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accession-icon GSE18893
TNF activates a distinct cellular program in human regulatory T cells
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Here we show that tumor necrosis factor (TNF) induced in human T-regulatory cells (Treg), as compared to conventional T cells (Tcon), a transcription program highly enriched for typical NF-B target genes, such as: the cytokines LTA and TNF; the TNF-receptor super family members FAS, 4-1BB and OX-40; various anti-apoptotic genes; and other important immune-response genes.

Publication Title

TNF activates a NF-kappaB-regulated cellular program in human CD45RA- regulatory T cells that modulates their suppressive function.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE98216
Expression data from IMR90 cells expressing either E7-ca-STAT5A-shNTC vs E7-ca-STAT5a-shSOCS1 at 7 days post infection
  • organism-icon Homo sapiens
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.0 ST Array (hugene20st)

Description

SOCS1 plays a role in cellular senescence. Knocking down SOCS1 in senescence induced by the STAT5 oncogene results in senescence bypass by preventing p53 activation

Publication Title

SOCS1 regulates senescence and ferroptosis by modulating the expression of p53 target genes.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE70923
Expression data from xenograft in BALB/c 6-wk-old nude mice with PC3 prostate cancer cells stably expressing PML or a vector control after treatment of the mice with palbociclib
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.0 ST Array (hugene20st)

Description

Expression data from xenograft in BALB/c 6-wk-old nude mice with PC3 prostate cancer cells stably expressing PML or a vector control after treatment of the mice with palbociclib (100mg/kg/day diluted in sodium lactate 50mM pH4 given by gavage) during 5 consecutive days

Publication Title

A CDK4/6-Dependent Epigenetic Mechanism Protects Cancer Cells from PML-induced Senescence.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE49422
Expression data from H1299 human non-small cell lung carcinoma cell lines stably expressing CHES1 compared with H1299 infected with an empty vector
  • organism-icon Homo sapiens
  • sample-icon 1 Downloadable Sample
  • Technology Badge Icon Affymetrix Human Gene 2.0 ST Array (hugene20st)

Description

The expression of the forkhead transcription factor CHES1, also known as FOXN3, is reduced in many types of cancers. In vitro, CHES1 expression suppresses cell proliferation in tumor cell lines but not in normal cells. Conversely shRNA-mediated depletion of CHES1 increases tumor cell proliferation.

Publication Title

CHES1/FOXN3 regulates cell proliferation by repressing PIM2 and protein biosynthesis.

Sample Metadata Fields

Cell line

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accession-icon GSE76953
Gene expression analysis of MCF12A human breast cultures exposed to ethanol or acetaldehyde
  • organism-icon Homo sapiens
  • sample-icon 9 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

Long-term exposure of MCF-12A normal human breast epithelial cells to ethanol induces epithelial mesenchymal transition and oncogenic features.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE76951
Gene expression analysis of MCF12A human breast cultures exposed to ethanol or acetaldehyde [4 weeks]
  • organism-icon Homo sapiens
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Alcoholism is associated with breast cancer incidence and progression, and moderate chronic consumption of ethanol is a risk factor. The mechanisms involved in alcohol's oncogenic effects are unknown, but it has been speculated that they may be mediated by acetaldehyde. Here, we use the immortalized normal human epithelial breast cell line MCF-12A to determine whether short- or long-term exposure to ethanol or to acetaldehyde, using in vivo compatible ethanol concentrations, induces their oncogenic transformation and/or the acquisition of epithelial mesenchymal transition (EMT). Cultures of MCF-12A cells were incubated with 25 mM ethanol or 2.5 mM acetaldehyde for 1 week, or with lower concentrations (1.0-2.5 mM for ethanol, 1.0 mM for acetaldehyde) for 4 weeks. In the 4 wk incubation, cells were also tested for anchorage independence, including isolation of soft agar selected cells (SASC) from the 2.5 mM ethanol incubations. Cells were analyzed by immuno-cytofluorescence, flow cytometry, western blotting, DNA microarrays, RT/PCR, and assays for miRs. We found that short-term exposure to ethanol, but not, in general, to acetaldehyde, was associated with transcriptional upregulation of the metallothionein family genes, alcohol metabolism genes, and genes suggesting the initiation of EMT, but without related phenotypic changes. Long-term exposure to the lower concentrations of ethanol or acetaldehyde induced frank EMT changes in the monolayer cultures and in SASC as demonstrated by changes in cellular phenotype and mRNA expression. This suggests that low concentrations of ethanol, with little or no mediation by acetaldehyde, induce EMT and some traits of oncogenic transformation such as anchorage independence in normal breast epithelial cells.

Publication Title

Long-term exposure of MCF-12A normal human breast epithelial cells to ethanol induces epithelial mesenchymal transition and oncogenic features.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE76950
Gene expression analysis of MCF12A human breast cultures exposed to ethanol or acetaldehyde [1 week]
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Alcoholism is associated with breast cancer incidence and progression, and moderate chronic consumption of ethanol is a risk factor. The mechanisms involved in alcohol's oncogenic effects are unknown, but it has been speculated that they may be mediated by acetaldehyde. Here, we use the immortalized normal human epithelial breast cell line MCF-12A to determine whether short- or long-term exposure to ethanol or to acetaldehyde, using in vivo compatible ethanol concentrations, induces their oncogenic transformation and/or the acquisition of epithelial mesenchymal transition (EMT). Cultures of MCF-12A cells were incubated with 25 mM ethanol or 2.5 mM acetaldehyde for 1 week, or with lower concentrations (1.0-2.5 mM for ethanol, 1.0 mM for acetaldehyde) for 4 weeks. In the 4 wk incubation, cells were also tested for anchorage independence, including isolation of soft agar selected cells (SASC) from the 2.5 mM ethanol incubations. Cells were analyzed by immuno-cytofluorescence, flow cytometry, western blotting, DNA microarrays, RT/PCR, and assays for miRs. We found that short-term exposure to ethanol, but not, in general, to acetaldehyde, was associated with transcriptional upregulation of the metallothionein family genes, alcohol metabolism genes, and genes suggesting the initiation of EMT, but without related phenotypic changes. Long-term exposure to the lower concentrations of ethanol or acetaldehyde induced frank EMT changes in the monolayer cultures and in SASC as demonstrated by changes in cellular phenotype and mRNA expression. This suggests that low concentrations of ethanol, with little or no mediation by acetaldehyde, induce EMT and some traits of oncogenic transformation such as anchorage independence in normal breast epithelial cells.

Publication Title

Long-term exposure of MCF-12A normal human breast epithelial cells to ethanol induces epithelial mesenchymal transition and oncogenic features.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE20985
Comparison of gene expression in CD13 wild type versus Knock out Macrophages
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

The robust and consistent expression of the CD13 cell surface marker on very early as well as differentiated myeloid hematopoietic cells has prompted numerous investigations seeking to define roles for CD13 in myeloid cells. To directly address the function of myeloid CD13 we created a CD13 null mouse and assessed the responses of purified primary macrophages or dendritic cells from wild type and CD13 null animals in cell assays and inflammatory disease models where CD13 has been previously implicated. We find that mice lacking CD13 develop normally with normal hematopoietic profiles. Moreover, in in vitro assays, CD13 appears to be largely dispensable for the aspects of phagocytosis, proliferation and antigen presentation that we tested, but may contribute to adhesion to endothelial cells. In vivo assessment of four inflammatory disease models showed that lack of CD13 has little effect on disease onset or progression. Nominal alterations in gene expression levels between CD13 wild type and null macrophages argue against compensatory mechanisms. Analysis of the dataset with Ingenuity Pathway Analysis software did not suggest that loss of CD13 resulted in a purturbation of any specific biological pathways, processes or networks. Therefore, while CD13 is highly expressed on myeloid cells and is a reliable marker of the myeloid lineage of both normal and leukemic cells, it is not a critical regulator of hematopoietic development, hemostasis or myeloid cell function.

Publication Title

CD13 is dispensable for normal hematopoiesis and myeloid cell functions in the mouse.

Sample Metadata Fields

Specimen part

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accession-icon GSE72013
MCF-7 human breast cancer cells treated with ethanol: DNA microarray expression data and microRNA prevalence data
  • organism-icon Homo sapiens
  • sample-icon 9 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

Long-term exposure of MCF-7 breast cancer cells to ethanol stimulates oncogenic features.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon SRP067740
Next generation sequencing analysis of epididymal adipose tissue (II)
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

We analyze the contribution of alternative splicing to the transcriptional complexity in adipose tissue and the development of diet-induced obesity. Overall design: We use Next generation sequencing analysis of eWAT from control and Nova1 and Nova2-deficient mice fed with a control diet

Publication Title

An alternative splicing program promotes adipose tissue thermogenesis.

Sample Metadata Fields

Sex, Age, Specimen part, Cell line, 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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