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accession-icon E-MEXP-70
Transcription profiling by array of human primary CD30+/CD38lo cells differentiating along the megakaryocyte lineage
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U95 Version 2 Array (hgu95av2)

Description

Gene expression profile of primary human CD34+/CD38lo cells differentiating along the megakaryocyte lineage.

Publication Title

Gene expression profile of primary human CD34+CD38lo cells differentiating along the megakaryocyte lineage.

Sample Metadata Fields

Specimen part, Time

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accession-icon GSE40367
Gene expression analysis of liver and colon cancer primary tumors and metastasis
  • organism-icon Homo sapiens
  • sample-icon 58 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Enriched tumor epithelium from 61 primary and metastasis tumor specimens was obtained by laser capture microdissection (LCM) as previously described (Boersma et al., 2007). In brief, frozen 8-m serial sections from OCT-preserved frozen tissues were prepared and mounted on plain, uncharged microscope slides. One Hematoxylin/eosin-stained section of each specimen was reviewed by a pathologist to confirm diagnosis and presence of tumor. The pathologist indicated which representative sections of the tumors should be microdissected. LCM was performed with the Pixcell II LCM system (Arcturus, Mountain View, CA). Total RNA was isolated using the PicoPure protocol (Arcturus, Mountain View, CA). The mRNA was amplified with two linear amplification steps by in vitro transcription using the MEGAscript T7 kit (Ambion, Austin, TX) followed by the labeling step using the BioArray HighYield RNA Transcript Labeling Kit T3 from Enzo Life Sciences (Farmingdale, NY). Labeled cRNA was hybridized onto Affymetix GeneChip HG-U133 Plus 2.0 Arrays.

Publication Title

Integrative genomic and transcriptomic characterization of matched primary and metastatic liver and colorectal carcinoma.

Sample Metadata Fields

Specimen part, Disease, Disease stage

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accession-icon SRP091903
cFos-Sox9 Axis Reprograms Bone Marrow-derived Mesenchymal Stem Cells into Chondroblastic Osteosarcoma [RNA-seq]
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

The goal is to profile cFos binding sites in an p53 knockout mouse bone marrow-derived stem cells (mBMSCs). Overall design: Four single clones (clone2, 4, 8, 12) of p53 knockout (p53KO) mouse bone marrow-derived mesenchymal stem cells were transduced with retroviruses expressing either luciferase (Luc) or cFos cDNAs. RNA was extracted from cells and subject to RNAseq.

Publication Title

cFOS-SOX9 Axis Reprograms Bone Marrow-Derived Mesenchymal Stem Cells into Chondroblastic Osteosarcoma.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE58671
Enhanced MET signaling in mouse epidermis activates EGFR and initiates squamous carcinogenesis
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

MET expression is elevated in a majority of human skin cancers but its contributions to pathogenesis have not been evaluated. In a mouse model of constitutive overexpression of HGF (MT-HGF), the incidence of squamous cell skin tumors induced by initiation with 7,12-dimethylbenz(a)anthracene (DMBA) followed by exposure to 12-O-tetradecanoyl-phorbol-13-acetate (TPA) is increased fivefold over control groups. Half of these tumors carry Hras1 or Kras mutations. Without DMBA initiation, tumors also erupt on MT-HGF mouse skin but only when TPA promotion is enhanced by crossing these mice with mice overexpressing cutaneous PKC. None of these tumors have Ras mutations. In culture, MT-HGF keratinocytes share identical MET mediated phenotypic and biochemical features with wildtype keratinocytes transformed by oncogenic RAS. In both cell types, these common features of initiated keratinocytes arise from autocrine activation of EGFR through elevated expression and release of EGFR ligands. Inhibition of EGFR ablates the initiated signature of MT-HGF keratinocytes in vitro and causes regression of MT-HGF induced tumors in vivo. Global gene expression data indicate that MT-HGF and RAS transformed keratinocytes share largely an identical profile of over 5000 mRNAs. Gene ontology analysis reveals the most affected concordant signature is enriched for functions relevant to tissue development and response to wounding, accompanied by cytokine and growth factor activity, and peptidase and endopeptidase activity previously not linked to initiated keratinocytes. Furthermore, gene co-expression analysis in skin cancer patients revealed a core RAS/MET co-expression network considerably activated in pre cancerous and cancerous lesions. Thus MET activation though EGFR contributes to human cutaneous cancers, and inhibitors could be efficacious in advanced lesions such as those seen in transplant recipient patients.

Publication Title

MET signaling in keratinocytes activates EGFR and initiates squamous carcinogenesis.

Sample Metadata Fields

Specimen part

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accession-icon SRP189075
Gene expression analysis of primary mouse prostate organoid culture with overexpression of FOXA1
  • organism-icon Mus musculus
  • sample-icon 32 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Gene expression analysis of primary mouse prostate organoid culture with overexpression of FOXA1 Overall design: Examination by genotypes and days elapsed prepared in 3 replicates

Publication Title

FOXA1 mutations alter pioneering activity, differentiation and prostate cancer phenotypes.

Sample Metadata Fields

Subject, Time

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accession-icon GSE151303
Articular cartilage regeneration by activated skeletal stem cells
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Osteoarthritis (OA) is a degenerative disease resulting in irreversible, progressive destruction of articular cartilage1. The etiology of OA is complex and involves a variety of factors, including genetic predisposition, acute injury and chronic inflammation2-4. Here we investigate the ability of resident skeletal stem-cell (SSC) populations to regenerate cartilage in relation to age, a possible contributor to the development of osteoarthritis. We demonstrate that aging is associated with progressive loss of SSCs and diminished chondrogenesis in the joints of both mice and humans. However, a local expansion of SSCs could still be triggered in the chondral surface of adult limb joints in mice by stimulating a regenerative response using microfracture (MF) surgery. Although MF-activated SSCs tended to form fibrous tissues, localized co-delivery of BMP2 and soluble VEGFR1 (sVEGFR1), a VEGF receptor antagonist, in a hydrogel skewed differentiation of MF-activated SSCs toward articular cartilage. These data indicate that following MF, a resident stem-cell population can be induced to generate cartilage for treatment of localized chondral disease in OA.

Publication Title

Articular cartilage regeneration by activated skeletal stem cells.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon SRP092159
Analysis of gene expression (RNAseq) from shTP53:RB1 LNCaP/AR cell lines
  • organism-icon Homo sapiens
  • sample-icon 11 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Some cancers evade targeted therapies through a mechanism known as lineage plasticity, whereby tumor cells acquire phenotypic characteristics of a cell lineage whose survival no longer depends on the drug target. Here we show, using in vitro and in vivo prostate cancer models, that these tumors can develop resistance to the antiandrogen drug enzalutamide by a phenotypic shift from androgen receptor (AR) dependent luminal epithelial cells to AR independent basal-like cells. This lineage plasticity is enabled by loss of TP53 and RB1 function, is mediated by increased expression of the reprogramming transcription factor SOX2 and can be reversed by restoring TP53 and RB1 function or by inhibiting SOX2 expression. Thus, mutations in tumor suppressor genes can create a state of increased cellular plasticity that, when challenged with antiandrogen therapy, promotes resistance through lineage switching. Overall design: LNCaP/AR prostate cell line was transduced with shNT or shTP53:RB1 hairpins and then RNA was harvested from these cell lines for gene epxression analysis.

Publication Title

SOX2 promotes lineage plasticity and antiandrogen resistance in TP53- and RB1-deficient prostate cancer.

Sample Metadata Fields

Cell line, Subject

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accession-icon SRP165279
Early response to loss of Argonaute proteins in embryonic stem cells activates the Tgf-ß/Smad Transcriptional Network [mRNA-Seq: DicerDgcr8_KOs]
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Argonaute (Ago) proteins, which act in post-transcriptional gene regulation directed by small RNAs, are vital for normal stem cell biology. Here we report the genomic characterization of stable Ago-deficient mouse embryonic stem cells (mESC) and determine the direct, primary and system level response to loss of Ago-mediated regulation. We find mESCs lacking all four Ago proteins are viable, do not repress microRNA (miRNA)-targeted cellular RNAs, and show distinctive gene network signatures. Profiling of RNA expression and epigenetic activity in an Ago mutant genetic series indicates that early responses to Ago loss are driven by transcriptional regulatory networks, in particular the Tgf-ß/Smad transcriptional network. This finding is confirmed using a time course analysis of Ago depletion and Ago rescue experiments. Detailed analysis places Tgf-ß/Smad activation upstream of cell cycle regulator activation, such as Cdkn1a, and repression of the c-Myc transcriptional network. The Tgf-ß/Smad pathway is directly controlled by multiple low-affinity miRNA interactions with Tgf-ß/Activin receptor mRNAs and receptor-mediated activation is required for Tgf-ß/Smad target induction with Ago loss. Our characterization reveals the interplay of post-transcriptional regulatory pathways with transcriptional networks in maintaining cell state and likely coordinating cell state transitions. Overall design: mRNA seq from stable genetic Dicer and Dgcr8 mutant mouse embryonic stem cells.

Publication Title

Temporal Control of the TGF-β Signaling Network by Mouse ESC MicroRNA Targets of Different Affinities.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon SRP167977
Gene expression profile in FTSEC cells (FT190 and FT194 cell lines) transduced with shRNA to knockdown RNF20 or with control shRNA using RNA-seq.
  • organism-icon Homo sapiens
  • sample-icon 36 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

We identified that downregulation of RNF20/H2Bub1 is involved in HGSOC progression through altering key immune signaling pathways. The goal of this RNA-seq is to analyze gene expression profile in FTSEC cells (FT190 and FT194 cell lines) with RNF20 knockdown (shRNF20) or control shRNA. Integrating the data from ATAC-seq for same samples, we observed that expression of immune signaling pathways have significantly changed by RNF20/H2Bub1 downregulation. Overall design: mRNA profiles of FT190 and FT194 shRNF20 (RNF20 knockdown) or control shRNA cells were generated by deep sequencing using Illumina HiSeq 2500, in triplicate.

Publication Title

Early Loss of Histone H2B Monoubiquitylation Alters Chromatin Accessibility and Activates Key Immune Pathways That Facilitate Progression of Ovarian Cancer.

Sample Metadata Fields

Subject

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accession-icon GSE13946
Comparison of gamma delta intraepithelial lymphocytes from DSS-treated and untreated colon
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

gamma delta intraepithelial lymphocytes were isolated from the colons of DSS-treated and untreated mice. Total RNAs were isolated and compared by Affymetrix DNA microarray.

Publication Title

Reciprocal interactions between commensal bacteria and gamma delta intraepithelial lymphocytes during mucosal injury.

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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