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accession-icon GSE97549
Global microarray analysis of ONECUT2 transcription factor overexpression in human prostate cancer cells
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Treatment of prostate cancer by hormone suppression leads to the appearance of aggressive variants with variable or no dependence on the androgen receptor. Here we show that the developmental transcription factor, ONECUT2, is a master regulator of the AR network that is highly active in castration-resistant prostate cancer (CRPC).

Publication Title

ONECUT2 is a targetable master regulator of lethal prostate cancer that suppresses the androgen axis.

Sample Metadata Fields

Cell line, Treatment

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accession-icon GSE97548
ONECUT2 inhibition by chemical compound treatment in 22Rv1
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

To evaluate the specificity for inhibition of expression of OC2 target genes we generated microarray data of 22Rv1 cells treated for 4, 6 and 16 hours with the small molecule inhibitor.

Publication Title

ONECUT2 is a targetable master regulator of lethal prostate cancer that suppresses the androgen axis.

Sample Metadata Fields

Cell line, Treatment, Time

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accession-icon GSE12407
Gene expression in erythroid cell differentiation
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

Human mononuclear cells were cultured in 2 phases. In the 1st phase the culture medium contained cyclosporine A the 2nd phase contained SCF and erythropoietin. Cells were collected at 3 stages of differentiation; on day 6, 10, 12 and represented early erythroblasts, medium stage and normoblasts.

Publication Title

Identification of gene networks associated with erythroid differentiation.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE30239
Mis-expression of Tramtrack in Drosophila embryos
  • organism-icon Drosophila melanogaster
  • sample-icon 19 Downloadable Samples
  • Technology Badge Icon Affymetrix Drosophila Genome 2.0 Array (drosophila2)

Description

We profiled the transcriptome of Drosophila melanogaster embryos in ttk2D50 embryos or after over-expression using btl-GAL4; UAS-ttk, respectively. We further isolated cells that express btl-enh-RFPmoe (Cabernard and Affolter 2005) and FACS sorting, and profiled their transcriptomes in the same genetic backgrounds.

Publication Title

Tramtrack is genetically upstream of genes controlling tracheal tube size in Drosophila.

Sample Metadata Fields

Specimen part

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accession-icon GSE71416
Gene Expression Profiling in Omental Adipose Tissue of Morbidly Obese Diabetic African Americans
  • organism-icon Homo sapiens
  • sample-icon 19 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Adipose tissues play an important role in the pathophysiology of obesity-related disease including type 2 diabetes. To describe gene expression patterns and functional pathways in obesity-related type 2 diabetes, we performed global transcript profiling of omental adipose tissue in morbidly obese individuals with or without diabetes.

Publication Title

Global Gene Expression Profiling in Omental Adipose Tissue of Morbidly Obese Diabetic African Americans.

Sample Metadata Fields

Sex

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accession-icon SRP156461
Transcriptome analysis of mesenchymal CSC-like cells harboring mutant p53
  • organism-icon Mus musculus
  • sample-icon 17 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

We show that mesenchymal CSC-like cells express an embryonic stem cell signature that is mutant p53 dependent Overall design: Examination of three p53 mutant mesenchymal stem cells and ten derived CSC-like cell lines and 2 derived p53 mutant KO clones compared to control clones

Publication Title

A Mutant p53-Dependent Embryonic Stem Cell Gene Signature Is Associated with Augmented Tumorigenesis of Stem Cells.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE15648
AML1-ETO induction and knockdown
  • organism-icon Homo sapiens
  • sample-icon 30 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U95A Array (hgu95a)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Identification of AML1-ETO modulators by chemical genomics.

Sample Metadata Fields

Cell line

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accession-icon GSE91002
caArray_stegm-00394: Broad: Identification of AML1-ETO modulators by chemical genomics
  • organism-icon Homo sapiens
  • sample-icon 30 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U95A Array (hgu95a)

Description

Somatic rearrangements of transcription factors are common abnormalities in the acute leukemias. With rare exception, however, the resultant protein products have remained largely intractable as pharmacologic targets. One example is AML1-ETO, the most common translocation reported in acute myeloid leukemia (AML). To identify AML1-ETO modulators, we screened a small molecule library using a chemical genomic approach. Gene expression signatures were used as surrogates for the expression versus loss of the translocation in AML1-ETO-expressing cells. The top classes of compounds that scored in this screen were corticosteroids and dihydrofolate reductase (DHFR) inhibitors. In addition to modulating the AML1-ETO signature, both classes induced evidence of differentiation, dramatically inhibited cell viability, and ultimately induced apoptosis via on-target activity. Furthermore, AML1-ETO-expressing cell lines were exquisitely sensitive to the effects of corticosteroids on cellular viability compared with nonexpressers. The corticosteroids diminished AML1-ETO protein in AML cells in a proteasome- and glucocorticoid receptor-dependent manner. Moreover, these molecule classes demonstrated synergy in combination with standard AML chemotherapy agents and activity in an orthotopic model of AML1-ETO-positive AML. This work suggests a role for DHFR inhibitors and corticosteroids in treating patients with AML1-ETO-positive disease.

Publication Title

Identification of AML1-ETO modulators by chemical genomics.

Sample Metadata Fields

Disease, Disease stage, Cell line

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accession-icon GSE15647
U937 AML1-ETO inducible samples
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U95A Array (hgu95a)

Description

U937 AML cells that express an inducible AML1-ETO construct under the control of the tetracycline promoter.

Publication Title

Identification of AML1-ETO modulators by chemical genomics.

Sample Metadata Fields

Cell line

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accession-icon GSE15646
Kasumi-1 AML1-ETO knockdown samples
  • organism-icon Homo sapiens
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U95A Array (hgu95a)

Description

Kasumi-1 AML cells that were transfected in triplicate with AML1-ETO or luciferase siRNA constructs by either Amaxa nucleofection or Biorad siLentFect and incubated for 96 hours.

Publication Title

Identification of AML1-ETO modulators by chemical genomics.

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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Developed by the Childhood Cancer Data Lab

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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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