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accession-icon GSE74407
Epidermal Growth Factor Receptor inhibition triggers Type 1 Interferon signature in human keratinocytes
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

The Epidermal Growth Factor Receptor (EGFR)/ligand system is centrally involved in multiple homeostatic functions of the epithelia. Epithelial cells are the primary targets of humanized antibodies and small molecule inhibitors against this system, whereby the constellation of skin-specific side effects of these drugs stems from a profound disturbance of keratinocyte biology. So far, the molecular mechanisms underlying these toxic events have been investigated only broadly. Here we show that keratinocyte response to anti-EGFR drugs comprises the development of a type 1 interferon (IFN) molecular signature including enhanced expression of IFN-kappa. Mechanistically, nuclear accumulation of IRF1 precedes this signature as well as the enhanced expression of a chemokine cluster we previously identified as a relevant pro-inflammatory component of EGFR inhibition. In fact, either silencing of IRF1 transcript expression, or antibody-mediated blockade of type 1 IFN receptor function and consequent abrogation of STAT1 activation, leads to impairment of this gene transcription profile. High levels of IRF1 and IFN-kappa can be clearly observed in the early skin lesions of patients treated with cetuximab. Type 1 IFN signaling could be crucially implicated in the triggering of the inflammatory mechanisms active in the skin of patients under treatment with anti-EGFR drugs.

Publication Title

Epidermal growth factor receptor inhibitors trigger a type I interferon response in human skin.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE116660
Human NK cells under normoxic and hypoxic conditions
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Hypoxia, which characterizes most tumor tissues, can alter the function of different immune cell types, favoring tumor escape mechanisms. In this study, we show that hypoxia profoundly acts on NK cells by influencing their transcriptome, affecting their immunoregulatory functions, and changing the chemiotactic responses of different NK cell subsets.

Publication Title

Hypoxia Modifies the Transcriptome of Human NK Cells, Modulates Their Immunoregulatory Profile, and Influences NK Cell Subset Migration.

Sample Metadata Fields

Specimen part

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accession-icon GSE104003
Analysis of transcriptome changes arising from MIR205HG modulation in prostate cells
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

LEADeR role of miR-205 host gene as long noncoding RNA in prostate basal cell differentiation.

Sample Metadata Fields

Cell line

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accession-icon GSE29958
Mast cell targeting hampers prostate adenocarcinoma development but promotes the occurrence of highly malignant neuroendocrine cancers.
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconIllumina mouseRef-8 v1.1 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Mast cell targeting hampers prostate adenocarcinoma development but promotes the occurrence of highly malignant neuroendocrine cancers.

Sample Metadata Fields

Age, Specimen part, Cell line

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accession-icon GSE11701
Genes modulated by miR-205 in DU145 prostate cancer cells
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina humanRef-8 v2.0 expression beadchip

Description

The study was aimed at identifying genes directly or indirectly regulated by miR-205 in the prostate. To this purpose, DU145 prostate cancer cells, which express miR-205 at very low levels, were transfected with miR-205 synthetic precursor and consequent alterations of gene expression analyzed using a microarray approach.

Publication Title

miR-205 Exerts tumor-suppressive functions in human prostate through down-regulation of protein kinase Cepsilon.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE29956
Gene expression analysis of prostate tumors arisen in TRAMP mice in which mast cells are pharmacologically stabilized or genetically ablated.
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina mouseRef-8 v1.1 expression beadchip

Description

Analysis of gene expression of prostate tumors arisen in TRAMP mice in which mast cells are pharmacologically stabilized or genetically ablated.The hypothesis tested in the present study was that mast cells inhibition or absence impacted prostate tumor development and histotype. Results demonstrate that prostate tumors arisen in TRAMP mice in which mast cells are pharmacologically stabilized or genetically ablated have a neuroendocrine signature.

Publication Title

Mast cell targeting hampers prostate adenocarcinoma development but promotes the occurrence of highly malignant neuroendocrine cancers.

Sample Metadata Fields

Age, Specimen part

View Samples
accession-icon GSE103655
Effects of deletion of a portion of the Alu element from MIR205HG transcript
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

We aimed at analyzing the transcriptome changes associated with the deletion of a portion of the Alu element from MIR205HG transcript

Publication Title

LEADeR role of miR-205 host gene as long noncoding RNA in prostate basal cell differentiation.

Sample Metadata Fields

Cell line

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accession-icon GSE29957
Gene expression analysis of 2 different prostate tumor cell lines isolated from 30 wks old TRAMP mice compared to normal prostate
  • organism-icon Mus musculus
  • sample-icon 1 Downloadable Sample
  • Technology Badge IconIllumina mouseRef-8 v1.1 expression beadchip

Description

Analysis of gene expression of 2 novel prostate tumor cell lines isolated from TRAMP mice and compared to normal prostate. T1525 cell line is a well differentiated adenocarcinoma with epithelial features, whereas T23 cell line displays the molecular signature of epithelial-to-mesenchymal transition.

Publication Title

Mast cell targeting hampers prostate adenocarcinoma development but promotes the occurrence of highly malignant neuroendocrine cancers.

Sample Metadata Fields

Age, Specimen part, Cell line

View Samples
accession-icon GSE32373
Gene expression analysis of OX40-triggered mouse Treg
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina MouseRef-8 v2.0 expression beadchip

Description

Regulatory T (Treg) maintain the tumor microenvironment in an immunosuppressive state preventing effective anti-tumor immune response. A possible strategy to overcome Treg cell suppression focuses on OX40, a costimulatory molecule expressed constitutively by Treg cells while induced in activated effector T (Teff) cells. OX40 stimulation by the agonist mAb OX86 inhibits Treg cell suppression and boosts Teff cell activation. Here we uncover the mechanisms underlying the therapeutic activity of OX86 treatment dissecting its distinct effects on Treg and on effector memory T (Tem) cells, which are the most abundant CD4+ populations strongly expressing OX40 at the tumor site. In response to OX86, tumor-infiltrating Treg cells produced significantly less interleukin 10 (IL-10), possibly in relation to a decrease in the transcription factor IRF1. Tem cells responded to OX86 by upregulating surface CD40L expression, providing a licensing signal to dendritic cells (DCs). The CD40L/CD40 axis was required for Tem cell-mediated in vitro DC maturation and in vivo DC migration. Accordingly, OX86 treatment was no longer therapeutic in CD40 KO mice. In conclusion, following OX40 stimulation, blockade of Treg cell suppression and enhancement of the Tem cell adjuvant effect both concurred to free DCs from immunosuppression and to activate the immune response against the tumor.

Publication Title

Intratumor OX40 stimulation inhibits IRF1 expression and IL-10 production by Treg cells while enhancing CD40L expression by effector memory T cells.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE103656
Effects of MIR205HG silencing
  • organism-icon Homo sapiens
  • sample-icon 1 Downloadable Sample
  • Technology Badge Icon

Description

We aimed at analyzing the transcriptome changes associated with MIR205HG knock-down in RWPE-1 cells

Publication Title

LEADeR role of miR-205 host gene as long noncoding RNA in prostate basal cell differentiation.

Sample Metadata Fields

No sample metadata fields

View Samples
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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)

fund-icon Fund the CCDL

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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