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accession-icon E-MEXP-1269
Transcription profiling by array of three human multiple myeloma cell lines treated with 5-aza-2-deoxycytidine and/or trichostatin A
  • organism-icon Homo sapiens
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

To identify epigenetically silenced genes in multiple myeloma (MM) cell lines and to determine the effects of 5-aza-2-deoxycytidine and trichostatin A on gene expression. We treated 3 multiple myeloma cell lines (MM1, NCI-H929, U266) with 5-aza-2-deoxycytidine and/or trichostatin A.

Publication Title

Genome-wide transcriptional response to 5-aza-2'-deoxycytidine and trichostatin a in multiple myeloma cells.

Sample Metadata Fields

Specimen part, Disease, Cell line

View Samples
accession-icon SRP132194
Differential expression in wild type and mutant HAP1 cells [RNA-seq I]
  • organism-icon Homo sapiens
  • sample-icon 41 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

using RNA-seq we characterized gene expression changes occuring upon knockout of BAP1, ASXL1, ASXL2, ASXL1/2 or Polycomb genes RING1B and EZH2. We also investigated the response to retinoic acid treatment in wild-type and BAP1 KO cells. Overall design: Examination of transcript abundance in wild-type HAP1 cells and in 9 different HAP1-mutated cell lines as well as upon retinoic acid treatment in wild-type and BAP1 KO cells. Two biological replicated were performed for each condition.

Publication Title

BAP1 complex promotes transcription by opposing PRC1-mediated H2A ubiquitylation.

Sample Metadata Fields

Cell line, Treatment, Subject

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accession-icon SRP159677
Differential expression in wild type and mutant HAP1 cells [RNA-seq II]
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Characterization of gene expression changes occuring upon knockout of RING1A, RING1B, and BAP1. Overall design: Four Samples

Publication Title

BAP1 complex promotes transcription by opposing PRC1-mediated H2A ubiquitylation.

Sample Metadata Fields

Specimen part, Treatment, Subject

View Samples
accession-icon GSE32497
GENOME-WIDE CpG ISLAND METHYLATION ANALYSIS IN NON-SMALL CELL LUNG CANCER PATIENTS
  • organism-icon Homo sapiens
  • sample-icon 15 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

Genome-wide CpG island methylation analyses in non-small cell lung cancer patients.

Sample Metadata Fields

Specimen part, Disease, Cell line, Treatment

View Samples
accession-icon GSE32496
GENOME-WIDE CpG ISLAND METHYLATION ANALYSIS IN NON-SMALL CELL LUNG CANCER PATIENTS [Affymetrix expression data]
  • organism-icon Homo sapiens
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Epigenetic changes largely contribute to the regulation of gene expression in cancer cells. DNA methylation is part of the epigenetic gene regulation complex which is relevant for the pathogenesis of cancer. We performed a genome-wide search for methylated CpG islands in tumors and corresponding non-malignant lung tissue samples of 101 stage I-III non-small cell lung cancer (NSCLC) patients by combining methylated DNA immunoprecipitation and microarray analysis using NimbleGens 385K Human CpG Island plus Promoter arrays. By testing for differences in methylation between tumors and corresponding non-malignant lung tissues, we identified 298 tumor-specifically methylated genes. From many of these genes epigenetic regulation was unknown so far. Gene Ontology analysis revealed an over-representation of genes involved in regulation of gene expression and cell adhesion. Expression of 182 of 298 genes was found to be upregulated after 5-aza-2-deoxycytidine (Aza-dC) and/or trichostatin A (TSA) treatment of 3 NSCLC cell lines by Affymetrix microarray analysis. In addition, methylation of selected genes in primary NSCLCs and corresponding non-malignant lung tissue samples were analyzed by methylation-sensitive high resolution melting analysis (MS-HRM). Our results obtained by MS-HRM analysis confirmed our data obtained by MeDIP-chip analysis. Moreover, by comparing methylation results from MeDIP-chip analysis with clinico-pathological parameters of the patients we observed methylation of HOXA2 as potential parameter for shorter disease-free survival of NSCLC patients. In conclusion, using a genome-wide approach we identified a large number of tumor-specifically methylated genes in NSCLC patients. Our results stress the importance of DNA methylation for the pathogenesis of NSCLCs.

Publication Title

Genome-wide CpG island methylation analyses in non-small cell lung cancer patients.

Sample Metadata Fields

Cell line, Treatment

View Samples
accession-icon SRP156474
Differential expression in wild-type and mutant neurofibroma and MPNST cell lines
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Using RNA-seq we characterized gene expression changes occuring upon knockout of EZH2, EZH1, EZH1+EZH2 or SUZ12 in a neurofibroma cell line. We also investigated the transcriptional consequences of EZH1+EZH2 double knockout in a SUZ12-mutant MPNST cell line. Overall design: Examination of transcript abundance in wild-type and mutant ipNF05.5 or 88.14 cells. Two biological replicates were performed for wild-type and mutant ipNF05.5 cell lines. Three biological replicates were performed for wild-type and mutant 88.14 cell lines.

Publication Title

EZH1/2 function mostly within canonical PRC2 and exhibit proliferation-dependent redundancy that shapes mutational signatures in cancer.

Sample Metadata Fields

Cell line, Subject

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accession-icon SRP152952
RNAseq of (Dimethylfumarate)DMF-induced changes in murine Tc17 CD8+ cells
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

IL-17-producing CD8+ (Tc17)T cells are implicated in the pathogenesis of multiple sclerosis (MS), thereby representing a promising target for therapy. We found that dimethyl fumarate (DMF), a first-line medication for MS upregulated reactive oxygen species (ROS) by glutathione depletion in murine Tc17 cells, which limited IL-17 and diverted Tc17 cells towards cytotoxic T lymphocyte (CTL) signature. DMF enhanced PI3K-AKT-FOXO1-T-bet- as well as STAT5-signaling leading to restricted permissive histone state at the Il17 locus. T-bet-deficiency, inhibiting PI3K-AKT, STAT5 or histone deacetylases prevented DMF-ROS-mediated IL-17 suppression. In MS patients with stable response, DMF suppressed IL-17 production by CD8+ T-cells and triggered diversion from Tc17 towards CTL signature along with enriched ROS-, PI3K-AKT-FOXO1-signaling, demonstrating comparable regulation across species. Accordingly, in the mouse model for MS, DMF limited Tc17-encephalitogenicity. Our findings disclose DMF-ROS-AKT-driven pathway, which selectively modulates Tc17 fate to ameliorate MS, thus opening avenue to develop markers and targets for specific therapy. Overall design: Examination of DMF-induced expression changes in 3 conditions, 3 samples each: murine TC17 cells without treatment as control group, murine Tc17 cells treated with DMF and murine Tc17 cells treated with DMF and Glutathione(GSH)

Publication Title

IL-17<sup>+</sup> CD8<sup>+</sup> T cell suppression by dimethyl fumarate associates with clinical response in multiple sclerosis.

Sample Metadata Fields

Specimen part, Cell line, Subject

View Samples
accession-icon SRP152951
RNAseq of (Dimethylfumarate)DMF-induced changes in human CD8+ memory cells
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

IL-17-producing CD8+ (Tc17)T cells are implicated in the pathogenesis of multiple sclerosis (MS), thereby representing a promising target for therapy. We found that dimethyl fumarate (DMF), a first-line medication for MS upregulated reactive oxygen species (ROS) by glutathione depletion in murine Tc17 cells, which limited IL-17 and diverted Tc17 cells towards cytotoxic T lymphocyte (CTL) signature. DMF enhanced PI3K-AKT-FOXO1-T-bet- as well as STAT5-signaling leading to restricted permissive histone state at the Il17 locus. T-bet-deficiency, inhibiting PI3K-AKT, STAT5 or histone deacetylases prevented DMF-ROS-mediated IL-17 suppression. In MS patients with stable response, DMF suppressed IL-17 production by CD8+ T-cells and triggered diversion from Tc17 towards CTL signature along with enriched ROS-, PI3K-AKT-FOXO1-signaling, demonstrating comparable regulation across species. Accordingly, in the mouse model for MS, DMF limited Tc17-encephalitogenicity. Our findings disclose DMF-ROS-AKT-driven pathway, which selectively modulates Tc17 fate to ameliorate MS, thus opening avenue to develop markers and targets for specific therapy. Overall design: CD8+ memory cells from human blood

Publication Title

IL-17<sup>+</sup> CD8<sup>+</sup> T cell suppression by dimethyl fumarate associates with clinical response in multiple sclerosis.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE12885
Genome-wide changes in DNA methylation and copy number play a role in deregulation of gene expression in osteosarcoma
  • organism-icon Homo sapiens
  • sample-icon 14 Downloadable Samples
  • Technology Badge IconAgilent-014693 Human Genome CGH Microarray 244A (Feature number version), Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Identification of interactive networks of gene expression associated with osteosarcoma oncogenesis by integrated molecular profiling.

Sample Metadata Fields

Specimen part

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accession-icon GSE11416
Comparison of osteosarcoma cell lines and normal human osteoblasts
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconAgilent-014693 Human Genome CGH Microarray 244A (Feature number version), Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

In vitro analysis of integrated global high-resolution DNA methylation profiling with genomic imbalance and gene expression in osteosarcoma.

Sample Metadata Fields

No sample metadata fields

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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