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accession-icon GSE138660
Ets1 confers context-dependent activation of Notch signaling in T-cell leukemia
  • organism-icon Homo sapiens
  • sample-icon 4 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

Combinatorial ETS1-dependent control of oncogenic NOTCH1 enhancers in T-cell leukemia.

Sample Metadata Fields

Sex, Specimen part, Disease, Cell line

View Samples
accession-icon GSE138803
Expression data from the HPB-ALL T-ALL cell line transduced with shETS1
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

To formally address the biological activity of ETS1 in vitro, we measured the transcriptional effect of ETS1 knock down by transducing HPB-ALL leukemia cell lines with a plKO - shETS1 and plko shLUC control. Samples were hybridized to Affymetrix Human Genome U133 Plus 2.0 arrays. Log2 abundance estimates were obtained using gcrma package of Bioconductor, which is a version of the Robust Multi-Array Average (RMA) algorithm. We provide a supplementary file with gene annotation, which performs a two-sample T-test and computes an average fold-change.

Publication Title

Combinatorial ETS1-dependent control of oncogenic NOTCH1 enhancers in T-cell leukemia.

Sample Metadata Fields

Sex, Cell line

View Samples
accession-icon SRP147921
Insights into the Biology of Hearing and Deafness Revealed by Single-Cell RNA Sequencing
  • organism-icon Mus musculus
  • sample-icon 127 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500, Illumina HiSeq 4000, MinION

Description

The goal of this study was to isolate individual cochlear hair cells and supporting cells from wild type animals in order to characterize the transcriptome of functionally mature auditory hair cells in the mammalian cochlea. Overall design: Single-cell RNA sequencing is a powerful tool by which to characterize the transcriptional profile of low-abundance cell types, however its application to the inner ear has been hampered by the bony labyrinth, tissue sparsity and difficulties in dissociating the ultra-rare cells of the membranous cochlea.  Herein, we present a method to isolate individual inner hair cells (IHCs), outer hair cells (OHCs) and Deiters' cells (DCs) from the murine cochlea at any post-natal time point. We isolated of 132 single cells from OHC, IHC, and DC cell types at postnatal day 15 (p15) and performed RNA-Sequencing of these cells using smartseq2 and Illumina HiSeq. An additional 12 single OHCs from the same timepoint were isolated and sequenced using smartseq2 and the Nanopore MinION 1D reads. We leverage single-cell RNA sequencing to analyze these three cell types and generate a multidimensional overview of their transcriptomes. The data provide new insights into OHC motility and the architecture of gene products implicated in hereditary hearing loss. This refined view of transcription in the organ of Corti will enhance to our understanding of the biology of hearing and deafness.

Publication Title

Insights into the Biology of Hearing and Deafness Revealed by Single-Cell RNA Sequencing.

Sample Metadata Fields

Specimen part, Subject

View Samples
accession-icon GSE43112
Expression data comparing human DKK1 and control vector transfected murine osteochondrosarcoma cells (MOS-J)
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Canonical Wnt signaling controls proliferation and differentiation of osteogenic progenitor cells, and tumor-derived secretion of the Wnt antagonist Dickkopf-1 (Dkk1) is correlated with osteolyses and metastasis in many bone malignancies. However, the role of Dkk1 in the oncogenesis of primary osteosarcoma (OS) remains unexplored. Here, we over-expressed Dkk1 in the OS cell line MOS-J. Contrary to expectations, Dkk1 had autocrine effects on MOSJ cells in that it increased proliferation and resistance to metabolic stress in vitro. In vivo, Dkk1 expressing MOS-J cells formed larger and more destructive tumors than controls. These effects were attributed in part to up-regulation of the stress response enzyme and cancer stem cell marker aldehyde-dehydrogenase-1 (ALDH1) through Jun-N-terminal kinase signaling. This is the first report linking Dkk1 to tumor stress resistance, further supporting the targeting of Dkk1 not only to prevent and treat osteolytic bone lesions but also to reduce numbers of stress-resistant tumor cells.

Publication Title

An unexpected role for a Wnt-inhibitor: Dickkopf-1 triggers a novel cancer survival mechanism through modulation of aldehyde-dehydrogenase-1 activity.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon GSE102287
Gene and microRNA expression data from African Americans and European Americans with non-small cell lung cancer
  • organism-icon Homo sapiens
  • sample-icon 66 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

Comparative Transcriptome Profiling Reveals Coding and Noncoding RNA Differences in NSCLC from African Americans and European Americans.

Sample Metadata Fields

Sex, Age, Specimen part, Disease, Race, Subject

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accession-icon GSE44962
Minor compensatory changes in SAGE Mdr1a (P-gp), Bcrp, and Mrp2 knockout rats do not detract from their utility in the study of transporter-mediated pharmacokinetics.
  • organism-icon Rattus norvegicus
  • sample-icon 111 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

Mdr1a-, Bcrp-, and Mrp2-knockout rats are a more practical species for ADME studies than murine models and previously demonstrated expected alterations in pharmacokinetics of various probe substrates. At present, gene expression and pathology changes were systematically studied in small intestine, liver, kidney, and brain tissue from male SAGE Mdr1a-, Bcrp-, and Mrp2-knockout rats versus wild-type Sprague Dawley controls. Gene expression data supported the relevant knockout genotype. As expected, Mrp2-knockout rats were hyperbilirubinemic and exhibited upregulation of hepatic Mrp3. Overall, few alterations were observed within 137 ADME-relevant genes. The two most consequential changes were upregulation of intestinal carboxylesterase in Mdr1a-knockouts and catechol-O-methyltransferase in all tissues of Bcrp-knockout rats. Previously reported upregulation of hepatic Mdr1b P-glycoprotein in proprietary Wistar Mdr1a-knockout rats was not observed in the SAGE counterpart investigated herein. Relative liver and kidney weights were 22-53% higher in all three knockouts, with microscopic increases in hepatocyte size in Mdr1a- and Mrp2-knockout rats, and glomerular size in Bcrp- and Mrp2-knockouts. Increased relative weight of clearing organs is quantitatively consistent with reported increases in clearance of drugs that are not substrates of the knocked-out transporter. Overall, SAGE knockout rats demonstrated modest compensatory changes, which do not preclude their general application to study transporter-mediated pharmacokinetics. However until future studies elucidate the magnitude of functional change, caution is warranted in rare instances of extensive metabolism by catechol-O-methyltransferase in Bcrp-knockouts and intestinal carboxylesterase in Mdr1a-knockout rats, specifically for molecules with free catechol groups and esters subject to gut wall hydrolysis.

Publication Title

Minor compensatory changes in SAGE Mdr1a (P-gp), Bcrp, and Mrp2 knockout rats do not detract from their utility in the study of transporter-mediated pharmacokinetics.

Sample Metadata Fields

Sex, Specimen part

View Samples
accession-icon GSE101929
Gene expression data from African Americans and European Americans with non-small cell lung cancer
  • organism-icon Homo sapiens
  • sample-icon 66 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Translational Relevance

Publication Title

Comparative Transcriptome Profiling Reveals Coding and Noncoding RNA Differences in NSCLC from African Americans and European Americans.

Sample Metadata Fields

Sex, Age, Race, Subject

View Samples
accession-icon GSE66792
Reprogramming of primary human Philadelphia chromosome-positive B cell acute lymphoblastic leukemia cells into nonleukemic macrophages
  • organism-icon Homo sapiens
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

BCRABL1+ precursor B-cell acute lymphoblastic leukemia (BCR ABL1+ B-ALL) is an aggressive hematopoietic neoplasm characterized by a block in differentiation due in part to the somatic loss of transcription factors required for B-cell development. We hypothesized that overcoming this differentiation block by forcing cells to reprogram to the myeloid lineage would reduce the leukemogenicity of these cells. We found that primary human BCRABL1+ B-ALL cells could be induced to reprogram into macrophage-like cells by exposure to myeloid differentiation-promoting cytokines in vitro or by transient expression of the myeloid transcription factor C/EBP or PU.1. The resultant cells were clonally related to the primary leukemic blasts but resembled normal macrophages in appearance, immunophenotype, gene expression, and function. Most importantly, these macrophage-like cells were unable to establish disease in xenograft hosts, indicating that lineage reprogramming eliminates the leukemogenicity of BCRABL1+ B-ALL cells, and suggesting a previously unidentified therapeutic strategy for this disease. Finally, we determined that myeloid reprogramming may occur to some degree in human patients by identifying primary CD14+ monocytes/ macrophages in BCRABL1+ B-ALL patient samples that possess the BCRABL1+ translocation and clonally recombined VDJ regions.

Publication Title

Reprogramming of primary human Philadelphia chromosome-positive B cell acute lymphoblastic leukemia cells into nonleukemic macrophages.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP073734
High-dose maternal folic acid supplementation before conception impairs reversal learning in offspring mice
  • organism-icon Mus musculus
  • sample-icon 11 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Folic acid supplements prior to and during gestation are recommended and necessary to prevent neural tube defects in developing embryos. But there are also studies suggesting possible adverse effects of high-dose folic acid supplementation. Here, we address whether maternal dietary folic acid supplementation at 40 mg/kg chow (FD), restricted to a period prior to conception, affects gene expression in the offspring generation. Overall design: Total RNA extracted from hippocampi of 6 control (CD) F1 mice and 5 FD F1 mice at the age of 14 weeks.

Publication Title

High-dose maternal folic acid supplementation before conception impairs reversal learning in offspring mice.

Sample Metadata Fields

Sex, Age, Specimen part, Cell line, Subject

View Samples
accession-icon GSE30952
Microarray expression data from human renal mesangial cells (HMC) treated with a Cyclosporine A (CsA) time course.
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

HMCs were treated with CsA (4.2 M) for 0 12 and 48 hours. To exmaine global gene changes in the renal mesangium following CsA treatment in order to identify novel contributors to CsA-induced renal dysfunction

Publication Title

Cyclosporine A--induced oxidative stress in human renal mesangial cells: a role for ERK 1/2 MAPK signaling.

Sample Metadata Fields

Specimen part, Treatment

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)

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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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