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accession-icon SRP151594
RNA-seq in wild type and dCAP-D3 mutant tissues
  • organism-icon Drosophila melanogaster
  • sample-icon 11 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

The goal of this experiment was to identify transcripts that are differentially expressed in dCAP-D3 mutant tissues. Overall design: RNA was isolated from wing discs and salivary glands of wild type (w1118) or dCap-D3 homozygous mutant (dCap-D3c07081/c07081) larvae. Directional (wing disc) or nondirectional (salivary gland) cDNA libraries (50 bp, paired end) were made at the University of Chicago Genomics Core and sequenced on an Illumina HiSeq2500, according to standard protocols.

Publication Title

Comparing and Contrasting the Effects of <i>Drosophila</i> Condensin II Subunit dCAP-D3 Overexpression and Depletion <i>in Vivo</i>.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE59928
Expression data from 24 hours of Sox17 overexpression in pancreatic islets of a 16-week old mice
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Secretion of insulin by pancreatic cells in response to glucose is central for glucose homeostasis, and dysregulation of this process is a hallmark of the early stages of diabetes. We utilized a tetracycline-inducible approach to investigate the immediate impact of a pulse of Sox17 expression on the insulin secretory pathway. Sox17 gain-of-function animals (Sox17-GOF) were generated using an Ins2-rtTA mouse line and a line in which Sox17 expression is regulated by the tetracycline transactivator (tetO-Sox17). Administering doxycycline to 16-week old mice resulted in Sox17 overexpression in mature cells in the islets.

Publication Title

Sox17 regulates insulin secretion in the normal and pathologic mouse β cell.

Sample Metadata Fields

Age, Specimen part

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accession-icon SRP022043
A blood based 12-miRNA signature of Alzheimer patients
  • organism-icon Homo sapiens
  • sample-icon 70 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

We applied Next-Generation Sequencing (NGS) to miRNAs from blood samples of 48 AD (Alzheimer''s Disease) patients and 22 unaffected controls, yielding a total of 140 unique mature miRNAs with significantly changed expression level. Of these, 82 were higher and 58 lower abundant in samples from AD patients. We selected a panel of 12 miRNAs for a qRT-PCR analysis on a larger cohort of 202 samples including not only AD patients and healthy controls but also patients with other CNS illnesses: Multiple Sclerosis, Parkinson''s Disease, Major Depression, Bipolar Disorder, Schizophrenia, and Mild Cognitive Impairment, which is assumed to represent a transitional period before the development of AD. MiRNA target enrichment analysis of the selected 12 miRNAs indicated an involvement of miRNAs in nervous system development, neuron projection, neuron projection development, and neuron projection morphogenesis, respectively. Using this 12-miRNA signature we were able to differentiate between AD and controls with an accuracy of 93.3%, a specificity of 95.1%, and a sensitivity of 91.5%. The differentiation of AD from other neurological diseases was possible with accuracies between 73.8% and 77.8%. The differentiation of the other CNS disorders from controls yielded even higher accuracies. Overall design: Examination of the miRNA profile in blood samples of 48 AD patients and 22 controls

Publication Title

A blood based 12-miRNA signature of Alzheimer disease patients.

Sample Metadata Fields

Sex, Age, Subject

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accession-icon GSE57612
Characterization of genomic imbalances in diffuse large B-cell lymphoma by high resolution SNP-chip analysis
  • organism-icon Homo sapiens
  • sample-icon 148 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Characterization of genomic imbalances in diffuse large B-cell lymphoma by detailed SNP-chip analysis.

Sample Metadata Fields

Sex, Age

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accession-icon GSE57611
HGU133A expression array data for diffuse large B cell lymphoma samples
  • organism-icon Homo sapiens
  • sample-icon 148 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

The pathogenesis of diffuse large B cell lymphomas (DLBCL) is only partly understood. We analyzed 148 DLBCL by high resolution single nucleotide polymorphism (SNP)-chips to characterize genomic imbalances. Seventy-nine cases were of the germinal center B-cell like (GCB) type of DLBCL, 49 of the activated B-cell like (ABC) subtype and 20 were type 3 DLBCL. Twenty-four regions of recurrent genomic gains and 38 regions of recurrent genomic losses were identified over the whole cohort, with a median of 25 imbalances per case for ABC-DLBCL and 19 per case for GCB-DLBCL. Several recurrent copy number changes showed differential frequencies in the GCB- and ABC-DLBCL subgroups, including gains of HDAC7A predominantly in GCB-DLBCL (38% of cases) and losses of BACH2 and CASP8AP2 predominantly in ABC-DLBCL (35%), hinting at disparate pathogenetic mechanisms in these entities. Correlating gene expression and copy number revealed a strong gene dosage effect in all tumors, with 34% of probesets showing a concordant expression change in affected regions. Two new potential tumor suppressor genes emerging from the analysis, CASP3 and IL5RA, were sequenced in 10 and 16 candidate cases, respectively. However, no mutations were found, pointing to a potential haploinsufficiency effect of these genes, considering their reduced expression in cases with deletions. This work thus describes differences and similarities in the landscape of genomic aberrations in the DLBCL subgroups in a large collection of cases, confirming already known targets, but also discovering novel copy number changes with possible pathogenetic relevance.

Publication Title

Characterization of genomic imbalances in diffuse large B-cell lymphoma by detailed SNP-chip analysis.

Sample Metadata Fields

Sex, Age

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accession-icon GSE45626
Expression data from IGF-1R targeting in 33 NCI-H526 SCLC (small-cell lung cancer) xenografts
  • organism-icon Homo sapiens
  • sample-icon 33 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Insulin-like growth factor receptor-1 (IGF-1R) inhibition could be a relevant therapeutic approach in small cell lung cancer (SCLC) given the importance of an IGF-1R autocrine loop and its role in DNA damage repair processes. We assessed IGF-1R and pAkt protein expression in 83 SCLC human specimens. The efficacy of R1507 (a monoclonal antibody directed against IGF-1R) alone or combined with cisplatin or ionizing radiation (IR) was evaluated in H69, H146 and H526 cells in vitro and in vivo. Innovative genomic and functional approaches were conducted to analyze the molecular behavior under the different treatment conditions. A total of 53% and 37% of human specimens expressed IGF-1R and pAkt, respectively. R1507 demonstrated single agent activity in H146 and H526 cells but not in H69 cells. R1507 exhibited synergistic effects with both Cisplatin and IR in vitro. The triple combination R1507-Cisplatin-IR led to a dramatic delay in tumor growth compared to Cisplatin-IR in H526 cells. Analyzing the apparent absence of antitumoral effect of R1507 alone in vivo, we observed a transient reduction of IGF-1R staining intensity in vivo, concomitant to the activation of multiple cell surface receptors and intracellular proteins involved in proliferation, angiogenesis and survival. Finally, we identified that the nucleotide excision repair pathway (NER) was mediated after exposure to R1507-CDDP and R1507-IR in vitro and in vivo. In conclusion, adding R1507 to the current standard Cisplatin-IR doublet reveals remarkable chemo- and radiosensitizing effects in selected SCLC models and warrants to be investigated in the clinical setting.

Publication Title

IGF-1R targeting increases the antitumor effects of DNA-damaging agents in SCLC model: an opportunity to increase the efficacy of standard therapy.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE64052
Gene expression changes during resistance toward vascular endothelial growth factor receptor (VEGFR) tyrosine kinase inhibitor (TKI) therapy in renal cell carcinoma (RCC)
  • organism-icon Homo sapiens
  • sample-icon 25 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

This study was performed to understand the gene expression changes that accompany treatment of renal cell carcinoma (RCC) with vascular endothelial growth factor receptor (VEGFR) tyrosine kinase inhibitor (TKI) therapy. Human RCC cell lines were implanted into the flanks of nude beige mice, allowed to reach 12mm in long axis, and then treated with TKIs (sunitinib or sorafenib). Tumors were excised at 2 timepoints (prior to any therapy and at the 20mm endpoint of the study) and gene expression analysis was performed.

Publication Title

Anti-S1P Antibody as a Novel Therapeutic Strategy for VEGFR TKI-Resistant Renal Cancer.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon SRP049063
RNA-sequencing of mRNAs from control and CAP-D3 deficient Salmonella infected HT-29 cells
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2500

Description

BACKGROUND & AIMS- More frequent interaction of bacteria with the colonic epithelium is associated with ulcerative colitis (UC). The identities of all proteins which promote bacterial clearance in colonic epithelial cells are unknown. Previously, we discovered that dCAP-D3 (Chromosome Associated Protein-D3), regulates responses to bacterial infection. We examined whether CAP-D3 promotes bacterial clearance in human colonic epithelium. METHODS- Clearance of Salmonella or adherent-invasive Escherichia coli LF82 was assessed by gentamycin protection assays in HT-29 and Caco-2 cells expressing CAP-D3 shRNA. CAP-D3 levels in colonic epithelial cells from healthy and UC patient tissues were analyzed by immunoblot. RNA-sequencing identified bacterially-induced CAP-D3 target genes. The role of CAP-D3 target genes in bacterial clearance was analyzed by gentamycin protection assays, immunofluorescent staining, and by using pharmacologic inhibitors. RESULTS- CAP-D3 expression was reduced in colonic epithelial cells from UC patients with active disease. Reduction of CAP-D3 expression inhibited autophagy and decreased intracellular bacterial clearance. The components of the heterodimeric SLC7A5/SLC3A2 amino acid transporter were identified as CAP-D3 target genes; their levels increased in infected, CAP-D3 deficient cell lines and in cells from UC patients. In HT-29 cells, this resulted in earlier SLC7A5 recruitment to Salmonella-containing vacuoles, increased mTOR activity, and enhanced bacterial survival. Inhibition of SLC7A5/SLC3A2 or mTOR activity rescued the bacterial clearance defect in CAP-D3 deficient cells. CONCLUSIONS- CAP-D3 attenuates amino acid transporter transcription to promote bacterial autophagy in colon epithelial cells. CAP-D3 protein levels are decreased in patients with active UC, suggesting that CAP-D3 is a potential therapeutic target to restore mucosal homeostasis in UC patients. Overall design: Three RNA samples from 3 independent experiments including timepoints taken at 0, 0.5 and 7 hours post-infection were analyzed on a bioanalyzer for quality; one of the 0.5 hour post-infection samples was excluded at this time due to poor RNA purity. Directional, cDNA libraries made from cellular mRNAs were generated from the other 8 samples and sequenced (paired-end sequencing of 100 bp reads) in the Genomics Core at the University of Chicago on an Illumina HiSeq2000.

Publication Title

Chromosome-associated protein D3 promotes bacterial clearance in human intestinal epithelial cells by repressing expression of amino acid transporters.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP188673
A time course study by mRNA Sequencing to identify transcriptional changes in mice lung development
  • organism-icon Mus musculus
  • sample-icon 27 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Mammalian fetal lung development is a complex biological process.Despite considerable progress, a comprehensive understanding of the dynamic regulatory networks that govern postnatal alveolar lung development is still lacking. The purpose of this study as part of the LungMAP consortium (www.lungmap.net) is to understand the transcriptional changes in the process of mammalian lung development. Overall design: Method: We isolated alveolar septa from c57BL/6 mice by laser capture microdissection from 14 time points (E16.5, P0.5, P1, P1.5, P2.5, P4, P5, P7, P10, P13.5, P15, P19, P23, and P28) and performed RNA-Sequencing by Illumina Hi-Seq 2500 .

Publication Title

LungMAP: The Molecular Atlas of Lung Development Program.

Sample Metadata Fields

Sex, Specimen part, Cell line, Subject

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accession-icon GSE86575
MicroRNA-196b-5p is a prognostic factor in colorectal cancer patients and influences cancer cell migration and metastases formation through regulation of HOXB7 and GalNT5
  • organism-icon Homo sapiens
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.0 ST Array (hugene20st)

Description

Background: MicroRNA-196b-5p (miR-196b-5p) has been previously involved in carcinogenesis, though its role in colorectal cancer (CRC) patients and biology remains controversially. In our current study, we systematically explored the clinical significance and biological relevance of miR-196b-5p, as well as the underlying molecular mechanisms regulated by miR-196b-5p in colorectal cancer.

Publication Title

miR-196b-5p Regulates Colorectal Cancer Cell Migration and Metastases through Interaction with HOXB7 and GALNT5.

Sample Metadata Fields

Cell line

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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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