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accession-icon GSE95214
Ventral prostate in male F344 rats: Control vs. PhIP treatment
  • organism-icon Rattus norvegicus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

The gene expression profling between Control and 300 mg/kg PhIP treatment in ventral prostate lobe of male F344 rats

Publication Title

Early detection of prostate carcinogens by immunohistochemistry of HMGB2.

Sample Metadata Fields

Specimen part

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accession-icon GSE54957
Functional analysis of the TRIB1 associated locus (TRIBAL) linked to plasma triglycerides and coronary artery disease
  • organism-icon Homo sapiens
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Transcriptome Array 2.0 (hta20), Agilent-028004 SurePrint G3 Human GE 8x60K Microarray (Probe Name Version)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Functional analysis of the TRIB1 associated locus linked to plasma triglycerides and coronary artery disease.

Sample Metadata Fields

Cell line

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accession-icon GSE85429
Gene expression profiles in Drosophila phagocytes after incubation with apototic cell fragments
  • organism-icon Drosophila melanogaster
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Drosophila Genome 2.0 Array (drosophila2)

Description

The phagocytic elimination of cells undergoing apoptosis is an evolutionarily conserved innate immune mechanism for eliminating unnecessary cells. Previous studies showed an increase in the level of engulfment receptors in phagocytes after the phagocytosis of apoptotic cells, which leads to the enhancement of their phagocytic activity. However, precise mechanisms underlying this phenomenon require further clarification. We found that the pre-incubation of a Drosophila phagocyte cell line with the fragments of apoptotic cells enhanced the subsequent phagocytosis of apoptotic cells, accompanied by an augmented expression of the engulfment receptors Draper and integrin PS3. The DNA-binding activity of the transcription repressor Tailless was transiently raised in those phagocytes, depending on two partially overlapping signal-transduction pathways for the induction of phagocytosis as well as the occurrence of engulfment. The RNAi knockdown of tailless in phagocytes abrogated the enhancement of both phagocytosis and engulfment receptor expression. Furthermore, the hemocyte-specific RNAi of tailless reduced apoptotic cell clearance in Drosophila embryos. Taken together, we propose the following mechanism for the activation of Drosophila phagocytes after an encounter with apoptotic cells: two partially overlapping signaltransduction pathways for phagocytosis are initiated; transcription repressor Tailless is activated; expression of engulfment receptors is stimulated; and phagocytic activity is enhanced. This phenomenon most likely ensures the phagocytic elimination of apoptotic cells that stimulated phagocytes find thereafter and is thus considered as a mechanism to prime phagocytes in innate immunity.

Publication Title

Signaling pathway for phagocyte priming upon encounter with apoptotic cells.

Sample Metadata Fields

Cell line, Treatment, Time

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accession-icon GSE54937
TRIBAL overexpression in HepG2 cells
  • organism-icon Homo sapiens
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Transcriptome Array 2.0 (hta20), Agilent-028004 SurePrint G3 Human GE 8x60K Microarray (Probe Name Version)

Description

Objective - The TRIB1 locus has been linked to hepatic triglyceride metabolism in mice and to plasma triglycerides and coronary artery disease (CAD) in humans. The lipid associated SNPs identified by genome-wide association studies (GWAS) are located ~ 30 kb downstream from TRIB1 suggesting complex regulatory effects on genes or pathways relevant to hepatic triglyceride metabolism. The goal of this study was to investigate the functional relationship between common SNPs at the TRIB1 locus and plasma lipid traits.

Publication Title

Functional analysis of the TRIB1 associated locus linked to plasma triglycerides and coronary artery disease.

Sample Metadata Fields

Cell line

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accession-icon SRP148597
Single-cell Map of Diverse Immune Phenotypes in the Breast Tumor Microenvironment 3'' RNA Sequencing
  • organism-icon Homo sapiens
  • sample-icon 168 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 4000, Illumina HiSeq 2500

Description

Knowledge of immune cell phenotypes in the tumor microenvironment is essential for understanding mechanisms of cancer progression and immunotherapy response. We created an immune map of breast cancer using single-cell RNA-seq data from 45,000 immune cells from eight breast carcinomas, as well as matched normal breast tissue, blood, and lymph node. We developed a preprocessing pipeline, SEQC, and a Bayesian clustering and normalization method, Biscuit, to address computational challenges inherent to single-cell data. Despite significant similarity between normal and tumor tissue-resident immune cells, we observed continuous phenotypic expansions specific to the tumor microenvironment. Analysis of paired single-cell RNA and T cell receptor (TCR) sequencing data from 27,000 additional T cells revealed the combinatorial impact of TCR utilization on phenotypic diversity. Our results support a model of continuous activation in T cells and do not comport with the macrophage polarization model in cancer, with important implications for characterizing tumor-infiltrating immune cells.  Overall design: Single-cell RNA sequencing was performed on eight donors using the InDrop v2 protocol. For each donor populations of CD45+ immune cells were assayed for trancriptome-wide RNA-sequence. At least one replicate was taken for each donor.

Publication Title

Single-Cell Map of Diverse Immune Phenotypes in the Breast Tumor Microenvironment.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP148594
Single-cell Map of Diverse Immune Phenotypes in the Breast Tumor Microenvironment - 5'' RNA sequencing and TCR sequencing
  • organism-icon Homo sapiens
  • sample-icon 29 Downloadable Samples
  • Technology Badge IconNextSeq 500, Illumina HiSeq 2500

Description

Knowledge of immune cell phenotypes in the tumor microenvironment is essential for understanding mechanisms of cancer progression and immunotherapy response. We created an immune map of breast cancer using single-cell RNA-seq data from 45,000 immune cells from eight breast carcinomas, as well as matched normal breast tissue, blood, and lymph node. We developed a preprocessing pipeline, SEQC, and a Bayesian clustering and normalization method, Biscuit, to address computational challenges inherent to single-cell data. Despite significant similarity between normal and tumor tissue-resident immune cells, we observed continuous phenotypic expansions specific to the tumor microenvironment. Analysis of paired single-cell RNA and T cell receptor (TCR) sequencing data from 27,000 additional T cells revealed the combinatorial impact of TCR utilization on phenotypic diversity. Our results support a model of continuous activation in T cells and do not comport with the macrophage polarization model in cancer, with important implications for characterizing tumor-infiltrating immune cells.  Overall design: Single-cell RNA sequencing was performed on three patients using the 10x genomics TCR profiling kits. For each patient, populations of T-cells were assayed for both TCR sequence and trancriptome-wide RNA-sequence. Two donors have a replicate experiment.

Publication Title

Single-Cell Map of Diverse Immune Phenotypes in the Breast Tumor Microenvironment.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE67529
In vivo gene expression changes in EW5 Ewing sarcoma xenografts after IGF-1R or mTOR blockade
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

Ewing Sarcoma is caused by a pathognomonic genomic translocation that places an N-terminal EWSR1 gene in approximation with one of several ETS genes (typically FLI1). This aberration, in turn, alters the transcriptional regulation of more than five hundred genes and perturbs a number of critical pathways that promote oncogenesis, cell growth, invasion, and metastasis. Among them, translocation-mediated up-regulation of the insulin-like growth factor receptor 1 (IGF-1R) and mammalian target of rapamycin (mTOR) are of particular importance since they work in concert to facilitate IGF-1R expression and ligand-induced activation, respectively, of proven importance in ES transformation. When used as a single agent in Ewing sarcoma therapy, IGF-1R or mTOR inhibition leads to rapid counter-regulatory effects that blunt the intended therapeutic purpose. Therefore, identify new mechanisms of resistance that are used by Ewing sarcoma to evade cell death to single-agent IGF-1R or mTOR inhibition might suggest a number of therapeutic combinations that could improve their clinical activity.

Publication Title

IGF-1R and mTOR Blockade: Novel Resistance Mechanisms and Synergistic Drug Combinations for Ewing Sarcoma.

Sample Metadata Fields

Specimen part

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accession-icon GSE24671
The nucleic-acid recognizing Toll-like receptors -3, -7 and -9 cooperatively protect against murine T cell lymphoma caused by endogenous retrovirus
  • organism-icon Mus musculus
  • sample-icon 13 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

The genome of vertebrates contains endogenous retroviruses (ERVs) that have resulted from ancestral infections by exogenous retroviruses. ERVs are germline encoded, transmitted in a Mendelian fashion and account for about 8% of the human and 9.9% of the murine genome, respectively1, 2. By spontaneous activation and reintegration ERVs may cause insertional mutagenesis and thus participate in the process of malignant transformation or progression of tumor growth3, 4. However, if the innate immune system is able to recognize and control ERVs has not yet been elucidated. Here we report that, in vitro, nucleic-acid sensing TLRs on dendritic cells are activated by retroviral RNA and DNA from infected cells in vitro. Infection of TLR competent wild type mice with murine leukemia virus (MuLV)-like ERV isolates results in non-canonical gene upregulation, independent of type I IFN. In vivo, TLR3, -7 and -9 triple deficient mice (TLR379-/-) and mice with non functional TLR3, 7 and 9 signaling due to a mutation in UNC93B develop spontaneous ERV-induced viremia. More importantly, in TLR379-/- mice ERV-induced viremia correlates with acute T cell lymphoblastic leukemia (T-ALL). Multiple independent TLR379-/- T cell leukemia lines produce infectious MuLV of endogenous origin. These cell lines display de novo retroviral integration into the Nup214 or Notch1 gene locus leading to gene dysregulation that is reminiscent of aberrant Nup214 and Notch1 expression in human T-ALLs5. Overall, our results demonstrate that in addition to their role in innate immune defense against exogenous pathogens, TLR3,-7, and -9 may be essential for the control of endogenous retroviral mediated T-cell lymphomagenesis.

Publication Title

Nucleic acid-sensing Toll-like receptors are essential for the control of endogenous retrovirus viremia and ERV-induced tumors.

Sample Metadata Fields

Specimen part

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accession-icon GSE70526
Expression data from plant tissues during incompatible interaction between the rice host and its major pest, the Asian rice gall midge
  • organism-icon Oryza sativa
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Rice Genome Array (rice)

Description

During an incompatible or compatible interaction between rice (Oryza sativa) and the Asian rice gall midge (Orseolia oryzae), a lot of genetic reprogamming occurs in the plant host

Publication Title

Metabolic and transcriptomic changes induced in host during hypersensitive response mediated resistance in rice against the Asian rice gall midge.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE36868
Simvastatin treated Lymphoblastoid Cell lines from Cholesterol and Pharmacogenomics (CAP) Trial
  • organism-icon Homo sapiens
  • sample-icon 960 Downloadable Samples
  • Technology Badge IconIllumina HumanRef-8 v3.0 expression beadchip

Description

Statins reduce cardiovascular disease risk by lowering plasma low density lipoprotein (LDL)-cholesterol. To identify novel pathways that modulate statin response, we assessed the influence of simvastatin exposure on expression quantitative trait locus (eQTL) associations across the genome in 480 lymphoblastoid cell lines (LCLs). Cell lines were derived blood samples collected ant entry visit from participants in the Cholesterol and Pharmacogenomics (CAP) trial, who underwent a 6 week 40mg/day simvastatin trial. We identified 4590 cis-eQTLS that were independent of treatment status (FDR=1%) and six cis-eQTLS for which there was evidence of an interaction with treatment (FDR=20%). Genotypes and Phenotypes derived from these indivudals are available through dbGaP (Accession Number). eQTL results are available at: http://eqtl.uchicago.edu/cgi=bin/gbrowse/eqtl/

Publication Title

HNRNPA1 regulates HMGCR alternative splicing and modulates cellular cholesterol metabolism.

Sample Metadata Fields

Sex, Subject

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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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