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accession-icon GSE41146
Expression data from uninfected and VSV-infected Drosophila cells at 4 hours post-infection
  • organism-icon Drosophila melanogaster
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Drosophila Genome 2.0 Array (drosophila2)

Description

Expression profiling of rapidly-induced genes upon VSV infection at 4 hours post-infection in Drosophila cells

Publication Title

Transcriptional pausing controls a rapid antiviral innate immune response in Drosophila.

Sample Metadata Fields

Cell line

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accession-icon GSE41242
Global analysis of Cdk9-dependence for VSV-induced genes in Drosophila cells
  • organism-icon Drosophila melanogaster
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Drosophila Genome 2.0 Array (drosophila2)

Description

To determine the Cdk9 targets of VSV-induced genes in Drosophila cells at 4 hours post-infection

Publication Title

Transcriptional pausing controls a rapid antiviral innate immune response in Drosophila.

Sample Metadata Fields

Cell line, Treatment

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accession-icon GSE93527
Expression analysis of human TAG2 primary bladder tumours
  • organism-icon Homo sapiens
  • sample-icon 35 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Transcriptome Array 2.0 (hta20)

Description

Expression data derived from this analysis was used to compare expression signatures between genomic subgroups identified from DNA copy number analysis.

Publication Title

Genomic Subtypes of Non-invasive Bladder Cancer with Distinct Metabolic Profile and Female Gender Bias in KDM6A Mutation Frequency.

Sample Metadata Fields

Sex, Age

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accession-icon GSE21147
Express data from Du145 cells
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

The retinoblastoma (Rb) tumor suppressor is often inactivated in cancers. To identify genes that can be used to specifically target such cancers, we carried out a genetic screen in Drosophila. We identified gig (fly TSC2) and found that inactivation of rbf (fly Rb) and gig synergistically induced cell death. Interestingly, inactivation of TSC2 specifically kills Rb mutant cancer cells under stress conditions, which is correlated with an inhibition of tumor growth. We show that cancer cell killing induced by concomitant inactivation of Rb and TSC2 is mediated by increased cellular stress, including oxidative stress. Inactivation of TSC2 and Rb synergistically induce oxidative stress via increased protein synthesis, inhibited de novo lipid synthesis, and decreased ROS scavenger enzyme SOD2 induction.

Publication Title

Specific killing of Rb mutant cancer cells by inactivating TSC2.

Sample Metadata Fields

Cell line

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accession-icon GSE40227
Expression variation between VHLR200w homozygous verse wildtype control
  • organism-icon Homo sapiens
  • sample-icon 45 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

Hypoxia may cause pulmonary and brain edema, pulmonary hypertension, aberrant metabolism and early mortality. To better understand pathological processes associated with hypoxia, we examined gene expression in Chuvash polycythemia (CP) blood mononuclear cells. CP is a congenital disorder of up-regulated hypoxic response at normoxia wherein VHLR200W homozygosity leads to elevated hypoxia inducible factor (HIF)-1 and HIF-2 levels, thromboses, pulmonary hypertension, lower systemic blood pressure (SBP) and increased mortality. VHLR200W homozygotes are often treated by phlebotomy resulting in iron deficiency, allowing us to evaluate an interaction of augmented hypoxia sensing with iron deficiency.

Publication Title

Iron deficiency modifies gene expression variation induced by augmented hypoxia sensing.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE53441
Associations of inflammation, iron and early death in sickle cell disease
  • organism-icon Homo sapiens
  • sample-icon 32 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Expression profiling using a defined set of iron regulated genes identifies co-regulation of genes and pathways related to inflammatory cytokines

Publication Title

Iron, inflammation, and early death in adults with sickle cell disease.

Sample Metadata Fields

Specimen part, Disease

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accession-icon GSE79641
Gene expression signature baesd screening identifies ribonucleotide reductase as a candidate therapeutic target in Ewing sarcoma
  • organism-icon Homo sapiens
  • sample-icon 32 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

There is a critical need in cancer therapeutics to identify targeted therapies that will improve outcomes and decrease toxicities compared to conventional, cytotoxic chemotherapy. Ewing sarcoma is a highly aggressive bone and soft tissue cancer that is caused by the EWS-FLI1 fusion protein. Although EWS-FLI1 is specific for cancer cells, and required for tumorigenesis, directly targeting this transcription factor has proven challenging. Consequently, targeting unique dependencies or key downstream mediators of EWS-FLI1 represent important alternative strategies. We used gene expression data derived from a genetically defined model of Ewing sarcoma to interrogate the Connectivity Map and identify a class of drugs, iron chelators, that downregulate a significant number of EWS-FLI1 target genes. We then identified ribonucleotide reductase M2 (RRM2), the iron-dependent subunit of ribonucleotide reductase (RNR), as one mediator of iron chelator toxicity in Ewing sarcoma cells. Inhibition of RNR in Ewing sarcoma cells led to apoptosis and cell death in vitro and attenuated tumor growth in vivo in a xenograft model. Additionally, we discovered that the sensitivity of Ewing sarcoma cells to inhibition or suppression of RNR is mediated, in part, by high levels of SLFN11, a protein that sensitizes cells to DNA damage. This work demonstrates a unique dependency of Ewing sarcoma cells on RNR and supports further exploration of clinically used inhibitors of RNR as a therapeutic approach in treating this cancer.

Publication Title

Gene expression signature based screening identifies ribonucleotide reductase as a candidate therapeutic target in Ewing sarcoma.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon GSE64686
Expression data from the inducible expression of EWS-FLI1 (EF) in embryoid bodies
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Oncogenic transformation in Ewing sarcoma tumors is driven by the fusion oncogene EWS-FLI1. The inducible expression of EWS-FLI1 (EF) in embryoid bodies, or collections of differentiating stem cells, generates cells with properties of Ewing sarcoma tumors, including characteristics of transformation. These cell lines exhibit anchorage-independent growth, a lack of contact inhibition and a strong Ewing sarcoma gene expression signature. These cells also demonstrate a requirement for the persistent expression of EWS-FLI1 for cell survival and growth.

Publication Title

Modeling the initiation of Ewing sarcoma tumorigenesis in differentiating human embryonic stem cells.

Sample Metadata Fields

Specimen part

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accession-icon GSE6419
Expression data from mouse bladder urothelium
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

Host responses to intracellular UPEC communities

Publication Title

Functional genomic studies of uropathogenic Escherichia coli and host urothelial cells when intracellular bacterial communities are assembled.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP074246
Gene expression changes upon NUSAP1 over- or under-expression in PC-3 or DU145 cells.
  • organism-icon Homo sapiens
  • sample-icon 40 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

By transcriptome (RNA-Seq) analysis of PC-3 or DU145 prostate cancer cell lines over- or under-expressing NUSAP1, we determined genes that become differentially expressed upon expression changes of NUSAP1. Ingenuity Pathway Analysis revealed that the differentially expressed genes correlated with increased tumor progression and are involved in functions that include cancer, cellular movement, and cell morphology Overall design: Lentiviral infections were used to over- or under-express NUSAP1 or controls in triplicate in PC-3 or DU145 cell lines. Seventy-two or ninety-six hours after infection, total RNA was extracted and purified. The sequencing libraries were prepared with the TruSeq RNA Sample Preparation Kit v2 (Illumina) or TruSeq Stranded mRNA Sample Preparation Kit (Illumina) as directed by the manufacturer’s protocol. Pooled libraries were run on a Hiseq 2000 Sequencing System (Illumina) with 101 base pair single-end reads.

Publication Title

NUSAP1 promotes invasion and metastasis of prostate cancer.

Sample Metadata Fields

Specimen part, Subject

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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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