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accession-icon GSE42320
IKKe coordinates invasion and metastasis
  • organism-icon Homo sapiens
  • sample-icon 17 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

IKKe was identified previously as a breast cancer oncogene and was associated with poor clinical outcome in ovarian cancer.

Publication Title

IKK-ε coordinates invasion and metastasis of ovarian cancer.

Sample Metadata Fields

Specimen part, Cell line, Treatment

View Samples
accession-icon GSE94358
Expression data from ovarian cancer cells grown in different culture condtions
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Cells grown in culture conditions that enrich for cancer stem cells are more tumoigenic and have higher resistance to chemotherapy.

Publication Title

NFκB Promotes Ovarian Tumorigenesis via Classical Pathways That Support Proliferative Cancer Cells and Alternative Pathways That Support ALDH<sup>+</sup> Cancer Stem-like Cells.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP172679
A Preformed Chromatin Architecture Ensures Robust Shh Transcription during Limb Development [RNA-Seq]
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

During embryogenesis, enhancer-promoter interactions control gene transcriptional activation. These interactions can be tissue-specific or tissue-invariant and occur mostly within larger insulated regulatory domains called Topologically Associating Domains (TADs). Boundary elements, which delineate the extent of TADs, frequently interact with each other and have been associated with constitutive transcription and CTCF/Cohesin binding. In this work, we set out to investigate the regulatory role of a tissue-invariant, preformed interaction between two boundaries that involve the Shh gene and its unique limb enhancer, the ZRS, located one megabase away. Using CRISPR/Cas9 we specifically perturb CTCF binding sites or constitutive transcription at the ZRS-containing boundary, without altering the enhancer sequence. Using capture-HiC (cHiC) we show that both types of perturbation result in altered preformed chromatin interactions and lead to a reduction of Shh expression in developing limb buds. Finally, we demonstrate that the disruption of the chromatin structure in combination with a hypomorphic ZRS allele results in a dramatic Shh loss- of- function and digit agenesis. We thus propose that preformed chromatin structures can ensure stable enhancer promoter communication during development and robustness of gene transcriptional activation. Overall design: We performed transcriptome analysis to confirm the complete loss of the Lmbr1 transcript due to the deletion of its promoter and to detect other potential non-coding transcripts at the locus.

Publication Title

Preformed chromatin topology assists transcriptional robustness of <i>Shh</i> during limb development.

Sample Metadata Fields

Cell line, Subject

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accession-icon GSE110545
Transcriptome data from Eomes-overexpressing Th17 cells
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Th17 cells were sorted ex vivo from PB of healthy donors as CD4+CD161+CCR6+CXCR3-. Following, cells were transduced with a lentiviral vector carrying the Eomes gene or with an empty vector. Infected cells were then enriched by MACS separation using the reporter gene NGFR as selection marker. Finally, cells were frozen for RNA analysis.

Publication Title

Eomes controls the development of Th17-derived (non-classic) Th1 cells during chronic inflammation.

Sample Metadata Fields

Cell line

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accession-icon GSE51927
Expression analysis of murine primary and derived orthotopic SEOC tumors
  • organism-icon Mus musculus
  • sample-icon 56 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

We previously generated genetically engineered mouse (GEM) models based on perturbation of Tp53, Rb with or without Brca1 or Brca2 that develop serous epithelial ovarian cancer (SEOC) closely resembling the human disease on histologic and molecular levels. We have adapted these GEM models to orthotopic allografts that uniformly develop tumors with short latency in immunocompetent recipients and are ideally suited for routine preclinical studies. To monitor passaged tumors at the molecular level, we analyzed transcriptional profiles of a set of primary SEOC and matching derived passaged tumors. We have merged this dataset with previously published ( doi: 10.1158/0008-5472.CAN-11-3834; PMID 22617326) dataset of murine primary ovarian tumors from our GEM models (GSE46169) and merged and compared them to expression profiles of human dataset published previously (doi: 10.1038/nature10166).

Publication Title

Pathway-specific engineered mouse allograft models functionally recapitulate human serous epithelial ovarian cancer.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE117935
Whole transcriptome analysis of circulating B cells from multiple sclerosis (MS) patients and healthy donors (HD)
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

Whole transcriptome analysis of circulating B cells from multiple sclerosis (MS) patients and healthy donors (HD).

Publication Title

Analysis of coding and non-coding transcriptome of peripheral B cells reveals an altered interferon response factor (IRF)-1 pathway in multiple sclerosis patients.

Sample Metadata Fields

Specimen part, Disease

View Samples
accession-icon GSE22611
NOD2 and desease associated variant NOD2-L1007fsinsC dependent genomewide transcriptional regulation in stable Flp-In HEK cells
  • organism-icon Homo sapiens
  • sample-icon 25 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

NOD2 is an intracellular receptor for the bacterial cell wall component muramyl dipeptide (MDP) and variants of NOD2 are associated with chronic inflammatory diseases of barrier organs e.g. Crohn disease, asthma and atopic eczema. It is known that activation of NOD2 induces a variety of inflammatory and antibacterial factors. The exact transcriptomal signatures that define the cellular programs downstream of NOD2 activation and the influence of the Crohn-associated variant L1007fsinsC are yet to be defined. To describe the MDP-induced activation program, we analyzed the transcriptomal reactions of isogenic HEK293 cells expressing NOD2wt or NOD2L1007fsinsC to stimulation with MDP. Importantly, a clear loss-of-function could be observed in the cells carrying the Crohn-associated variant L1007fsinsC, while the NOD2wt cells showed differential regulation of growth factors, chemokines and several antagonists of NF-B, e.g. TNFAIP3 (A20) and IER3.

Publication Title

Genome-wide expression profiling identifies an impairment of negative feedback signals in the Crohn's disease-associated NOD2 variant L1007fsinsC.

Sample Metadata Fields

Cell line, Time

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accession-icon GSE10616
Human colon expression in healthy controls, colon-only CD, ileo-colonic CD, and UC
  • organism-icon Homo sapiens
  • sample-icon 58 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Colon gene expression in human IBD. The three major clinical subsets of Inflammatory Bowel Disease (IBD) include colon-only Crohn's Disease (CD), ileo-colonic CD, and Ulcerative Colitis (UC). These experiments tested differential colon gene expression in these three types of IBD, relative to healthy control samples, and the local degree of mucosal inflammation as measured by the CD Histological Index of Severity (CDHIS). Colon biopsy samples were obtained from IBD patients at diagnosis and during therapy, and healthy controls. The global pattern of gene expression was determined using GeneSpring software, with a focus upon candidate genes identified in a recent genome wide association study in pediatric onset IBD. Data suggested that two of these candidate genes are up regulated in pediatric IBD, partially influenced by local mucosal inflammation.

Publication Title

Loci on 20q13 and 21q22 are associated with pediatric-onset inflammatory bowel disease.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP066244
Activation of the pluripotency factor OCT4 in smooth muscle cells is atheroprotective. doi: 10.1038/nm.4109
  • organism-icon Mus musculus
  • sample-icon 80 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

The multiple claims about reactivation of the embryonic stem cell (ESC) pluripotency factor OCT4 in somatic cells are highly controversial due to the fact that there is no direct evidence that OCT4 has a functional role in cells other than ESCs. Herein we demonstrate that smooth muscle cell (SMC)-specific knockout of Oct4 within atherosclerotic mice resulted in increased lesion size and multiple changes consistent with decreased plaque stability. SMC-lineage tracing studies showed that lesions from SMC-specific conditional Oct4 KO mice had a reduced number of SMCs likely due to impaired SMC migration. RNA-seq analysis of lesion specimens showed that loss of Oct4 in SMCs was associated with marked activation of genes associated with inflammation and suppression of genes associated with cell migration, a number of which were shown to be activated in cultured SMCs by the combination of hypoxia and oxidized phospholipids in an OCT4-dependent manner. Activation of Oct4 within SMCs was associated with hydroxymethylation of the Oct4 promoter and was HIF1a- and KLF4-dependent. Results provide the first genetic evidence that OCT4 plays a functional role in somatic cells and highlight the importance of further investigation of possible OCT4 functions in somatic cells. Overall design: In vivo: mRNA profiles of 18 week fed Western diet wild type (WT) and Oct4-/- mice were generated by deep sequencing, four animals per group, using Illumina HiSeq 2000. In vitro: a smooth muscle cell wild type (WT) and Oct4-/- (KO) primary aortic cell line was generated and used. mRNA profiles were generated by deep sequencing, in triplicates, using Illumina HiSeq 2000, for the following groups: WT-normoxia-vehicle; WT-normoxia-POVPC; KO-normoxia-vehicle; KO-normoxia-POVP; WT-hypoxia-vehicle; WT-hypoxia-POVPC; KO-hypoxia-vehicle; and KO-hypoxia-POVPC.

Publication Title

Perivascular cell-specific knockout of the stem cell pluripotency gene Oct4 inhibits angiogenesis.

Sample Metadata Fields

Specimen part, Cell line, Treatment, Subject

View Samples
accession-icon GSE20281
The transcriptional network for mesenchymal transformation of brain tumours
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 108 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

The transcriptional network for mesenchymal transformation of brain tumours.

Sample Metadata Fields

Time

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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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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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