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accession-icon GSE41802
Isocitrata Dehydrogenase (IDH) Mutations Promote a Reversible ZEB1/mir-200-Dependent Epithelial Mesenchymal Transition (EMT)
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Mutations in the genes encoding isocitrate dehydrogenase 1 and 2 (IDH1/2) occur in a variety of tumor types, resulting in production of the proposed oncometabolite, 2-hydroxyglutarate (2-HG). How mutant IDH and 2-HG alter signaling pathways to promote cancer, though, remains unclear. Additionally, there exist relatively few cell lines with IDH mutations. To examine the effect of endogenous IDH mutations and 2-HG, we created a panel of isogenic epithelial cell lines with either wild-type IDH1/2 or clinically relevant IDH1/2 mutations. Differences were noted in the ability of IDH mutations to cause robust 2-HG accumulation. IDH1/2 mutants that produce high levels of 2-HG cause an epithelial-mesenchymal transition (EMT)-like phenotype, characterized by changes in EMT-related gene expression and cellular morphology. 2-HG is sufficient to recapitulate aspects of this phenotype in the absence of an IDH mutation. In the cells types examined, mutant IDH-induced EMT is dependent on upregulation of the transcription factor ZEB1 and downregulation of the mir-200 family of microRNAs. Furthermore, sustained knockdown of IDH1 in IDH1 R132H mutant cells is sufficient to reverse many characteristics of EMT, demonstrating that continued expression of mutant IDH is required to maintain this phenotype. These results suggest mutant IDH proteins can reversibly deregulate discrete signaling pathways that contribute to tumorigenesis

Publication Title

Isocitrate dehydrogenase (IDH) mutations promote a reversible ZEB1/microRNA (miR)-200-dependent epithelial-mesenchymal transition (EMT).

Sample Metadata Fields

Cell line

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accession-icon GSE60771
Testing gene expression changes in VCaP upon depletion of the mutated ETS transcription factor ERG
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

VCaP cells expressing inducible shRNAs for either ERG or a non-targeting control were treated with Doxycycline for 1, 3, 7 and 10 days prior to collection

Publication Title

TMPRSS2:ERG blocks neuroendocrine and luminal cell differentiation to maintain prostate cancer proliferation.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP046010
Investigating gene expression changes in wildtype and TMPRSS2-ERG homozygous mouse prostate tissue
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

A transgenic TMPRSS2:ERG mouse model was engineered in FVB background and compared to its wildtype counterpart in the absence of any treatment This experiment is designed to look at ERG-dependent changes in phenotype and gene expression Overall design: A loxP-GFP-loxP-hERG exon 4-11 cassette was inserted into a BAC clone containing the TMPRSS2 locus using a recombineering kit. This modified BAC was used for pronuclear injection and generation of germline-transmitting mice. One line expressing high GFP was used for pronuclear injection of Cre protein and one sub-line that transmitted the TMPRSS2:ERG transgene into the germline was subsequently bred to homozygosity.

Publication Title

TMPRSS2:ERG blocks neuroendocrine and luminal cell differentiation to maintain prostate cancer proliferation.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE44927
Transcriptional responses of control and MDV3100 resistant lines to DMSO or MDV3100
  • organism-icon Homo sapiens
  • sample-icon 39 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

LNCaP-derived MDV3100-resistant clones were treated with MDV3100 for 24h prior to collection

Publication Title

An F876L mutation in androgen receptor confers genetic and phenotypic resistance to MDV3100 (enzalutamide).

Sample Metadata Fields

Cell line

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accession-icon GSE44924
Testing rescue of AR signaling by ectopic expression of mutant AR allele in the presence of MDV-3100
  • organism-icon Homo sapiens
  • sample-icon 13 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Genetically engineered LNCaPs overexpressing various AR alleles were treated with 0.1% DMSO or 10uM MDV3100 for 24h prior to collection

Publication Title

An F876L mutation in androgen receptor confers genetic and phenotypic resistance to MDV3100 (enzalutamide).

Sample Metadata Fields

Cell line

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accession-icon GSE9280
The effect of dietary calcium and dairy proteins on adipose tissue gene expression profile in diet induced obesity
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The effect of dietary calcium and dairy proteins on adipose tissue gene expression profile in diet induced obesity

Publication Title

Effect of dietary calcium and dairy proteins on the adipose tissue gene expression profile in diet-induced obesity.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE20940
Lactobacillus rhamnosus LGG and LC705 effects on human primary macrophages
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Analysis of human primary macrophages after live Lactobacillus rhamnosus GG (LGG) or LC705 stimulation for 6h and 24h. The results reveal novel mechanisms for probiotics-induced activation of the healthy human innate immune system.

Publication Title

Nonpathogenic Lactobacillus rhamnosus activates the inflammasome and antiviral responses in human macrophages.

Sample Metadata Fields

Specimen part, Time

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accession-icon GSE6013
Gene expression in asbestos exposed lung cells
  • organism-icon Homo sapiens
  • sample-icon 25 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Asbestos has been shown to cause chromosomal damage and DNA aberrations. The fiber is associated with many different lung diseases such as asbestosis, malignant mesothelioma, and lung cancer, but the disease-related processes are still largely unknown. Our aim was to identify specific gene expression profiles by using Affymetrix arrays, in human cell lines A549, Beas-2B, and MeT5A exposed to asbestos in a time-dependent manner. The hybridization data was analyzed using an algorithm specifically designed for clustering short time series expression data, a canonical correlation analysis (CCA) for identifying correlations between the cell lines, and a Gene Ontology (GO) analysis method for the identification of enriched differentially expressed biological processes.

Publication Title

Gene expression profiles in asbestos-exposed epithelial and mesothelial lung cell lines.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE49559
Gene expression data from PC3 prostate cells overexpressing control miR or miR-95
  • organism-icon Homo sapiens
  • sample-icon 1 Downloadable Sample
  • Technology Badge Icon Affymetrix Human Gene 2.0 ST Array (hugene20st)

Description

We used microarrays to detail the global changes in gene expression resulting from miR-95 overexpression

Publication Title

miRNA-95 mediates radioresistance in tumors by targeting the sphingolipid phosphatase SGPP1.

Sample Metadata Fields

Cell line, Treatment

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accession-icon GSE23310
Uncovering Genes and Regulatory Pathways Related to Urinary Albumin Excretion in Mice
  • organism-icon Mus musculus
  • sample-icon 173 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Identifying the genes underlying quantitative trait loci (QTL) for disease has proven difficult, mainly due to the low resolution of the approach and the complex genetics involved. However, recent advances in bioinformatics and the availability of genetic resources now make it possible to narrow the genetic intervals and test candidate genes. In addition to identifying the causative genes, defining the pathways that are affected by these QTL is of major importance as it can give us insight into the disease process and provide evidence to support candidate genes. In this study we mapped three significant and one suggestive QTL on Chromosomes (Chrs) 1, 4, 15, and 17, respectively, for increased albumin excretion (measured as albumin-to-creatinine ratio) in a cross between the MRL/MpJ and SM/J mouse inbred strains. By combining data from several sources and by utilizing gene expression data, we identified Tlr12 as a likely candidate for the Chr 4 QTL. Through the mapping of 33,881 transcripts measured by microarray on kidney RNA from each of the 173 male F2 animals, we identified several downstream pathways associated with these QTL. Among these were the glycan degradation, leukocyte migration, and antigen presenting pathways. We demonstrate that by combining data from multiple sources, we can identify not only genes that are likely to be causal candidates for QTL, but also the pathways through which these genes act to alter phenotypes. This combined approach provides valuable insights into the causes and consequences of renal disease.

Publication Title

Uncovering genes and regulatory pathways related to urinary albumin excretion.

Sample Metadata Fields

Sex, Age

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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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