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accession-icon GSE31287
Gene expression from head and neck squamous cell carcinoma (SCCHN) cancer cells before and after figitumumab
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Patients with palliative SCCHN were treated with figitumumab, an IGF-1R inhibitor. This receptor plays an important role in cell growth, proliferation and differentiation and is often overexpressed in SCCHN. No significant clinical activity was observed in our study

Publication Title

Phase II study of figitumumab in patients with recurrent and/or metastatic squamous cell carcinoma of the head and neck: clinical activity and molecular response (GORTEC 2008-02).

Sample Metadata Fields

Specimen part

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accession-icon SRP098901
Retinal degeneration triggers the activation of YAP/TEAD in reactive Müller cells
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

PURPOSE. During retinal degeneration, Müller glia cells respond to photoreceptor loss by undergoing reactive gliosis, with both detrimental and beneficial effects. Increasing our knowledge of the complex molecular response of Müller cells to retinal degeneration is thus essential for the development of new therapeutic strategies. The purpose of this work was to identify new factors involved in Müller cell response to photoreceptor cell death. METHODS. Whole transcriptome sequencing was performed from wild-type and degenerating rd10 mouse retinas at P30. The changes in mRNA abundance for several deregulated genes were assessed by RT-qPCR. Protein expression level and retinal cellular localization were determined by western-blot and immunohistochemistry, respectively. RESULTS. Pathway-level analysis from whole transcriptomic data revealed the Hippo/YAP pathway as one of the main signaling pathways altered in response to photoreceptor degeneration in rd10 retinas. We found that downstream effectors of this pathway, YAP and TEAD1, are specifically expressed in Müller cells and that their expression, at both the mRNA and protein levels, is increased in rd10 reactive Müller glia after the onset of photoreceptor degeneration. The expression of Ctgf and Cyr61, two target genes of the transcriptional YAP/TEAD complex, is also upregulated following photoreceptor loss. CONCLUSIONS. This work reveals for the first time that YAP and TEAD1, key downstream effectors of the Hippo pathway, are specifically expressed in Müller cells. We also uncovered a deregulation of the expression and activity of Hippo/YAP pathway components in reactive Müller cells under pathological conditions. Overall design: Retinal samples were harvested from C57Bl6/J and rd10 mouse retina at postnatal days 30 for whole transcriptome sequencing (RNAseq). Each sample included 2 frozen retina and experiments were performed in triplicate. RNA-seq transcriptome libraries were constructed from 1 ug of total RNA.

Publication Title

Retinal Degeneration Triggers the Activation of YAP/TEAD in Reactive Müller Cells.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE58525
Expression data from WIF1 induced LN-229 (GBM cell line)
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Glioblastoma is the most aggressive primary brain tumor in adults and due to the invasive nature it cannot be completely removed. We have recently shown that the WNT inhibitory factor 1 (WIF1), a secreted inhibitor of WNTs, is downregulated in glioblastoma and acts as strong tumor suppressor. In search of a mediator for this function differential gene expression profiles of WIF1-expressing cells were performed. MALAT1, a long non-coding RNA and key positive regulator of invasion, emerged as the top downregulated gene. Indeed, knock-down of MALAT1 reduced migration in glioblastoma cells, without effect on proliferation.

Publication Title

WIF1 re-expression in glioblastoma inhibits migration through attenuation of non-canonical WNT signaling by downregulating the lncRNA MALAT1.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE106260
Immunopathology of childhood celiac disease-Key role of intestinal epithelial cells
  • organism-icon Homo sapiens
  • sample-icon 52 Downloadable Samples
  • Technology Badge IconIllumina HumanRef-8 v3.0 expression beadchip, Illumina HumanHT-12 V4.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Immunopathology of childhood celiac disease-Key role of intestinal epithelial cells.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon GSE829
Laminin binding/non-binding germ cells
  • organism-icon Mus musculus
  • sample-icon 21 Downloadable Samples
  • Technology Badge Icon Affymetrix Murine Genome U74A Version 2 Array (mgu74av2), Affymetrix Murine Genome U74A Array (mgu74a)

Description

Comparison of laminin binding and laminin non-binding germ cells

Publication Title

Defining the spermatogonial stem cell.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE830
Rat germ cells
  • organism-icon Rattus norvegicus
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Expression 230A Array (rae230a)

Description

Rat germ cells

Publication Title

Defining the spermatogonial stem cell.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE103374
Gene expression assessed by genome wide hybridization bead array in T84 polarized tight monolayers after challenge with celiac disease-associated bacteria and gluten [CTR glut bmix, bmix and gluten]
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

Analysis of the influence of celiac disease-associated bacteria and gluten on intestinal epithelial cells

Publication Title

Immunopathology of childhood celiac disease-Key role of intestinal epithelial cells.

Sample Metadata Fields

Cell line, Treatment

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accession-icon GSE103100
Gene expression assessed by genome wide hybridization bead array in T84 polarized tight monolayers after challenge with celiac disease-associated bacteria and gluten [A grav, Bmix Bmix glut]
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

Analysis of the influence of celiac disease-associated bacteria and gluten on intestinal epithelial cells

Publication Title

Immunopathology of childhood celiac disease-Key role of intestinal epithelial cells.

Sample Metadata Fields

Cell line, Treatment

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accession-icon GSE103107
Gene expression assessed by genome wide hybridization bead array in T84 polarized tight monolayers after challenge with celiac disease-associated bacteria [CTR 22 28 27]
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

Analysis of the influence of celiac disease-associated bacteria on intestinal epithelial cells

Publication Title

Immunopathology of childhood celiac disease-Key role of intestinal epithelial cells.

Sample Metadata Fields

Cell line, Treatment

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accession-icon GSE102993
Gene expression assessed by genome wide hybridization bead array in intraepithelial lymphocytes (IELs) isolated from small intestinal biopsies of celiac disease patients with active disease and clinical controls
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HumanRef-8 v3.0 expression beadchip

Description

Analysis of role of small intestinal intraepithelial lymphocytes (IELs) in the immunopathology of celiac disease

Publication Title

Immunopathology of childhood celiac disease-Key role of intestinal epithelial cells.

Sample Metadata Fields

Specimen part

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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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