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accession-icon GSE30391
Expression data from human Wharton's jelly stem cells
  • organism-icon Homo sapiens
  • sample-icon 30 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Human umbilical cord Whartons jelly stem cells (WHJSC) are gaining attention as a possible clinical source of mesenchymal stem cells for use in cell therapy and tissue engineering due to their high accessibility, expansion potential and plasticity. However, the cell viability changes that are associated to sequential cell passage of these cells are not known. In this analysis, we have identified the gene expression changes that are associated to cell passage in WHJSC.

Publication Title

Evaluation of the cell viability of human Wharton's jelly stem cells for use in cell therapy.

Sample Metadata Fields

Specimen part

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accession-icon GSE64573
The UBC-40 Urothelial Bladder Cancer Cell Line Index
  • organism-icon Homo sapiens
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

The UBC-40 Urothelial Bladder Cancer cell line index: a genomic resource for functional studies.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE64279
The UBC-40 Urothelial Bladder Cancer Cell Line Index [gene expression]
  • organism-icon Homo sapiens
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

This is a comprehensive genomic characterization of 40 urothelial bladder carcinoma (UBC) cell lines including information on origin, mutation status of genes implicated in bladder cancer (FGFR3, PIK3CA, TP53, and RAS), copy number alterations assessed using high density SNP arrays, uniparental disomy (UPD) events, and gene expression. Based on gene mutation patterns and genomic changes we identify lines representative of the FGFR3-driven tumor pathway and of the TP53/RB tumor suppressor-driven pathway. High-density array copy number analysis identified significant focal gains (1q32, 5p13.1-12, 7q11, and 7q33) and losses (i.e. 6p22.1) in regions altered in tumors but not previously described as affected in bladder cell lines. We also identify new evidence for frequent regions of UPD, often coinciding with regions reported to be lost in tumors. Previously undescribed chromosome X losses found in UBC lines also point to potential tumor suppressor genes. Cell lines representative of the FGFR3-driven pathway showed a lower number of UPD events. Overall, there is a predominance of more aggressive tumor subtypes among the cell lines. We provide a cell line classification that establishes their relatedness to the major molecularly-defined bladder tumor subtypes. The compiled information should serve as a useful reference to the bladder cancer research community and should help to select cell lines appropriate for the functional analysis of bladder cancer genes, for example those being identified through massive parallel sequencing.

Publication Title

The UBC-40 Urothelial Bladder Cancer cell line index: a genomic resource for functional studies.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon SRP150708
Functional interplay between c-Myc and Max in B lymphocyte differentiation
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

The Myc proteins (N-, L- and c-Myc) are transcription factors involved in many biological functions such as regulation of cell proliferation, differentiation, metabolism and apoptosis. A large number of human cancers show enhanced expression of myc family proto-oncogenes as one of their hallmarks. These proteins contain a basic region/helix-loop-helix/leucine zipper (bHLHZip) domain that mediates DNA binding and heterodimerization with its partner Max (Myc/Max heterodimer). Among Myc proteins, c-Myc is the most widely expressed and relevant in primary B lymphocytes. Some reports have implied that c-Myc can perform some functions without Max in different cell contexts. However, the functional interplay in vivo between c-Myc and Max during B lymphocyte differentiation is not well-known. Here we show that c-Myc requires Max. However, key biological processes such as cell differentiation and DNA replication can initially progress without c-Myc/Max heterodimer in primary B lymphocytes. We found that B lymphocytes lacking Myc, Max or both showed upregulation of signalling pathways associated with the B cell receptor. Our data suggest that c-Myc/Max heterodimers are not essential for the initiation of certain biological processes in B lymphocytes. Rather, c-Myc/Max are necessary for fine-tuning the initial response in these cells after activation. Overall design: B cell mRNA profiles of 8-week old control (HET) Myc deficient (MycKO), Max deficient (MaxKO) and double deficient (DKO) mice were generated by deep sequencing, in duplicate, using a HiSeq2500 (Illumina.

Publication Title

Functional interplay between c-Myc and Max in B lymphocyte differentiation.

Sample Metadata Fields

Age, Specimen part, Subject

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accession-icon GSE44272
The Long-HER Study
  • organism-icon Homo sapiens
  • sample-icon 53 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U219 Array (hgu219)

Description

Trastuzumab improves survival outcomes in patients with HER2+ metastatic breast cancer. Some of these patients may become long-term survivors. The Long-Her study was designed to identify clinical and molecular markers that could differentiate long-term survivors from patients having early progression to trastuzumab.

Publication Title

The Long-HER study: clinical and molecular analysis of patients with HER2+ advanced breast cancer who become long-term survivors with trastuzumab-based therapy.

Sample Metadata Fields

Age, Disease

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accession-icon SRP154527
Next Generation Sequencing Facilitates Quantitative Analysis of mock and tobacco ratle virus (TRV) Arabidopsis inflorescences Transcriptome [RNA-Seq]
  • organism-icon Arabidopsis thaliana
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Purpose: The goal of this study is to compare the transcriptome profilling (RNA-seq) of inflorescences infected with tobacco ratle virus (TRV) to mock inoculated inflorescences (negative controls), in Arabidopsis plants Methods: Inflorescences of systemically TRV infected or mock-inoculated plants were collected from more than 40 independent Arabidopsis plants, at 14 days post-inoculation (dpi). TRV and mock mRNA profiles were generated by deep sequencing by Illumina HiSeq 2000. The sequence reads that passed quality filters (SOAPnuke) were analysed by Burrows-Wheeler (BWA) followed by ANOVA (ANOVA) and TopHat followed by Cufflinks. Genes and isoforms were quantified by RSEM sofware package. qRT-PCR validation was performed using TaqMan and SYBR Green assays. Results: Here we report a significant repression of DNA methylation genes in inflorescences of Arabidopsis plants infected with Tobacco rattle virus (TRV) that coincides with dynamic changes in methylation at the whole genome level. Arabidopsis mutants deficient in DNA methylation were more resistant to this virus in early colonized tissues but more susceptible at later time points of infection, indicating that DNA methylation was critical to control both proliferation and antiviral defense. We found that TRV interference with DNA methylation leads to changes in the methylation and trancriptional status of transposable elements (TEs), including TEs located in the promoter of disease resistance genes that were significantly repressed in plants exposed to TRV. Activation of both TEs and their nearby disease resistance genes was altered in a range of hypo- and hyper-methylated Arabidopsis mutants, indicating that perturbations in DNA methylation contributes to modulate their expression in infected plants. Conclussion: Our study showed that TRV interferes with DNA methylation to alter the transcriptional silencing of TEs, which in turn compromises the expression of neighboring disease resistance genes. Overall design: TRV and mock mRNA profiles were generated from Arabidopsis inflorescences by deep sequencing with Illumina HiSeq 2000.

Publication Title

Crosstalk between epigenetic silencing and infection by tobacco rattle virus in Arabidopsis.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE17922
Immunomodulatory effect of 5-azacytidine (5-azaC): potential role in the transplantation setting.
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Cytokine genes are targets of multiple epigenetic mechanisms in T lymphocytes. 5-azacytidine (5-azaC) is a nucleoside-based DNA methyltransferases (DNMT) inhibitor which induces demethylation and gene reactivation. In the current study, we analyzed the effect of 5-azaC in T-cell function and observed that 5-azaC inhibits T-cell proliferation and activation, blocking cell cycle in G0-G1 phase and decreasing the production of proinflammatory cytokines such as TNF and IFN. This effect was not due to a pro-apoptotic effect of the drug but to the down-regulation of genes involved in T-cell cycle progression and activation such as CCNG2, MTCP1, CD58, and ADK and up-regulation of genes which induce cell growth arrest, such as DCUN1D2, U2AF2, GADD45B or p53. In spite of being also up-regulated, we did not find any effect of 5-azaC on the methylation pattern of FOXP3. Finally, the administration of 5-azaC at 60 and 84 hours post-transplant prevented the development of GVHD leading to a significant increase in survival in a fully mismatched BMT mouse model. In conclusion, the current study shows the effect of 5-azaC in T-lymphocytes and illustrates its role in the allogeneic transplantation setting as an immunomodulatory drug, describing new pathways which must be explored in order to prevent graft-versus-host disease.

Publication Title

Immunomodulatory effect of 5-azacytidine (5-azaC): potential role in the transplantation setting.

Sample Metadata Fields

Specimen part, Treatment, Time

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accession-icon SRP041313
Mismatch between mtDNA and nuclear DNA determines metabolism and healthy aging
  • organism-icon Mus musculus
  • sample-icon 29 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer IIx

Description

We postulate here that the two singular characteristics of the mitochondrial oxidative phosphorylation system—the integration of three potentially antagonistic functions in the same structure and the double genetic origin of the components that assemble together in these molecular machines—make the evolution of an optimal system impossible. As a consequence the system is intrinsically mismatched and has to be continuously monitored, Adjusted and regulated in order to achieve the necessary and variable performance. Systematic transcriptomic, Metabolomic and biochemical evaluation of animals with identical nuclear DNA but different mtDNA haplotype strongly support the existence of intrinsic mismatch and reveals profound lifelong metabolic consequences on reactive oxygen species generation, Insulin signaling, Tendency towards obesity, And healthy ageing parameters, Including telomere atresia Overall design: Transcriptome analysis of conplastic mice versus WT mice in Liver and Heart tissues Conplastic strains were obtained after 10 generations of backcrossing to create a new line harboring the nuclear genome of one strain and the mtDNA of another (C57BL/6 and NZB were purchased from Harlan Laboratories).

Publication Title

Mitochondrial and nuclear DNA matching shapes metabolism and healthy ageing.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP098927
A Cross-Species Approach Identifies MELK as a Potential Therapeutic Target in Prostate Cancer
  • organism-icon Mus musculus
  • sample-icon 912 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Genetically engineered mouse models of cancer represent valuable biological tools that can be used to filter genome-wide expression datasets generated from human prostate tumours, and identify gene expression alterations that are functionally important to cancer development and progression. In this study, we have generated RNASeq data from tumours arising in two established mouse models of prostate cancer, PB-Cre/PtenloxP/loxP and p53loxP/loxPRbloxP/loxP, and integrated this with published human prostate cancer expression data to pinpoint cancer-associated gene expression changes that are conserved between the two species. In order to identify potential therapeutic targets, we then filtered this information for genes that are either known or predicted to be druggable. Using this approach, we identified the serine/threonine kinase MELK as a potential therapeutic target in prostate cancer. MELK was overexpressed in both human and murine prostate cancers, and high expression of MELK was associated with biochemical recurrence in prostate cancer patients. Overall design: 92 Samples

Publication Title

Identification of potential therapeutic targets in prostate cancer through a cross-species approach.

Sample Metadata Fields

Cell line, Subject

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accession-icon GSE38829
Expression data from MCF7 and MCF7-LTED cells treated with YC-1
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U219 Array (hgu219)

Description

To identify novel therapeutic opportunities for patients with acquired resistance to endocrine treatments in breast cancer, we applied a high-throughput drug screen. The IC50 values were determined for MCF7 and MCF7-LTED cells.

Publication Title

VAV3 mediates resistance to breast cancer endocrine therapy.

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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