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accession-icon GSE54507
Lambda light chain knockdown in ALMC1 human myeloma cells
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

We used siRNA to knockdown lambda light chain expression in ALMC1 cells that express an intact IgG lambda monoclonal protein.

Publication Title

One siRNA pool targeting the λ constant region stops λ light-chain production and causes terminal endoplasmic reticulum stress.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE30888
Tumor-entrained neutrophils inhibit seeding in the pre-metastatic lung
  • organism-icon Mus musculus
  • sample-icon 22 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip, Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Tumor entrained neutrophils inhibit seeding in the premetastatic lung.

Sample Metadata Fields

Sex, Specimen part, Disease, Treatment

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accession-icon GSE30885
Pre-metastatic expression array day 7
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip, Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

Primary tumors have been shown to prepare distal organs for later colonization of metastatic cells by stimulating organ-specific infiltration of bone marrow-derived cells. Here we demonstrate that neutrophils accumulate in the lung prior to the arrival of metastatic cells in mouse models of breast cancer. Tumor-entrained neutrophils (TENs) inhibit metastatic seeding in the lungs by generating H2O2, and tumor-secreted CCL2 is a critical mediator of optimal anti-metastatic entrainment of G-CSF-stimulated neutrophils. TENs are present in the peripheral blood of breast cancer patients prior to surgical resection but not in healthy individuals. Thus, while tumor-secreted factors contribute to tumor progression at the primary site, they concomitantly induce a neutrophil-mediated inhibitory process at the metastatic site.

Publication Title

Tumor entrained neutrophils inhibit seeding in the premetastatic lung.

Sample Metadata Fields

Sex, Specimen part, Disease

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accession-icon GSE30887
Neutrophil expression array
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

Primary tumors have been shown to prepare distal organs for later colonization of metastatic cells by stimulating organ-specific infiltration of bone marrow-derived cells. Here we demonstrate that neutrophils accumulate in the lung prior to the arrival of metastatic cells in mouse models of breast cancer. Tumor-entrained neutrophils (TENs) inhibit metastatic seeding in the lungs by generating H2O2, and tumor-secreted CCL2 is a critical mediator of optimal anti-metastatic entrainment of G-CSF-stimulated neutrophils. TENs are present in the peripheral blood of breast cancer patients prior to surgical resection but not in healthy individuals. Thus, while tumor-secreted factors contribute to tumor progression at the primary site, they concomitantly induce a neutrophil-mediated inhibitory process at the metastatic site.

Publication Title

Tumor entrained neutrophils inhibit seeding in the premetastatic lung.

Sample Metadata Fields

Sex, Specimen part, Treatment

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accession-icon GSE50603
Effect of L-Proline on mouse embryonic stem cells (ESCs)
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

We found that the non-essential amino acid L-Proline (L-Pro) acts as a signaling molecule that promotes the conversion of embryonic stem cells (ESCs) into mesenchymal-like, spindle-shaped, highly motile, invasive pluripotent stem cells. This embryonic stem cell-to-mesenchymal-like transition (esMT) is accompanied by a genome-wide remodeling of the transcriptome

Publication Title

L-Proline induces a mesenchymal-like invasive program in embryonic stem cells by remodeling H3K9 and H3K36 methylation.

Sample Metadata Fields

Cell line

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accession-icon GSE5242
Hepatic gene expression in transgenic mice with conditional liver-specific expression of the SV40 17kT/LT oncoproteins
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Expression 430A Array (moe430a)

Description

The SV40 large (LT) and small (st) antigens are produced from a single alternatively spliced pre-mRNA, that when co-expressed, transform a variety of cells in vitro and in vivo. However, 17kT, a relatively uncharacterized third protein that is co-linear with LT for the first 131 amino acids, is also produced from the early viral pre-mRNA by removal of an additional intron from the LT transcript. Here we report a line of transgenic mice expressing a liver-specific dox-inducible viral transcript that fails to yield any detectable LT protein, yet produces abundant 17kT. Comparative analysis of livers of transgenic mice expressing either 17kT or LT demonstrates that while 17kT is a potent stimulator of cell proliferation, it is ineffective at inducing liver tumor development, due in part, to the failure of 17kT to effectively induce the expression of growth regulators and reactivate expression of imprinted and developmentally regulated hepatic genes. These studies highlight key functional differences between LT and 17kT in their ability to transform quiescent primary epithelial cells in vivo, and demonstrate how specific functional domains within LT impact cell-specific gene expression to promote oncogenesis.

Publication Title

Comparative analysis of SV40 17kT and LT function in vivo demonstrates that LT's C-terminus re-programs hepatic gene expression and is necessary for tumorigenesis in the liver.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE52721
Effects of O-GlcNAc modification on gene expression using O-GlcNAcase deleted Mouse Embryonic Fibroblast cells.
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Single O-GlcNAc modification orchestrate by O-GlcNAc Transferase (OGT) and O-GlcNAcase (OGA alias MGEA5) enzymes, affects signal transduction and gene expression by chromatin modulation. We developed Oga deleted MEF (mouse embryonic fibroblast) cells to investigate effects of O-GlcNAc modification in mice. RNA isolated from Mouse Embryonic Fibroblast cells generated from Oga Knock out (KO) Heterozygous (Het) and wild type (WT) cells and subjected to microarray analysis.

Publication Title

Conditional knock-out reveals a requirement for O-linked N-Acetylglucosaminase (O-GlcNAcase) in metabolic homeostasis.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE31180
Patterns of cancer development and progression in the protein-protein interaction network
  • organism-icon Homo sapiens
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

For this study we selected a gene, -synuclein (SNCA), that is consistently under-expressed in MCF7 cells and breast tumors. Following transfection with an SNCA expression construct, two stable MCF7 clones (named MCF7-SNCA #1 and 2) were selected and examined for expression differences relative to the parental MCF7 cells.

Publication Title

Cancer develops, progresses and responds to therapies through restricted perturbation of the protein-protein interaction network.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE22299
Role of the Yersinia pestis Virulence Plasmid in Evading a Protective Polymorphonuclear Leukocyte Response During the Early Stages of Bubonic Plague
  • organism-icon Rattus norvegicus
  • sample-icon 50 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

A delay in the mammalian inflammatory response is a prominent feature of infection with Yersinia pestis, the agent of bubonic and pneumonic plague. Y. pestis factors have been identified that either do not stimulate a normal inflammatory response, or actively suppress it. Prominent among these are components of the Type III secretion system that is encoded on the Yersinia virulence plasmid (pYV). We used a rat model of bubonic plague to characterize the kinetics and extent of the mammalian transcriptomic response to infection with wild-type or pYV-negative Y. pestis in the draining lymph node. Remarkably, dissemination and multiplication of wild-type Y. pestis during the bubonic stage of disease did not induce any detectable gene expression response by host lymph node cells. This was followed, however, by an extensive transcriptomic response, including upregulation of several cytokine, chemokine, and other immune response genes, after systemic spread during septicemic plague. Matched lymph node samples used for histopathology and extracellular cytokine measurements, combined with the microarray data set, broadly outlined the mammalian immune response to Y. pestis and how it is influenced by pYV-encoded factors. The results indicate that both WT and pYV Y. pestis induce primarily a Th17 response, and not a Th1 or Th2 response. In the absence of pYV, a sustained recruitment of polymorphonuclear leukocytes, the major Th17 effector cell, to the lymph node resulted in clearance of infection. Thus, the ability to counteract a Th17- driven PMN response in the lymph node appears to be a major function of the Y. pestis virulence plasmid. In contrast, classic markers of the proinflammatory response and macrophage activation, such as TNF- and IFN-, were not induced at all by pYV Y. pestis, and appeared only late in infection with WT Y. pestis.

Publication Title

Transcriptomic and innate immune responses to Yersinia pestis in the lymph node during bubonic plague.

Sample Metadata Fields

Sex, Specimen part, Treatment, Time

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accession-icon GSE10867
Biomarkers of human gastro-intestinal tract regions
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Background and aims: Dysregulation of intestinal epithelial cells performance associates with an array of pathologies whose onset mechanisms are incompletely understood. The aim of the present study was to provide a map of gene expresssion patterns along the human healthy adult gastro-intestinal tract and to implement a new procedure for microarray data noise filtering that would allow their use as a reference when screening for pathological deviations, such as inflammatory bowel disease (IBD). Methods: Gene expression profiles in antrum, duodenum, jejunum, ileum and transverse colon biopsies were measured with the Affymetrix U133A array and principal component analysis was used to identify region-selective biomarkers. These data were intersected with highly variable genes from a public dataset of gene expression in the ileal and colonic healthy regions of UC and Crohns disease patients. Moreover, gene sets covering gut functions not entirely accounted for by the available public tools were constructed to monitor their expression along the GI tract. Results: 166 genes were found to be responsible for distinguishing the five regions considered. Fourteen had never been described in the GI tract, including a semaphorin probably implicated in pathogen invasion, and six other novel genes. Similar analysis of the IBD datasets revealed that samples stratify based on disease rather than on the intestinal region. This withstanding, eleven genes were identified as possible early predictors of Crohns and/or UC in ileum and/or colon. These include CLCA4 and SLC26A2, both implicated in ion transport. Conclusions: This novel approach, validated by retrieving known gene profiles, allowed the identification of promising new leads both in health and IBD state.

Publication Title

Biomarkers of human gastrointestinal tract regions.

Sample Metadata Fields

Age

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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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