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accession-icon GSE7440
Early Response and Outcome in High-Risk Childhood Acute Lymphoblastic Leukemia: A Childrens Oncology Group Study
  • organism-icon Homo sapiens
  • sample-icon 96 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The cure rate for childhood ALL has improved considerably in part because therapy is routinely tailored to the predicted risk of relapse. Various clinical and laboratory variables are used in current risk-stratification schemes, but many children who fail therapy lack adverse prognostic factors at initial diagnosis. Using gene expression analysis, we have identified genes and pathways in a NCI high-risk childhood B-precursor ALL cohort at diagnosis that may play a role in early blast regression as correlated with the Day 7 marrow status. We have also identified a 47-probeset signature (representing 41 unique genes) that was predictive of long term outcome in our dataset as well as three large independent datasets of childhood ALL treated on different protocols.

Publication Title

Gene expression signatures predictive of early response and outcome in high-risk childhood acute lymphoblastic leukemia: A Children's Oncology Group Study [corrected].

Alternate Accession IDs

E-GEOD-7440

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE27280
Pompe disease induced pluripotent stem cells for pathogenesis modeling, drug testing and disease marker identification
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Pompe disease is caused by autosomal recessive mutations in the GAA gene, which encodes acid alpha-glucosidase. Although enzyme replacement therapy has recently improved patient survival greatly, the results in skeletal muscles and for advanced disease are still not satisfactory. Here, we report the derivation of Pompe disease induced pluripotent stem cells (PomD-iPSCs) and their potential for pathogenesis modeling, drug testing and disease marker identification. PomD-iPSCs maintained pluripotent features, and had low GAA activity and high glycogen content. Cardiomyocyte-like cells (CMLCs) differentiated from PomD-iPSCs recapitulated the hallmark Pompe disease pathophysiological phenotypes, including high levels of glycogen, abundant intracellular LAMP-1- or LC3-positive granules, and multiple ultrastructural aberrances. Drug rescue assessment showed that exposure of PomD-iPSC-derived CMLCs to rhGAA reversed the major pathologic phenotypes. Further, L-carnitine and 3- methyladenine treatment reduced defective cellular respiration and buildup of phagolysosomes, respectively, in the diseased cells. By comparative transcriptome analysis, we identified glycogen metabolism, lysosome and mitochondria related marker genes whose expression robustly correlated with the therapeutic effect of drug treatment in PomD-iPSC-derived CMLCs. Collectively, these results demonstrate that PomD-iPSCs are a promising in vitro disease model for development of novel therapeutic strategies for Pompe disease.

Publication Title

Human Pompe disease-induced pluripotent stem cells for pathogenesis modeling, drug testing and disease marker identification.

Alternate Accession IDs

E-GEOD-27280

Sample Metadata Fields

Specimen part

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accession-icon GSE12885
Genome-wide changes in DNA methylation and copy number play a role in deregulation of gene expression in osteosarcoma
  • organism-icon Homo sapiens
  • sample-icon 14 Downloadable Samples
  • Technology Badge IconAgilent-014693 Human Genome CGH Microarray 244A (Feature number version), Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Identification of interactive networks of gene expression associated with osteosarcoma oncogenesis by integrated molecular profiling.

Alternate Accession IDs

E-GEOD-12885

Sample Metadata Fields

Specimen part

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accession-icon GSE80767
Transcriptional response to mouse and human AIM2-like receptor activation
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip, Illumina MouseWG-6 v2.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

The AIM2-like Receptors Are Dispensable for the Interferon Response to Intracellular DNA.

Alternate Accession IDs

E-GEOD-80767

Sample Metadata Fields

Treatment, Time

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accession-icon GSE80766
Transcriptional response to intracellular DNA in cells lacking AIM2-like receptors
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

Analysis of ALR-deficient cells indicates that ALRs are not required for the IFN response to intracellular DNA. To explore whether AIM2-like receptors activated another innate signaling pathway upon

Publication Title

The AIM2-like Receptors Are Dispensable for the Interferon Response to Intracellular DNA.

Alternate Accession IDs

E-GEOD-80766

Sample Metadata Fields

Treatment, Time

View Samples
accession-icon GSE12865
Gene expression of human paediatric osteosarcoma tumour samples relative to normal human osteoblasts
  • organism-icon Homo sapiens
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Gain or loss of genes and deregulation of gene expression can result in cumulative and progressive disruptions of normal cellular functions.

Publication Title

Identification of interactive networks of gene expression associated with osteosarcoma oncogenesis by integrated molecular profiling.

Alternate Accession IDs

E-GEOD-12865

Sample Metadata Fields

Specimen part

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accession-icon GSE17115
Gene Expression upon Doxorubicin Treatments
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

Murine C26 tumor xenografts displayed different responses to the treatments of PBS, Doxorubicin (Dox), and chimeric polypeptide (CP)-Dox conjugates. We used microarrays to globally study gene expression underlying these different responses and identified distinct classes of up-regulated or down-regulated genes upon treatment.

Publication Title

Self-assembling chimeric polypeptide-doxorubicin conjugate nanoparticles that abolish tumours after a single injection.

Alternate Accession IDs

E-GEOD-17115

Sample Metadata Fields

Age, Specimen part

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accession-icon SRP144795
Alternative splicing Hltf: intron retention-dependent activation of immune tolerance at the feto-maternal interface (RNA-Seq)
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Purpose: we tested the hypothesis that Hltf deletion in placenta either caused or exacerbated neonatal hypoglycemia via Hif-1a regulation of nutrient transporters. Methods: Individual samples [1 term placenta/sample x 5 biological replicates for test and control littermate female mice = 10 total samples] were flash frozen and sent to Otogenetics Corp. (Norcross, GA) for RNA-seq assays. Paired-end 100 nucleotide reads were aligned to genomic assembly mm10 and analyzed using the platform provided by DNAnexus, Inc. (Mountain View, CA). Results: There was no measureable evidence of uteroplacental dysfunction or fetal compromise. Conclusion: Our study is the first to show only the truncated Hltf isoform is expressed in E18.5 term placenta, and we identified a functional link between alternative splicing of Hltf and immunosuppression at the feto-maternal interface. Overall design: Placental mRNA profiles of E18.5 term placenta from five wild type control and five Hltf null mouse samples were generated by deep sequencing by Illumina HiSeq2000/2500.

Publication Title

Alternative splicing of helicase-like transcription factor (Hltf): Intron retention-dependent activation of immune tolerance at the feto-maternal interface.

Alternate Accession IDs

GSE114144

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE7768
Expression data from spleens of mice immunized using LPS vs MPL as adjuvant.
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Expression 430A Array (moe430a)

Description

An unresolved issue in immunology is the extent to which inflammatory effects are needed for robust T cell responses. In this study, mice were immunized by iv injection using either high toxicity lipopolysaccharide (LPS) or low toxicity monophosphoryl lipid A (MPL) as adjuvant. Six hours after iv immunization, whole spleens were harvested and gene expression was measured in unfractionated splenic populations of cells. The analysis indicated that the low toxicity adjuvanticity of MPL was associated with TLR4-mediated signaling that was biased to the TRIF branch of TLR4, while LPS generated balanced MyD88 and TRIF-associated outcomes.

Publication Title

The vaccine adjuvant monophosphoryl lipid A as a TRIF-biased agonist of TLR4.

Alternate Accession IDs

E-GEOD-7768

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE35603
Network Biology of Tumor Stem-like Cells Identified a Regulatory Role of CBX5 in Lung Cancer
  • organism-icon Homo sapiens
  • sample-icon 74 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Mounting evidence points to a link between a cancer possessing stem-like properties and a worse prognosis. To understand the biology, a common approach is to integrate network biology with signal processing mechanics. That said, even with the right tools, predicting the risk for a highly susceptible target using only a handful of gene signatures remains very difficult. By compiling the expression profiles of a panel of tumor stem-like cells (TSLCs) originating in different tissues, comparing these to their parental tumor cells (PTCs) and the human embryonic stem cells (hESCs), and integrating network analysis with signaling mechanics, we propose that network topologically-weighted signaling processing measurements under tissue-specific conditions can provide scalable and predicable target identification.

Publication Title

Network biology of tumor stem-like cells identified a regulatory role of CBX5 in lung cancer.

Alternate Accession IDs

E-GEOD-35603

Sample Metadata Fields

Specimen part

View Samples
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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)

fund-icon Fund the CCDL

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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