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accession-icon GSE9801
Human Monocytes to M-CSF differentiated Macrophages
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

This dataset was created to study M-CSF dependent in vitro differentiation of human monocytes to macrophages as a model process to demonstrate that independent component analysis (ICA) is a useful tool to support and extend knowledge-based strategies and to identify complex regulatory networks or novel regulatory candidate genes.

Publication Title

Analyzing M-CSF dependent monocyte/macrophage differentiation: expression modes and meta-modes derived from an independent component analysis.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE69754
VEGF blockade enhances the antitumor effect of BRAFV600E inhibition
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 14 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip, Illumina HumanHT-12 V4.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

VEGF blockade enhances the antitumor effect of BRAFV600E inhibition.

Sample Metadata Fields

Cell line, Treatment

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accession-icon GSE69744
VEGF blockade enhances the antitumor effect of BRAFV600E inhibition (mouse)
  • organism-icon Mus musculus
  • sample-icon 11 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

In this work we investigated the combined effects of the BRAF inhibition and of the VEGF blockade in a preclinical model of melanoma. The purpose of this dataset was to examine the transcriptional responses of a A375 xenograft model to PLX472 and bevacizumab, either as single agents or as combination therapy. We performed species-specific analysis of gene expression to discriminate the effects of the different therapeutic regimens on tumor cells (human) and stromal microenvironment (mouse). Here, Illumina Mouse BeadChips were used to profile the transcriptome after 12 days treatment. We reported that dispensing the dual treatment is more efficient than the single compounds and the occurrence of resistance by modifying the tumor genetic programs regulating myeloid cells recruitment and extracellular matrix remodeling.

Publication Title

VEGF blockade enhances the antitumor effect of BRAFV600E inhibition.

Sample Metadata Fields

Cell line, Treatment

View Samples
accession-icon GSE69742
VEGF blockade enhances the antitumor effect of BRAFV600E inhibition (human)
  • organism-icon Homo sapiens
  • sample-icon 3 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip, Illumina HumanHT-12 V4.0 expression beadchip

Description

In this work we investigated the combined effects of the BRAF inhibition and of the VEGF blockade in a preclinical model of melanoma. The purpose of this dataset was to examine the transcriptional responses of a A375 xenograft model to PLX472 and bevacizumab, either as single agents or as combination therapy. We performed species-specific analysis of gene expression to discriminate the effects of the different therapeutic regimens on tumor cells (human) and stromal microenvironment (mouse). Here, Illumina Human BeadChips were used to profile the transcriptome after 12 days treatment. We reported that dispensing the dual treatment is more efficient than the single compounds and the occurrence of resistance by modifying the tumor genetic programs regulating myeloid cells recruitment and extracellular matrix remodeling.

Publication Title

VEGF blockade enhances the antitumor effect of BRAFV600E inhibition.

Sample Metadata Fields

Cell line, Treatment

View Samples
accession-icon GSE7360
Equine Laminitis vs Control.
  • organism-icon Equus caballus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Bovine Genome Array (bovine)

Description

Equine lameller tissues were collected to compare normal vs laminitis generated differences in transcriptom level.

Publication Title

Gene expression in the lamellar dermis-epidermis during the developmental phase of carbohydrate overload-induced laminitis in the horse.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE69454
Expression data from decitabine-treated and non-treated BR5FVB1-Akt cells
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

The DNA methyl transferase inhibitor decitabine regulates gene expression in cancer cells.

Publication Title

Decitabine Enhances Lymphocyte Migration and Function and Synergizes with CTLA-4 Blockade in a Murine Ovarian Cancer Model.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon GSE34948
Expression data from three endothelial cell lines derived from murine embryonic stem cells expressing VE-cadherin, N-cadherin or both
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Endothelial cells (ECs) express two members of the cadherin family, VE- and N-cadherin. While VE-cadherin induces EC homotypic adhesion, N-cadherin function in ECs remains largely unknown. EC-specific inactivation of either VE- or N-cadherin leads to early foetal lethality suggesting that these cadherins play a non-redundant role in vascular development.

Publication Title

Overlapping and divergent signaling pathways of N-cadherin and VE-cadherin in endothelial cells.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon SRP078332
H3.3 depletion has a mild effect on the global transcriptome
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Transcriptomic analysis of H3.3 KO/Kd mouse embryonic fibroblasts (MEFs) Overall design: We isolated total RNA from control shRNA treated or shH3.3A treated H3.3B KO MEFs and carried out Ribozero RNA-seq analysis. RNA-seq analysis was carried out on pooled datasets from biological duplicate experiments.

Publication Title

Histone H3.3 regulates mitotic progression in mouse embryonic fibroblasts.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE11674
Genes up-regulated by VE-cadherin expression and clustering at junctions
  • organism-icon Mus musculus
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)

Description

In order to identify genes regulated by VE-cadherin expression, we compared a mouse VE-cadherin null cell line (VEC null) with the same line reconstituted with VE-cadherin wild type cDNA (VEC positive). The morphological and functional properties of these cell lines were described previously [Lampugnani,M.G. et al. Contact inhibition of VEGF-induced proliferation requires vascular endothelial cadherin, beta-catenin, and the phosphatase DEP-1/CD148. J. Cell Biol. 161, 793-804 (2003)]. By Affymetrix gene expression analysis we found several genes up-regulated by VE-cadherin, among which claudin-5 reached remarkably high levels. The up-regulation of these genes required not only VE-cadherin expression but also cell confluence suggesting that VE-cadherin clustering at junctions was needed.

Publication Title

Endothelial adherens junctions control tight junctions by VE-cadherin-mediated upregulation of claudin-5.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP071580
Interleukin 4 induces apoptosis of acute myeloid leukemia cells in a Stat6-dependent manner
  • organism-icon Mus musculus
  • sample-icon 14 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

Acute myeloid leukemia (AML) is associated with poor prognosis, and there is a strong need to develop new therapeutic strategies to improve treatments. We performed a cytokine screen with 114 recombinant proteins to identify selective negative regulators of primitive murine AML cells relative to normal bone marrow cells. The top candidate identified was interleukin 4 (IL4), as it showed the most selective inhibition of leukemia cell growth. Stimulating leukemia cells ex vivo with IL4 and transplanting the cells into mice resulted in reduced leukemia burden and prolonged survival compared with controls. In contrast, IL4 did not inhibit the function of normal hematopoietic stem and progenitor cells in long-term bone marrow repopulation assays. Moreover, we found that IL4 treatment of leukemia cells induced Stat6 phosphorylation, and that leukemia cells with Stat6 knocked out using CRISPR/Cas9-genetic engineering were partially resistant to IL4 stimulation, revealing Stat6 as a critical mediator of the IL4 effect. To evaluate whether IL4 has in vivo therapeutic efficacy, we expressed IL4 ectopically in leukemia cells in vivo and also injected IL4 into leukemic mice; both strategies resulted in the suppression of the leukemia cell burden and increased survival. Further analysis revealed that IL4 treatment induces apoptosis in the leukemia cells. Importantly, IL4 exposure also inhibited the growth and survival of primary AML patient cells. In summary, these findings demonstrate that IL4 selectively inhibits AML cells in a Stat6-dependent manner, thus revealing IL4 as a candidate therapeutic agent in AML. IL4 (ProSpec, East Brunswick NJ, USA) was resuspended following the provider guidelines and stored in aliquotes at -80 °C. Mouse MLL-AF9 leukemia cells were provided by Dr. Benjamin Ebert (Brigham and Women’s Hospital, Boston MA, USA). The murine leukemia cells were cultured in SFEM (StemCell Tech) supplemented with 1% penicillin/streptomycin at 37 °C with 5% CO2. Overall design: Mouse MLL-AF9 leukemia cells were grown in 20 ng/mL IL3 with or without IL4 (100 ng/mL) for 18 hours.

Publication Title

Interleukin 4 induces apoptosis of acute myeloid leukemia cells in a Stat6-dependent manner.

Sample Metadata Fields

Specimen part, Subject

View Samples

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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