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accession-icon GSE4188
Drosophila whole testis gene expression
  • organism-icon Drosophila melanogaster
  • sample-icon 13 Downloadable Samples
  • Technology Badge Icon Affymetrix Drosophila Genome Array (drosgenome1)

Description

Whole testes were dissected from adult males. RNA from five or six biological replicates were generated and the expression profiles were determined using Affymetrix Drosophila Genechip 1 arrays. Comparisons between the bgcn- and Os+bgcn- groups allowed for the identification of stem cell genes.

Publication Title

Novel regulators revealed by profiling Drosophila testis stem cells within their niche.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE23980
Expression data from human soft tissue sarcomas with complex genomics
  • organism-icon Homo sapiens
  • sample-icon 164 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Differentially expressed genes between 171 human soft tissue sarcomas with complex genomics

Publication Title

From PTEN loss of expression to RICTOR role in smooth muscle differentiation: complex involvement of the mTOR pathway in leiomyosarcomas and pleomorphic sarcomas.

Sample Metadata Fields

Sex, Specimen part, Cell line

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accession-icon GSE35306
Combined hepatocellular-cholangiocarcinomas exhibit progenitor features and activation of Wnt and TGFbeta signaling pathways
  • organism-icon Homo sapiens
  • sample-icon 30 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Primary liver tumours include hepatocellular carcinomas (HCC), cholangiocarcinomas (CC) and a group of rare tumours exhibiting biliary and hepatocytic differentiation called combined hepatocholangiocarcinomas (cHCC-CC). To better define this latter group, we take advantage of a series of these tumours based on their morphological characteristics and we performed transcriptional analysis allowing thereafter global comparison with published data. We show that most cHCC-CCs express progenitor cell traits, are committed to biliary lineage and are mainly associated to the activation of Wnt/beta-catenin and TGFbeta signalling pathways. Wnt/beta-catenin pathway activation in cHCC-CC is evidenced by the expression of both its direct targets such as LEF1 and EPCAM. In addition, extracellular matrix (ECM) genes and ECM-remodelling genes which are upon the control of TGF profibrotic program were found up-regulated in cHCC-CC. Interestingly, we show that CC and most cHCC-CC share characteristics associated to a subtype of poorly differentiated HCC suggesting that these tumours could originate from a stem/progenitor cell. The plasticity of these cells may explain the phenotypical heterogeneity of these tumors with the maintenance of some hepatocellular differentiation features such as albumin expression. Interestingly, this is shared by at least one third of CC, raising the hypothesis of a potential continuum between CC, cHCC-CC and poorly differentiated HCC.

Publication Title

Combined hepatocellular-cholangiocarcinomas exhibit progenitor features and activation of Wnt and TGFβ signaling pathways.

Sample Metadata Fields

Sex, Specimen part

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accession-icon SRP068845
Next generation sequencing based analysis of the embryonic (E15.5) transcriptome of wild type and ß1-integrin-cKO lenses
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

ß1-integrin is the major ß-integrin subunit expressed in both lens epithelial and fiber cells. Our previous research indicated that ß1-integrin is essential for the maintenance of lens epithelial integrity and survival in late embryonic lens development (Simirskii et al, 2009). Lack of ß1-integrin in the lens will lead to severe micropthalmia and lack of lens in adult mice. In order to study the mechanisms involved, high throughput RNA sequencing (RNAseq) was performed to determine the genes that are differentially expressed between E15.5 wild type (WT) lenses and lenses that lack ß1-integrin expression due to the action of MLR10 CRE (ß1-cKO). The methodology used here is similar to the other RNAseq experiments that were previously performed in our lab (Manthey et al., 2014a and Audette et al, 2015) (Geo accession: GSE 49949 and GSE69940) . Meanwhile, the filtering criteria and processing procedures were also published (Manthey et al., 2014b). Compared to WT, 120 genes were found to be differentially expressed in ß1-cKO lenses. Moreover, bioinformatics tools (DAVID (the database for Annotation, Visulization and Integrated Discovery), and PANTHER (Protein Analysis through Evolutionary Relationship) classification system) as well as manual literature searching was applied for further data analysis. It showed that genes involved in EMT and stress-responses were differentially expressed in ß1-cKO compared to that of WT. Description of filtering criteria: To identify the differentially expressed genes, pair-wise qCML method exact tests with a Benjamini Hochberg false discovery rate correction greater than the threshold of P<0.05 was applied, which identified 5120 genes. As previously described (Manthey et al., 2014b), most of the genes differentially expressed between inbred C57Bl/6 <har> and mice with a mixed background were below a threshold of 2.5 fold change. Therefore, all differentially expressed genes with a less than 2.5 fold change were filtered out. Further, genes whose expression level were not high enough to be biologically significant were also filtered out, based on the RPMK (Reads per Kilobase per million reads) value. Any gene in the final list has RPKM greater that 2 in either WT or ß1-cKO samples, a value that corresponds to approximately 1 mRNA molecule per cell. By applying a combination of these filtering criteria, 120 differentially expressed genes were found, which could potentially elucidate the molecular connections between conditional deletion of ß1-intergrin from the lens and the observed phenotypic abnormalities. Manthey, A. L., Lachke, S. A., FitzGerald, P. G., Mason, R. W., Scheiblin, D. A., McDonald, J. H. and Duncan, M. K. (2014a) ''Loss of Sip1 leads to migration defects and retention of ectodermal markers during lens development'', Mech Dev 131: 86-110. Manthey, A. L., Terrell, A. M., Lachke, S. A., Polson, S. W. and Duncan, M. K. (2014b) ''Development of novel filtering criteria to analyze RNA-sequencing data obtained from the murine ocular lens during embryogenesis'', Genom Data 2: 369-374. Overall design: RNA-Seq comparison of C57Bl/6 <har> wild type controls and ß1-integrin conditional knockout lenses at E15.5, three biological replicates were used in each group

Publication Title

β1-Integrin Deletion From the Lens Activates Cellular Stress Responses Leading to Apoptosis and Fibrosis.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE11732
Runx transcriptional program for control of cell adhesion and survival
  • organism-icon Mus musculus
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The Runx genes are important in development and cancer, where they can act either as oncogenes or tumour supressors. We compared the effects of ectopic Runx expression in established fibroblasts, where all three genes produce an indistinguishable phenotype entailing epithelioid morphology and increased cell survival under stress conditions. Gene array analysis revealed a strongly overlapping transcriptional signature, with no examples of opposing regulation of the same target gene. A common set of 50 highly regulated genes was identified after further filtering on regulation by inducible RUNX1-ER. This set revealed a strong bias toward genes with annotated roles in cancer and development, and a preponderance of targets encoding extracellular or surface proteins reflecting the marked effects of Runx on cell adhesion.

Publication Title

Gene array analysis reveals a common Runx transcriptional programme controlling cell adhesion and survival.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE12836
PDGF-B induces a homogeneous class of oligodendrogliomas from embryonic neural progenitors
  • organism-icon Mus musculus
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

We analyzed the generation of mouse gliomas following the overexpression of PDGF-B in embryonic neural progenitors. Comparison of our microarray data, with published gene expression data sets for many different murine neural cell types, revealed a closest relationship between our tumor cells and oligodendrocyte progenitor cells, confirming definitively that PDGF-B-induced gliomas are pure oligodendrogliomas.

Publication Title

PDGF-B induces a homogeneous class of oligodendrogliomas from embryonic neural progenitors.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE71121
Expression data (micro-array and RNA-seq, frozen tumors and FFPE blocks) from various sarcomas
  • organism-icon Homo sapiens
  • sample-icon 259 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

RNA sequencing validation of the Complexity INdex in SARComas prognostic signature.

Sample Metadata Fields

Time

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accession-icon GSE71118
Expression data (micro-array, frozen tumors) from various sarcomas
  • organism-icon Homo sapiens
  • sample-icon 259 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

We validated the technological and material transfers of the CINSARC signature.

Publication Title

RNA sequencing validation of the Complexity INdex in SARComas prognostic signature.

Sample Metadata Fields

Time

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accession-icon GSE58697
Expression data from 128 Desmoids
  • organism-icon Homo sapiens
  • sample-icon 123 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

One of the main problems in managing desmoids tumors is their locoregional aggressiveness and their high ability to recur after initial treatment. In our work, with the goal to identify molecular markers that can predict Progression-Free Survival, gene-expression screening was conducted on 128 available independent untreated primary desmoid tumors using cDNA microarray. By analyzing expression profiles, we have identified, for the first time, a gene expression signature that is able to predict Progression-Free Survival. This molecular signature identified two groups with clearly distinct Progression-Free Survival in the two sets of subjects. Patients in good prognostic group had achieved a progression-free 2-year survival rate of 86% while patients in poor prognostic group had a progression-free 2-year survival rate of 44%.

Publication Title

Gene Expression Profiling of Desmoid Tumors by cDNA Microarrays and Correlation with Progression-Free Survival.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE32697
Thrombospondin-1 type 1 repeats in a model of inflammatory bowel disease: genetic profile and therapeutic effects
  • organism-icon Mus musculus
  • sample-icon 28 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Thrombospondin 1 (TSP-1) is an anti-angiogenic matricellular protein with regulatory functions in inflammation and cancer. The type 1 repeats (TSR) domains of TSP-1 have been shown to interact with a wide range of proteins that result in the anti-angiogenic and anti-tumor properties of TSP-1. To evaluate potential therapeutic effects of TSRs in inflammatory bowel disease, we conducted clinical, histological and gene microarray analyses on a mouse model of induced colitis.

Publication Title

Thrombospondin-1 type 1 repeats in a model of inflammatory bowel disease: transcript profile and therapeutic effects.

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)

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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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