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accession-icon GSE69512
Tetraspanin 3 is Required for the Development and Propagation of Acute Myelogenous Leukemia
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Msi2 is a critical regulatior of myeoid leukemia, and these data identify genes that are changed following Msi2 deletion in bcCML and de novo AML stem cells.

Publication Title

Tetraspanin 3 Is Required for the Development and Propagation of Acute Myelogenous Leukemia.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE36947
Elevating Sox2 levels deleteriously affects the growth of glioblastoma and medulloblastoma cells.
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Induction of the transcription factor Sox2 from a doxycycline-inducible promoter in iSox2-DAOY medulloblastoma cells.

Publication Title

Elevating SOX2 levels deleteriously affects the growth of medulloblastoma and glioblastoma cells.

Sample Metadata Fields

Specimen part

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accession-icon GSE33882
Musashi2 is required for the self-renewal and pluripotency of embryonic stem cells
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Recent studies have shown that the RNA binding protein Musashi 2 (Msi2) plays prominent roles during development and leukemia. Additionally, in embryonic stem cells (ESC) undergoing the early stages of differentiation, Msi2 has been shown to associate with Sox2, which is required for the self-renewal of ESC. These findings led us to examine the effects of Msi2 on the behavior of ESC. Using an shRNA sequence that targets Msi2 and a scrambled shRNA sequence, we determined that knockdown of Msi2 disrupts the self-renewal of ESC and promotes their differentiation. Collectively, our findings argue that Msi2 is required to support the self-renewal and pluripotency of ESC.

Publication Title

Musashi2 is required for the self-renewal and pluripotency of embryonic stem cells.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE34801
Determination of the protein interactome of the transcription factor Sox2 in embryonic stem cells engineered for inducible expression of four reprogramming factors
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Coordinate expression of the somatic cell reprogramming factors Oct4, Sox2, Klf4 and c-Myc within embryonic stem cells preserves the self-renewal of these cells, while allowing for the expression epitope tagged Sox2. Taking advantage of this observation, we engineered embryonic stem cells (i-OSKM-ESC) to inducibly express Oct4, Klf4, c-Myc and an epitope tagged form of Sox2 from a polycistronic element, in the presence of doxycycline. We isolated Sox2 and its associated protein complexes by co-immunoprecipitation. Subsequently, we identified the Sox2-protein interactome in self-renewing embryonic stem cells using an unbiased proteomic screen (Multidimensional Protein Identification Technology [MudPIT]).

Publication Title

Determination of protein interactome of transcription factor Sox2 in embryonic stem cells engineered for inducible expression of four reprogramming factors.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE95794
Platelet-derived growth factor receptor signaling is required for postnatal tendon growth
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.1 ST Array (mogene21st)

Description

Platelet-derived growth factor receptor (PDGFR) signaling plays an important role in the embryonic formation of many different tissues. There is a family of PDGF isoforms which signal through the PDGF receptors (PDGFR) and (PDGFR). PDGF regulates many key cellular processes of mesenchymal cell function including proliferation, differentiation, migration and extracellular matrix (ECM) synthesis. While PDGF has been used to enhance flexor tendon healingin vivo, its role in postnatal tendon growth has remained largely unexplored. To determine the importance of PDGFR signaling in postnatal tendon growth, we performed pharmacological blockade of PDGFR and PDGFR, and then induced tendon growth via mechanical overload using the hindlimb synergist ablation model. Our hypothesis was that inhibition of PDGFR signaling will restrict normal growth of tendon tissue in response to mechanical loading.

Publication Title

Postnatal tendon growth and remodeling require platelet-derived growth factor receptor signaling.

Sample Metadata Fields

Sex, Treatment

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accession-icon GSE43606
Genetic Heterogeneity of DLBCL
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Diffuse large B-cell lymphoma (DLBCL) is the most common form of lymphoma in adults. The disease exhibits a striking heterogeneity in gene expression profiles and clinical outcomes, but its genetic causes remain to be fully defined. Through whole genome and exome sequencing, we characterized the genetic diversity of DLBCL. In all, we sequenced 73 DLBCL primary tumors (34 with matched normal DNA). Separately, we sequenced the exomes of 21 DLBCL cell lines. We identified 322 DLBCL cancer genes that were recurrently mutated in primary DLBCLs. We identified recurrent mutations implicating a number of known and not previously identified genes and pathways in DLBCL including those related to chromatin modification (ARID1A and MEF2B), NF-B (CARD11 and TNFAIP3), PI3 kinase (PIK3CD, PIK3R1, and MTOR), B-cell lineage (IRF8, POU2F2, and GNA13), and WNT signaling (WIF1). We also experimentally validated a mutation in PIK3CD, a gene not previously implicated in lymphomas. The patterns of mutation demonstrated a classic long tail distribution with substantial variation of mutated genes from patient to patient and also between published studies. Thus, our study reveals the tremendous genetic heterogeneity that underlies lymphomas and highlights the need for personalized medicine approaches to treating these patients.

Publication Title

Genetic heterogeneity of diffuse large B-cell lymphoma.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE22898
Deep Sequencing of the Small RNA Transcriptome of Normal and Malignant Human B cells Identifies Hundreds of Novel MicroRNAs
  • organism-icon Homo sapiens
  • sample-icon 26 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Deep sequencing of the small RNA transcriptome of normal and malignant human B cells identifies hundreds of novel microRNAs.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE48435
The genetic landscape of mutations in Burkitt lymphoma
  • organism-icon Homo sapiens
  • sample-icon 17 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Burkitt lymphoma is characterized by deregulation of MYC, but the contribution of other genetic mutations to the disease is largely unknown. Here, we describe the first completely sequenced genome from a Burkitt lymphoma tumor and germline DNA from the same affected individual. We further sequenced the exomes of 59 Burkitt lymphoma tumors and compared them to sequenced exomes from 94 diffuse large B-cell lymphoma (DLBCL) tumors. We identified 70 genes that were recurrently mutated in Burkitt lymphomas, including ID3, GNA13, RET, PIK3R1 and the SWI/SNF genes ARID1A and SMARCA4. Our data implicate a number of genes in cancer for the first time, including CCT6B, SALL3, FTCD and PC. ID3 mutations occurred in 34% of Burkitt lymphomas and not in DLBCLs. We show experimentally that ID3 mutations promote cell cycle progression and proliferation. Our work thus elucidates commonly occurring gene-coding mutations in Burkitt lymphoma and implicates ID3 as a new tumor suppressor gene.

Publication Title

Deep sequencing of the small RNA transcriptome of normal and malignant human B cells identifies hundreds of novel microRNAs.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE64328
Transcriptional Regulationand Chromatin Dynamics inHuman Epithelial Cell Differentiation
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer IIx

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Dynamic Transcriptional and Epigenetic Regulation of Human Epidermal Keratinocyte Differentiation.

Sample Metadata Fields

Specimen part, Disease

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accession-icon SRP070902
Transcriptional Regulationand Chromatin Dynamics inHuman Epithelial Cell Differentiation (RNA-seq)
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconNextSeq500

Description

Transcriptional profiling of KP and DK through RNA-seq Overall design: RNA-sequencing of KP and DK

Publication Title

Dynamic Transcriptional and Epigenetic Regulation of Human Epidermal Keratinocyte Differentiation.

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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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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