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accession-icon SRP023259
Transcriptome Sequencing (RNA-seq) of Ara-C Resistant Murine AML Cell Lines Identifies Mechanisms of Resistance
  • organism-icon Mus musculus
  • sample-icon 20 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

An RNA-seq study of altered gene expression and mutations in Ara-C resistant acute myeloid leukemia murine cell lines. The analysis of the RNA-seq data led to the identification of a large deletion within the Dck coding sequence of the B117H cell line, which produced an alternatively processed form of Dck mRNA. The RNA-seq analysis also identified the presence of an insertion mutation in Dck in the B140H cell line. The RNA-seq analysis also identified a number of significant expression changes which did not appear in a previous microarray analysis (GSE18322), as well as identified other mutations which may be contributing to Ara-C resistance. Overall design: Two highly Ara-C resistant cell lines, B117H and B140H were derived from Ara-C sensitive parental cell lines, B117P and B140P. Variations in gene expression as well identification of acquired mutations between these Ara-C resistant/sensitive sets were studied using various RNA-seq analysis tools.

Publication Title

Using RNA-seq and targeted nucleases to identify mechanisms of drug resistance in acute myeloid leukemia.

Sample Metadata Fields

Cell line, Subject

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accession-icon SRP090923
Next-gen RNA sequencing of mouse osteosarcoma tumors
  • organism-icon Mus musculus
  • sample-icon 175 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Trascriptome analysis of osteosarcoma samples were performed Overall design: Tumor samples were obtained from a previously published Sleeping Beauty forward genetic screen, cell lines were derived from previous primary tumors and sequenced using Illumina HiSeq 2000

Publication Title

Comparative Transcriptome Analysis Quantifies Immune Cell Transcript Levels, Metastatic Progression, and Survival in Osteosarcoma.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon SRP042212
Transcriptome Sequencing (RNA-seq) of Normal Human Osteoblasts
  • organism-icon Homo sapiens
  • sample-icon 15 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

Three normal human osteoblast samples, acquired from PromoCell, were used as controls to compare to RNA-seq data from prepublished osteosarcoma samples (submitted to the European Bioinformatics Institute; EGAS00001000263) for the purpose of evaluating expression levels of genes identified as common insertions sites in a Sleeping Beauty screen of osteosarcomas in mice. Overall design: Three normal human osteoblast samples (pellet form in RNAlater) were acquired from PromoCell (Heidelberg, Germany), and RNA was isolated from them immediately upon receipt.

Publication Title

A Sleeping Beauty forward genetic screen identifies new genes and pathways driving osteosarcoma development and metastasis.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE8699
Characterization of the gene expression changes associated with melanoma-endothelial cell communication
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Average life expectancy for patients with metastatic melanoma is less than 6 months, and only a handful of treatment options are available. If the disease can be stopped before it spreads to other organs, life expectancy is greatly increased. The goal of this project is to identify possible regulators of melanoma metastasis by determining genes whose expression is modulated when the cells are grown in contact with endothelial cells. Identification of genes involved in this cell-cell communication could have therapeutic implications.

Publication Title

Integration of genotypic and phenotypic screening reveals molecular mediators of melanoma-stromal interaction.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP167390
Next-gen RNA sequencing of Sleeping Beauty accelerated mouse brain tumors
  • organism-icon Mus musculus
  • sample-icon 57 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Expression profiling by high throughput sequencing Overall design: 23 Tumor samples were obtained from a Sleeping Beauty forward genetic screen and sequenced using Illumina HiSeq 2000

Publication Title

<i>Sleeping Beauty</i> Insertional Mutagenesis Reveals Important Genetic Drivers of Central Nervous System Embryonal Tumors.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE42568
Breast Cancer Gene Expression Analysis
  • organism-icon Homo sapiens
  • sample-icon 110 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Analysis of 104 breast cancer biopsies (removed prior to any treatment with tamoxifen or chemotherapeutic agents) from patients aged between 31 years and 89 years at the time of diagnosis (mean age = 58 years). Twenty were less than 50 years and seventy-seven women were 50 years, or older, at diagnosis. The size of the tumours ranged between 0.6 cm and 8.0 cm (mean = 2.79 cm). Eighteen tumours were T1 (<2 cm) in maximal dimension; 83 were T2 (25 cm) and 3 tumours were T3 (>5 cm). Eighty-two were invasive ductal carcinoma, 17 were invasive lobular and five were tumours of special type (two tubular and three mucinous). Eleven tumours were grade 1; 40 were grade 2; and 53 were grade 3. Sixty-seven tumours were oestrogen receptor (ER) positive and 34 were ER negative (ER status was determined by Enzyme Immuno-Assay (EIA); a positive result was defined as more than 200 fmol/g protein). ER status was not available for 3 patients. Forty-five tumours had no axillary metastases and 59 tumours had metastasised to axillary lymph nodes. Sixty-nine women were treated with post-operative tamoxifen; 26 did not receive tamoxifen. Fifty patients were treated with adjuvant systemic chemotherapy (CMF +/ adriamycin); 45 patients did not receive chemotherapy. Details regarding tamoxifen and systemic chemotherapy were not available for 9 patients. Maximal follow-up was 3,026 days with a mean follow-up of 1,887 days.

Publication Title

Correlating transcriptional networks to breast cancer survival: a large-scale coexpression analysis.

Sample Metadata Fields

Age, Specimen part, Disease stage

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accession-icon SRP174478
Disruption of FBXL5-mediated cellular iron homeostasis promotes liver carcinogenesis
  • organism-icon Mus musculus
  • sample-icon 22 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Hepatic iron overload is a risk factor for progression of hepatocellular carcinoma (HCC), although the molecular mechanisms underlying this association have remained unclear. We now show that the iron-sensing ubiquitin ligase FBXL5 is previously unrecognized oncosuppressor in liver carcinogenesis in mice. Hepatocellular iron overload evoked by FBXL5 ablation gives rise to oxidative stress, tissue damage, inflammation and compensatory proliferation in hepatocytes and to consequent promotion of liver carcinogenesis induced by exposure to a chemical carcinogen. The tumor-promoting effect of FBXL5 deficiency in the liver is also operative in a model of virus-induced HCC. FBXL5-deficient mice thus constitute the first genetically engineered mouse model of liver carcinogenesis induced by iron overload. Dysregulation of FBXL5-mediated cellular iron homeostasis was also found to be associated with poor prognosis in human HCC, implicating FBXL5 plays a significant role in defense against hepatocarcinogenesis. Overall design: Total RNA was extracted from the nontumor and tumor tissue of an Alb-Cre/Fbxl5F/F male mouse (nontumor, n = 5; tumor, n = 5) or two littermate control Fbxl5F/F mice (nontumor, n = 6; tumor, n = 6) at 45 weeks of age.

Publication Title

Disruption of FBXL5-mediated cellular iron homeostasis promotes liver carcinogenesis.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE24574
Expression data from BCL6-YFP-positive Tfh cells, BCL6-YFP-negative Tfh cells, non-Tfh cells, and nave helper T cells.
  • organism-icon Mus musculus
  • sample-icon 19 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

We found that a number of Tfh cells downmodulated BCL6 protein after their development, and we sought to compare the gene expression between BCL6-hi Tfh cells and BCL6-low Tfh cells.

Publication Title

Bcl6 protein expression shapes pre-germinal center B cell dynamics and follicular helper T cell heterogeneity.

Sample Metadata Fields

Specimen part

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accession-icon SRP092107
RNA-sequencing in TGF-beta treated MDA-231-D cells transfected with ZEB1/ZEB2 siRNAs [RNA-seq]
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIon Torrent Proton

Description

We searched for roles of ZEB1 during EMT by RNA-seq in breast cancer cells. Overall design: Expression of mRNA in a basal type breast cancer cell line MDA-231-D transfected with ZEB1/ZEB2 siRNAs and stimulated with TGF-beta for 24 h.

Publication Title

ZEB1-regulated inflammatory phenotype in breast cancer cells.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE141873
Establishment and Characterisation by Expression Microarray of Patient Derived Xenograft Panel of Human Pancreatic Adenocarcinoma Patients
  • organism-icon Homo sapiens
  • sample-icon 21 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.0 ST Array (hugene20st)

Description

mRNA expression profiling of pancreatic cancer, comparing adjacent normal tissue, patient tumour and first generation patient derived xenograft tumours

Publication Title

Establishment and Characterisation by Expression Microarray of Patient-Derived Xenograft Panel of Human Pancreatic Adenocarcinoma Patients.

Sample Metadata Fields

Specimen part

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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)

fund-icon Fund the CCDL

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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