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accession-icon GSE58697
Expression data from 128 Desmoids
  • organism-icon Homo sapiens
  • sample-icon 123 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

One of the main problems in managing desmoids tumors is their locoregional aggressiveness and their high ability to recur after initial treatment. In our work, with the goal to identify molecular markers that can predict Progression-Free Survival, gene-expression screening was conducted on 128 available independent untreated primary desmoid tumors using cDNA microarray. By analyzing expression profiles, we have identified, for the first time, a gene expression signature that is able to predict Progression-Free Survival. This molecular signature identified two groups with clearly distinct Progression-Free Survival in the two sets of subjects. Patients in good prognostic group had achieved a progression-free 2-year survival rate of 86% while patients in poor prognostic group had a progression-free 2-year survival rate of 44%.

Publication Title

Gene Expression Profiling of Desmoid Tumors by cDNA Microarrays and Correlation with Progression-Free Survival.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE21050
Expression data from Complex genetics sarcomas (cohort 1 and 2)
  • organism-icon Homo sapiens
  • sample-icon 303 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

For this study, we selected, from the French Sarcoma Group (FSG) database, soft tissue sarcomas with no recurrent chromosomal translocations and for which a frozen tissue of the untreated primary tumor was available. Three hundred and ten sarcomas have been studied. They are split in two cohorts.

Publication Title

Validated prediction of clinical outcome in sarcomas and multiple types of cancer on the basis of a gene expression signature related to genome complexity.

Sample Metadata Fields

Specimen part, Disease, Time

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accession-icon SRP057793
RNA-seq performed on sarcomas to identify various alterations
  • organism-icon Homo sapiens
  • sample-icon 149 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

No description.

Publication Title

Genomic and transcriptomic comparison of post-radiation versus sporadic sarcomas.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP113755
Transcriptome characterization of radiation-induced sarcomas
  • organism-icon Homo sapiens
  • sample-icon 73 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

No description.

Publication Title

Genomic and transcriptomic comparison of post-radiation versus sporadic sarcomas.

Sample Metadata Fields

Sex, Age, Specimen part, Disease, Disease stage

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accession-icon GSE46371
Expression data from zebrafish (Danio rerio) embryos exposed to methyl tert-butyl ether
  • organism-icon Danio rerio
  • sample-icon 36 Downloadable Samples
  • Technology Badge Icon Affymetrix Zebrafish Genome Array (zebrafish)

Description

Methyl tert-butyl ether (MTBE) has been shown to target developing vasculature in piscine and mammalian model systems. In the zebrafish, MTBE induces vascular lesions throughout development. These lesions result from exposure to MTBE at an early stage in development (6-somites to Prim-5 stages). During this time period, transcript levels of vegfa, vegfc, and vegfr1 were significantly decreased in embryos exposed to 5 mM MTBE.

Publication Title

Manipulation of the HIF-Vegf pathway rescues methyl tert-butyl ether (MTBE)-induced vascular lesions.

Sample Metadata Fields

Specimen part

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accession-icon SRP050275
Macrophage Gene Expression Upon Infection with Anaplasma phagocytophilum in the Presence and Absence of the Tick Salivary Protein SL2
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Previously, we observed that a tick salivary protein named sialostatin L2 (SL2) mitigates caspase 1-mediated inflammation upon Anaplasma phagocytophilum infection. Here we are performing next-generation sequencing to determine the global effect of SL2 upon A. phagocytophilum infection of macrophages. Overall design: BMDMs were treated by 4 different conditions (including non-treated, treated by SL2, treated by Anaplasma, and by Anaplasma and SL2, each treatment was performed in triplicate) followed by the extraction of total RNA and deep sequencing by Illumina

Publication Title

The Prostaglandin E2-EP3 Receptor Axis Regulates Anaplasma phagocytophilum-Mediated NLRC4 Inflammasome Activation.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE20257
Smoking-induced Disarray of the Apical Junctional Complex Gene Expression Architecture in the Human Airway Epithelium
  • organism-icon Homo sapiens
  • sample-icon 118 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Full Length HuGeneFL Array (hu6800), Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The apical junctional complex (AJC), composed of tight junctions and adherens junctions, is essential for maintaining epithelial barrier function. Since cigarette smoking and chronic obstructive pulmonary disease (COPD), the major smoking-induced disease, are both associated with increased lung epithelial permeability, we hypothesized that smoking alters the transcriptional program regulating AJC integrity in the small airway epithelium (SAE), the primary site of pathological changes in COPD. Transcriptome analysis revealed a global down-regulation of physiological AJC gene expression in the SAE of healthy smokers (n=53) compared to healthy nonsmokers (n=59), an observation associated with changes in molecular pathways regulating epithelial differentiation such as PTEN signaling and accompanied by induction of cancer-related AJC genes. Genome-wide co-expression analysis identified a smoking-sensitive AJC transcriptional network. The overall expression of AJC-associated genes was further decreased in COPD smokers (n=23). Exposure of human airway epithelial cells to cigarette smoke extract in vitro resulted in down-regulation of several AJC-related genes, accompanied by decreased transepithelial resistance. Thus, cigarette smoking alters the AJC gene expression architecture in the human airway epithelium, providing a molecular basis for the dysregulation of airway epithelial barrier function during the development of smoking-induced lung disease.

Publication Title

Cigarette smoking reprograms apical junctional complex molecular architecture in the human airway epithelium in vivo.

Sample Metadata Fields

Sex, Age

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accession-icon SRP033466
Transcriptome analysis of Jurkat T cells expressing MALT1 or its mutants MALT1-R149A and MALT1-C464A or the MALT1-R149A-C464A double mutant.
  • organism-icon Homo sapiens
  • sample-icon 36 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

Purpose: study the role of MALT1 auto-proteolysis in T cell receptor mediated activation of NF-kB. Methods: Jurkat cells were generated that express wild type MALT1, the auto-cleavage deficient MALT1-R149A mutant, the catalytic inactive MALT1-C464A mutant or the R149A-C464A double mutant (RACA). Expression of endogenous MALT1 was inactivated using TALEN technology for the Jurkat cells expressing MALT1-R149A (JDM-RA) and MALT1-C464A (JDM-CA). Illumina HISeq 2000 deep sequencing was performed to determine the mRNA profiles for MALT1, JDM-RA, JDM-CA and RACA cells in unstimulated conditions or after treatment with 75ng/ml PMA and 150 ng/ml ionomycin for 3 or 18 hrs. Results: PMA ionomycin stimulation of the MALT1 auto-cleavage defective JDM-RA cells fails to activate NF-kB-dependent transcription like for the MALT1 catalytic inactive JDM-CA cells and the double RACA mutant cells. Conclusion: MALT1 autoproteolysis is essential for transcription of NF-kB target genes Overall design: mRNA profiles of Jurkat expressing MALT1, MALT1-R149A, MALT1-C464A and MALT1-R149A-C464A after 0, 3 and 18 hours of stimulation with PMA and Ionomycin were generated by deep sequencing, in duplicate, using Illumina HISeq 2000

Publication Title

MALT1 auto-proteolysis is essential for NF-κB-dependent gene transcription in activated lymphocytes.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE94380
Gene expression data of Peyer's patch conventional dendritic cells and macrophages at steady state and under TLR7 ligand stimulation
  • organism-icon Mus musculus
  • sample-icon 25 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

The initiation of the mucosal immune response in Peyers patch (PP) relies on the sampling, processing and efficient presentation of foreign antigens by dendritic cells (DC). PP DC encompass five subsets, among which CD11b+ conventional DC (cDC) and LysoDC have distinct progenitors and functions but share many cell surface markers. This has previously led to confusion between these two subsets. In addition, another PP DC subset, termed double-negative (DN), remains poorly characterized. Here, we have studied the genetic relatedness of the different subsets of PP cDC at steady state and under TLR7 ligand stimulation. We also provide the transcriptional profiles of subepithelial TIM-4- and interfollicular TIM-4+ macrophages.

Publication Title

Distribution, location, and transcriptional profile of Peyer's patch conventional DC subsets at steady state and under TLR7 ligand stimulation.

Sample Metadata Fields

Sex, Age, Specimen part, Treatment

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accession-icon GSE78513
NPM-ALK expression levels identify two distinct signatures in Anaplastic Large Cell Lymphoma of Childhood
  • organism-icon Homo sapiens
  • sample-icon 33 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Anaplastic large-cell lymphoma (ALCL) makes up approximately 15% of paediatric non-Hodgkin's lymphomas of childhood. The vast majority of them is associated with the t(2;5)(p23;q35) translocation that results in the expression of a hybrid oncogenic tyrosine kinase, NPM-ALK. In order to investigate ALCL biological characteristics we used transcriptional profiling approach. Genome-wide gene expression profiling, performed on 23 paediatric ALCL and 12 reactive lymph nodes specimens, showed two novel ALCL subgroups based on their NPM-ALK expression levels (named (ALK low and ALK high). Gene set enrichment analysis revealed, in ALK low samples, a positive enrichment of genes involved in the Interleukin signaling pathway, whereas we found increased expression of genes related to cell cycle progression and division in ALK high tumour samples, such as Aurora Kinase A (AURKA) and B (AURKB). Growth inhibition was observed upon administration of AURKA and AURKB inhibitors Alisertib and Barasertib and it was associated with perturbation of the cell cycle and induction of apoptosis. In conclusion we identified two novel ALCL subgroups, which display unique biological characteristics suggesting sensitivity to distinct targeted therapies.

Publication Title

NPM-ALK expression levels identify two distinct subtypes of paediatric anaplastic large cell lymphoma.

Sample Metadata Fields

No sample metadata fields

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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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