 is modulated by TET2-mediated 5-hmC deposition on the gene body and at enhancers in cardiac cells. We thus provide the first genome-wide analysis of 5-hmC in the cardiomyocyte, and establish the role of this epigenetic modification in heart development and disease Overall design: Profiling of the transcriptome of embryonic, neonatal, adult, 1 week hypertrophic cardiomyocytes, sh-control and sh-TET2 cardiomyocytes. Two biological replicates were profiled for each cell type.

Publication Title

DNA hydroxymethylation controls cardiomyocyte gene expression in development and hypertrophy.

Sample Metadata Fields

Specimen part, Cell line, Subject

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refine.bio is a repository of uniformly processed and normalized, ready-to-use transcriptome data from publicly available sources. refine.bio is a project of the Childhood Cancer Data Lab (CCDL)

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Developed by the Childhood Cancer Data Lab

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Cite refine.bio

Casey S. Greene, Dongbo Hu, Richard W. W. Jones, Stephanie Liu, David S. Mejia, Rob Patro, Stephen R. Piccolo, Ariel Rodriguez Romero, Hirak Sarkar, Candace L. Savonen, Jaclyn N. Taroni, William E. Vauclain, Deepashree Venkatesh Prasad, Kurt G. Wheeler. refine.bio: a resource of uniformly processed publicly available gene expression datasets.
URL: https://www.refine.bio

Note that the contributor list is in alphabetical order as we prepare a manuscript for submission.

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