refine.bio
  • Search
      • Normalized Compendia
      • RNA-seq Sample Compendia
  • Docs
  • About
  • My Dataset
github link
Showing
of 383 results
Sort by

Filters

Technology

Platform

accession-icon GSE9520
Transcriptome changes in hMSCs during expansion
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Human mesenchymal stem cells or multipotent stromal cells (MSCs) are of interest for clinical therapy, in part because of their capacity for proliferation and differentiation. However, results from clinical trials and in vitro models have been variable, possibly due to MSC heterogeneity and a lack of standardization between MSC in vitro expansion protocols. Here we defined changes in MSCs during expansion in vitro. In low density cultures, MSCs expand through distinct lag, exponential growth and stationary phases. We assayed cultures of passage 2 human MSCs from three donors at low density (50 cells/cm2) at about 5% confluence on Day 2 and after the cultures had expanded to about 70% confluence on Day 7. On Day 2 genes involved in cell division were up-regulated. On Day 7 genes for cell development were up-regulated. The variations between three donors were less than the variation within the expansion of MSCs from a single donor. The microarray data for selected genes were confirmed by real-time PCR, ELISA and FACScan. About 50% of cells at Day 2 were in S-phase compared to 10% at Day 7. The results demonstrated major differences in early and late stage cultures of MSCs that should be considered in using the cells in experiments and clinical applications.

Publication Title

Human multipotent stromal cells undergo sharp transition from division to development in culture.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP062369
Genome-wide expression analysis of yeast with CRISPR-mediated inhibition of GAL10 ncRNA compared to wild-type.
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 49 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

We analyzed the genome-wide expression by RNA-seq of a yeast strain that expresses Cas9d and a guideRNA targeted to the GAL10 locus (called +116), which inhibits GAL10 ncRNA expression from the antisense strand. We compared this strain to a strain expressing a scrambled guideRNA. The goal was to examine the effects of ncRNA inhibition and to examine if CRISPR inhibition of gene expression has off-target effects. We find that CRISPR-mediated inhibtion of GAL10 ncRNA only significantly changes expression of transcripts at the GAL1-10 locus, showing that CRISPR is highly specific, and that GAL10 ncRNA only control genes at the GAL locus. Overall design: RNA-seq of 2 strains with CRISPR scrambled and 2 strains with CRISPR +116, the latter of which inhibits GAL10 ncRNA

Publication Title

Single-Molecule Imaging Reveals a Switch between Spurious and Functional ncRNA Transcription.

Sample Metadata Fields

Cell line, Subject

View Samples
accession-icon GSE18983
Effect of the explosive compound TNT on wild type seedlings
  • organism-icon Arabidopsis thaliana
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

The aim of this experiment was to identify the genes involved in the detoxification of the toxic pollutant and explosive compound 2,4,6-trinitrotolune (TNT). Fourteen-day-old, liquid culture grown, Arabidopsis seedlings, ecotype Col0 (NASC stock code N1093), were dosed with 60 uM TNT dissolved in 60 ul dimethyl formamide (DMF) solvent, or 60 ul DMF only. After six hours, RNA was extracted and used for the microarray analysis. Further details and characterisation of glucosyltransferases identified using this method are presented in citation below.

Publication Title

Detoxification of the explosive 2,4,6-trinitrotoluene in Arabidopsis: discovery of bifunctional O- and C-glucosyltransferases.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE40106
Pten deletion in neonatal brain induces an abnormal neural progenitor niche that can synergize with Trp53 loss to generate medulloblastoma
  • organism-icon Mus musculus
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

To investigate Pten function in neonatal developing brain, we conditionally inactivated Pten in neural stem/progenitor cells at birth using a Nestin-CreER transgenic driver. Pten inactivation created a novel perivascular proliferative niche in the cerebellum that did not progress to malignancy during the lifespan of the mouse. Co-deletion of Pten and Trp53 synergized to cause fully penetrant medulloblastoma originating from a perivascular niche. The Pten and Trp53 double knock-out medulloblastomas showed an extensive and abnormal blood vessel network and advanced neuronal differentiation of tumor cells compared to medulloblastomas arising in Nestin-creER;Trp53fl/fl mice, suggesting that Pten loss promoted angiogenesis and neuronal differentiation in medulloblastoma. EdU pulse-chase experiments demonstrated a lineage hierarchy of the double knock-out medulloblastomas consistent with a perivascular cancer stem cell population. The Pten and Trp53 double knock-out medulloblastomas showed somatic loss of chromosomes 7, 13 and 16, and inactivating mutations in the tumor suppressor gene Ptch1. Gene expression profiles showed that this model recapitulated the subgroup of human medulloblastomas with de-regulated SHH signaling.

Publication Title

PTEN Signaling in the Postnatal Perivascular Progenitor Niche Drives Medulloblastoma Formation.

Sample Metadata Fields

Sex, Specimen part

View Samples
accession-icon SRP167390
Next-gen RNA sequencing of Sleeping Beauty accelerated mouse brain tumors
  • organism-icon Mus musculus
  • sample-icon 57 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Expression profiling by high throughput sequencing Overall design: 23 Tumor samples were obtained from a Sleeping Beauty forward genetic screen and sequenced using Illumina HiSeq 2000

Publication Title

<i>Sleeping Beauty</i> Insertional Mutagenesis Reveals Important Genetic Drivers of Central Nervous System Embryonal Tumors.

Sample Metadata Fields

Specimen part, Subject

View Samples
accession-icon GSE1140
PMBCs and the effect of exercise
  • organism-icon Homo sapiens
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Analysis of peripheral blood mononuclear cells (PBMCs) separated from whole blood of healthy male subjects

Publication Title

Effects of exercise on gene expression in human peripheral blood mononuclear cells.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE15969
Changes in gene expression of hMSCs and NOD/scid mouse lung after IV infusion of hMSCs
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Quantitative assays for human DNA and mRNA were used to examine the paradox that intravenously (IV) infused human multipotent stromal cells (hMSCs) can enhance tissue repair without significant engraftment. After 2 X 106 hMSCs were IV infused into mice, most of the cells were trapped as emboli in lung. The cells in lung disappeared with a half-life of about 24 hr but < 1,000 cells appeared in 6 other tissues. The hMSCs in lung up-regulated expression of multiple genes with a large increase in the anti-inflammatory protein TSG-6. After myocardial infarction, IV hMSCs but not hMSCs transduced with TSG-6 siRNA decreased inflammatory responses, reduced infarct size, and improved cardiac function. IV administration of recombinant TSG-6 also reduced inflammatory responses and reduced infarct size. The results suggest improvements in animal models and patients after IV infusions of MSCs are at least in part explained by activation of MSCs to secrete TSG-6.

Publication Title

Intravenous hMSCs improve myocardial infarction in mice because cells embolized in lung are activated to secrete the anti-inflammatory protein TSG-6.

Sample Metadata Fields

Specimen part, Disease

View Samples
accession-icon GSE14618
Microarray analyses of induction failure in T-ALL
  • organism-icon Homo sapiens
  • sample-icon 77 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2), Affymetrix Human Genome U133A Array (hgu133a)

Description

The clinical and cytogenetic features associated with T-cell acute lymphoblastic leukemia (T-ALL) are not predictive of early treatment failure. Based on the hypothesis that microarrays might identify patients who fail therapy, we used the Affymetrix U133 Plus 2.0 chip and prediction analysis of microarrays (PAM) to profile 50 newly diagnosed patients who were treated in the Children's Oncology Group (COG) T-ALL Study 9404. We identified a 116-member genomic classifier that could accurately distinguish all 6 induction failure (IF) cases from 44 patients who achieved remission; network analyses suggest a prominent role for genes mediating cellular quiescence. Seven genes were similarly upregulated in both the genomic classifier for IF patients and T-ALL cell lines having acquired resistance to neoplastic agents, identifying potential target genes for further study in drug resistance. We tested whether our classifier could predict IF within 42 patient samples obtained from COG 8704 and, using PAM to define a smaller classifier for the U133A chip, correctly identified the single IF case and patients with persistently circulating blasts. Genetic profiling may identify T-ALL patients who are likely to fail induction and for whom alternate treatment strategies might be beneficial.

Publication Title

Identification of genomic classifiers that distinguish induction failure in T-lineage acute lymphoblastic leukemia: a report from the Children's Oncology Group.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP029742
Zea mays Transcriptome or Gene expression
  • organism-icon Zea mays
  • sample-icon 64 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Heterosis which is the improved vigor of F1-hybrids compared to their parents is widely exploited in maize (Zea mays L.) breeding to produce elite hybrids of superior yield. The transcriptomes of the maize inbred lines B73 and Mo17 and their reciprocal hybrid offspring were surveyed in the meristematic zone, the elongation zone, cortex and stele tissues of primary roots, prior to the developmental manifestation of heterosis. Single parent expression (SPE) is consistent with the dominance model for heterosis in that it denotes genes that are expressed in only one parent but in both reciprocal hybrids. In primary root tissues, between 1,027 (elongation zone) and 1,206 (stele) SPE patterns were observed. As a consequence, hybrids displayed in each tissue >400 active genes more than either parent. Analysis of tissue-specific SPE dynamics revealed that 1,233 of 2,233 SPE genes displayed SPE in all tissues in which they were expressed while 1,000 SPE genes displayed in at least one tissue a non-SPE pattern. In addition, 64% (17,351/ 27,164) of all expressed genes were assigned to the two subgenomes which are the result of an ancient genome duplication. By contrast, only between 18 and 25% of the SPE genes were assigned to a subgenome suggesting that a disproportionate number of SPE genes are evolutionary young and emerged after genome duplication. We hypothesize that this phenomenon is associated with human selection of favorable maize genotypes which might primarily affect younger genes rather than genes whose functions have been conserved for millions of years.

Publication Title

Nonsyntenic genes drive highly dynamic complementation of gene expression in maize hybrids.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE14615
Microarray analyses of induction failure in T-ALL (COG study 9404)
  • organism-icon Homo sapiens
  • sample-icon 35 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2), Affymetrix Human Genome U133A Array (hgu133a)

Description

The clinical and cytogenetic features associated with T-cell acute lymphoblastic leukemia (T-ALL) are not predictive of early treatment failure. Based on the hypothesis that microarrays might identify patients who fail therapy, we used the Affymetrix U133 Plus 2.0 chip and prediction analysis of microarrays (PAM) to profile 50 newly diagnosed patients who were treated in the Children's Oncology Group (COG) T-ALL Study 9404. We identified a 116-member genomic classifier that could accurately distinguish all 6 induction failure (IF) cases from 44 patients who achieved remission; network analyses suggest a prominent role for genes mediating cellular quiescence. Seven genes were similarly upregulated in both the genomic classifier for IF patients and T-ALL cell lines having acquired resistance to neoplastic agents, identifying potential target genes for further study in drug resistance. We tested whether our classifier could predict IF within 42 patient samples obtained from COG 8704 and, using PAM to define a smaller classifier for the U133A chip, correctly identified the single IF case and patients with persistently circulating blasts. Genetic profiling may identify T-ALL patients who are likely to fail induction and for whom alternate treatment strategies might be beneficial.

Publication Title

Identification of genomic classifiers that distinguish induction failure in T-lineage acute lymphoblastic leukemia: a report from the Children's Oncology Group.

Sample Metadata Fields

No sample metadata fields

View Samples
...

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

Powered by Alex's Lemonade Stand Foundation

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.

BSD 3-Clause LicensePrivacyTerms of UseContact