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accession-icon GSE11277
A2B5/OTMP+ rat perineuronal oligodendrocytes
  • organism-icon Rattus norvegicus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Expression 230A Array (rae230a)

Description

Oligodendrocytes are cells from the central nervous system that can be grouped into precursors, myelin-forming, and non-myelinating perineuronal. The function of perineuronal oligodendrocytes is unknown; it was suggested that they can ensheath denuded axons. We tested this hypothesis. Using cell-specific tags, microarray technology and bioinformatics tools to identify gene expression differences between these subpopulations allowed us to capture the genetic signature of perineuronal oligodendrocytes. Here we report that perineuronal oligodendrocytes are configured for a dual role. As perineuronal, they integrate a repertoire of transcripts designed to create a cell with its own physiological agenda. But they maintain a reservoir of untranslated transcripts encoding the major myelin proteins for we speculate a pathological eventuality. We posit that the signature molecules PDGFR-, cytokine PDGF-CC, and the transcription factor Pea3 used among others - to define the non-myelinating phenotype, may be critical for mounting a myelinating programme during demyelination. Harnessing this capability is of therapeutic value for diseases such as multiple sclerosis. This is the first molecular characterization of perineuronal oligodendrocytes.

Publication Title

The genetic signature of perineuronal oligodendrocytes reveals their unique phenotype.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE37060
Expression data from siSCR and siPRMT1 ES cells
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

The major type of protein arginine methyltransferase is PRMT1. Since the growth of embryos from Prmt1/ mice was arrested shortly after implantation, PRMT1 must play a critical role in early mouse development.

Publication Title

PRMT1 and PRMT8 regulate retinoic acid-dependent neuronal differentiation with implications to neuropathology.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE47214
Expression data from D3, siSCR, siPRMT1 and siPRMT8 ES cell derived neurons
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

PRMT1 and PRMT8 knockdown D3 embryonic stem cells were generated (siPRMT) or as a control, scrambled sequence was introduced (siSCR).

Publication Title

PRMT1 and PRMT8 regulate retinoic acid-dependent neuronal differentiation with implications to neuropathology.

Sample Metadata Fields

Cell line, Treatment

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accession-icon GSE10524
Genomic alterations and gene expression in primary diffuse large B cell lymphomas of immune privileged sites
  • organism-icon Homo sapiens
  • sample-icon 39 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Primary diffuse large B cell lymphomas of different immune-privileged sites (IP-DLBCL) share many clinical and biological features, such as a relatively poor prognosis, preferential dissemination to other immune-privileged sites and deletion of the HLA region, which suggests that IP-DLBCL represents a separate entity. To further investigate the nature of IP-DLBCL, we investigated site-specific genomic aberrations in 16 testicular, 9 central nervous system (CNS) and 15 nodal DLBCL using array-CGH. We also determined minimal common regions of gain and loss. Using robust algorithms, the array-CGH data were combined with gene expression data to explore pathways deregulated by chromosomal aberrations.

Publication Title

Genomic alterations and gene expression in primary diffuse large B-cell lymphomas of immune-privileged sites: the importance of apoptosis and immunomodulatory pathways.

Sample Metadata Fields

Specimen part

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accession-icon GSE29832
Expression data from pure/mixed blood and breast to test feasability of deconvolution of clinical samples
  • organism-icon Homo sapiens
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Samples collected from human subjects in clinical trials possess a level of complexity, arising from multiple cell types, that can obfuscate the analysis of data derived from them. Blood, for example, contains many different cell types that are derived from a distinct lineage and carry out a different immunological purpose. Failure to identify, quantify, and incorporate sources of heterogeneity into an analysis can have widespread and detrimental effects on subsequent statistical studies.

Publication Title

Optimal deconvolution of transcriptional profiling data using quadratic programming with application to complex clinical blood samples.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE19844
affy_xoo_rice-Transcriptomics-based identification of Xoo strain BAI3 Talc targets in rice
  • organism-icon Oryza sativa
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Rice Genome Array (rice)

Description

affy_xoo_rice - affy_xoo_rice - The Bacterial Leaf Blight disease of rice is due to Xanthomonas oryzae pv. oryzae. As for many pathogenic bacteria, it relies on a type 3 secretion system that is devoted to the injection of type 3 effectors into the eukaryotic host cell. These proteins are meant to suppress host basal defense responses and/or mimic some host regulatory function promoting bacterial survey in the plant. We are interested in the functional analysis of a subgroup of Xoo T3Es, that are specialized in host cell transcriptome remodelling. These effectors, therefore called TAL for Transcription Activator-Like proteins (also named AvrBs3/PthA-like), are often key virulence factors essential to Xoo pathogenicity such as the effector protein Talc of african Xoo strain BAI3. Our goal is to understand its function during disease development, by identifying rice host genes that are being directly up- or down-regulated by Talc. To that end, we aim at performing Affymetrix transcriptomic analysis, comparing leaf samples of a susceptible rice line inoculated with Xoo to leaves challenged with a Talc-deficient mutant and water-treated leaves. Highly induced genes are likely to be Talc primary targets and therefore potentially good susceptibility gene candidates.-The goal of the experiment is to identify the rice genes up- or down-regulated by the type III effector Talc from Xoo African strain BAI3, upon the inoculation of susceptible rice leaves 24 hours post-infection. To that end, the experimental design includes the inoculation of Nipponbare rice leaves with the virulent Xoo strain BAI3, that will be compared to Nipponbare rice leaves inoculated with a talc K.O. mutant strain and water.

Publication Title

Colonization of rice leaf blades by an African strain of Xanthomonas oryzae pv. oryzae depends on a new TAL effector that induces the rice nodulin-3 Os11N3 gene.

Sample Metadata Fields

Specimen part

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accession-icon GSE12902
Oncogenomic analysis of mycosis fungoides reveals major differences with Szary syndrome
  • organism-icon Homo sapiens
  • sample-icon 22 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Mycosis fungoides (MF), the most common cutaneous T-cell lymphoma (CTCL), is a malignancy of mature, skin-homing T cells. Szary syndrome (Sz) is often considered to represent a leukemic phase of MF. In this study the pattern of numerical chromosomal alterations in MF tumor samples was defined using array-based CGH; simultaneously gene expression was analyzed using microarrays. Highly recurrent chromosomal alterations in MF include copy number gain of 7q36, 7q21-7q22 and loss of 5q13 and 9p21. This pattern characteristic of MF differs markedly from chromosomal alterations observed in Sz. Integration of data from array-based CGH and gene expression analysis yielded several candidate genes with potential relevance in the pathogenesis of MF. We confirmed that the FASTK and SKAP1 genes, residing in loci with recurrent gain, demonstrated increased expression. The RB1 and DLEU1 tumor suppressor genes showed diminished expression associated with loss. In addition, it was found that presence of chromosomal alterations on 9p21, 8q24 and 1q21-1q22 was associated with poor prognosis in patients with MF. This study provides novel insight into genetic alterations underlying MF. Furthermore, our analysis uncovered genomic differences between MF and Sz, which suggest that the molecular pathogenesis and therefore therapeutic requirements of these CTCLs may be distinct.

Publication Title

Oncogenomic analysis of mycosis fungoides reveals major differences with Sezary syndrome.

Sample Metadata Fields

Specimen part

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accession-icon GSE89409
HOXA5 is a survival locus associated with chromosome 7 gain in IDH-wildtype glioblastoma
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

Glioblastomas (GBMs) are divided into CpG Island Methylator Phenotype (CIMP) and non-CIMP tumors. Non-CIMP GBMs derive from cells with non-disjunction of chromosome (chr7) and chromosome 10 (chr10), resulting in chr7 gain and chr10 loss, while CIMP GBMs have mutations in isocitrate dehydrogenase 1 or 2 (IDH1/2). Gain of chr7 is largely driven by PDGFA, but other genes on chr7 are likely to contribute to fitness gains and aggressiveness of these GBMs. We computationally investigated genes on chr7 whose gene expression correlated with survival, identifying HOXA5 as a potential driver of proneural gliomagenesis. Using a combination of human GBM cells and mouse PDGF-driven gliomas, we showed that HOXA5 drives increased proliferation and radiation resistance in culture and in vivo. These phenotypes appear to be in part due to effects on p53 and other apoptosis-related genes.

Publication Title

Increased <i>HOXA5</i> expression provides a selective advantage for gain of whole chromosome 7 in IDH wild-type glioblastoma.

Sample Metadata Fields

Disease

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accession-icon SRP096964
A de novo mouse model of C11orf95-RELA fusion-driven ependymoma identifies driver functions in addition to NF?B
  • organism-icon Mus musculus
  • sample-icon 38 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

The vast majority of supratentorial ependymomas (ST-EPNs) have few mutations other than chromosomal rearrangements on chromosome 11, most generating a fusion between C11orf95 and RELA (CR). This CR fusion can transform stem cells ex vivo rendering them oncogenic and may possess NF-?B activity, which has been proposed to be a mechanism of oncogenesis. However, it is not known whether CR is sufficient for EPN formation in vivo, and from what cell type and location. We found that CR is sufficient to form tumors from cells in the ependymal zone in mice that show many molecular and histologic similarities to human ST-EPN. Furthermore, the activation of NF-?B by this fusion protein appears minimal and not related to its oncogenic activity Overall design: C11orf95-RELA is a potent oncogene for supratentorial ependymoma

Publication Title

A De Novo Mouse Model of C11orf95-RELA Fusion-Driven Ependymoma Identifies Driver Functions in Addition to NF-κB.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE20368
1q gain clinical impact in Ewing's Sarcoma: role of DTL
  • organism-icon Homo sapiens
  • sample-icon 9 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

1q gain and CDT2 overexpression underlie an aggressive and highly proliferative form of Ewing sarcoma.

Sample Metadata Fields

Sex, Age, Specimen part, Disease, 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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