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accession-icon GSE146036
Chronic Inflammation Prediction for Inhaled Particles, the Impact of Material Cycling and Quarantining in the Lung Epithelium
  • organism-icon Mus musculus
  • sample-icon 45 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Clariom S Array (clariomsmouse)

Description

We are daily exposed to a multitude of health hazardous airborne particulate matter with notable deposition in the fragile alveolar region of our lungs. Hence, there is a great need for identification and prediction of material-associated diseases, currently hindered due to the lack of in-depth understanding of causal relationships, in particular between acute exposures and chronic symptoms. By applying advanced microscopies and omics to in vitro and in vivo systems, together with in silico molecular modelling, we have here determined that the long-lasting response to a single exposure can originate from the interplay between the newly discovered nanomaterial quarantining and nanomaterial cycling between different lung cell types. This new insight finally allows us to predict the spectrum of lung inflammation associated with materials of interest using only in vitro measurements and in silico modelling potentially relating outcomes to material properties for large number of materials thus boosting safe-by-design-based material development. Because of its profound implications for animal-free predictive toxicology, our work paves the way to a more efficient and hazard-free introduction of numerous new advanced materials into our lives.

Publication Title

Prediction of Chronic Inflammation for Inhaled Particles: the Impact of Material Cycling and Quarantining in the Lung Epithelium.

Sample Metadata Fields

Cell line

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accession-icon GSE73935
Expression data from A2780 cell line and wild type ovarian cancer cell line (with resistant sublines)
  • organism-icon Homo sapiens
  • sample-icon 48 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U219 Array (hgu219)

Description

The development of cytostatic-drug resistance renders chemotherapy ineffective in treating ovarian cancer, the most lethal gynaecological malignancy. In many cases, it is difficult to explain the development of drug resistance based on the expression patterns of genes known to be involved in this process. Microarray-based assays can provide information about new genes that are involved in the resistance to cytostatic drugs. This report describes alterations in the level of expression of genes in cisplatin- (CisPt), doxorubicin- (Dox), topotecan- (Top), and paclitaxel- (Pac) resistant variants of W1 and A2780 ovarian cancer cell lines. These drug-resistant variants of the W1 and A2780 cell lines were generated through the stepwise selection of cells tolerant of exposure to the indicated drugs at incrementally increased concentrations. Affymetrix GeneChip Human Genome Array Strips were used for hybridization assays. The genes with significantly altered expression levels (upregulated by more than fivefold or downregulated by less than fivefold relative to the level in the parental line) in the drug-resistant sublines were selected and were filtered using volcano plotting.

Publication Title

Microarray-based detection and expression analysis of extracellular matrix proteins in drug‑resistant ovarian cancer cell lines.

Sample Metadata Fields

Cell line

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accession-icon GSE58997
Expression data from livers from Sco1 liver-specific KO and WT adult mice
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

Sco1 is a gene required for cytochrome c oxidase biogenesis and the regulation of copper homeostasis. We characterized the transcriptional changes that occur as a result of liver-specific deletion of Sco1 in mice at 27 days of age

Publication Title

The Mitochondrial Metallochaperone SCO1 Is Required to Sustain Expression of the High-Affinity Copper Transporter CTR1 and Preserve Copper Homeostasis.

Sample Metadata Fields

Age, Specimen part

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accession-icon SRP057986
Context- and cell-type specific function of miR155-Socs1 interaction in immune regulation
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

The microRNA (miRNA) dependent regulation of gene expression confers robustness to cellular phenotypes and controls responses to extracellular stimuli. Although a single miRNA can regulate expression of hundreds of target genes, it is unclear whether any of its distinct biological functions can be due to the regulation of a single target. To explore in vivo the function of a single miRNA-mRNA interaction, we mutated the 3'' UTR of a major miR-155 target SOCS1 to specifically disrupt its regulation by miR-155. We found that under physiologic conditions and during autoimmune inflammation or viral infection some immunological functions of miR-155 were fully or largely attributable to the regulation of SOCS1, whereas others could be accounted only partially or not at all by this interaction. Our data suggest that the role of a single miRNA-mRNA interaction is cell type- and biological context-dependent. Overall design: Naïve WT, SOCS1KI and miR-155KO OVA-specific OT-1 TCR transgenic CD8+ T cells (1x10e4 per mouse) were adoptively transferred into CD45.1+ wt mice prior to infection with MCMV-OVA. WT, SOCS1KI and miR-155KO NK cells (2x10e5 per mouse) were adoptively transferred into CD45.1+ Klra8KO (Ly49H-deficient) mice prior to infection with MCMV. On d4 post infection, CD45.2+ CD44+ CD8+ OT-1 and CD45.2+ Ly49H+ NK1.1+ CD3- NK cells were FACS-sorted (BD FACS ARIA2). Each condition has 3 sequencing replicates.

Publication Title

A Single miRNA-mRNA Interaction Affects the Immune Response in a Context- and Cell-Type-Specific Manner.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP153037
Response of triple negative breast cancer to BAZ2A/B inhibition and BET bromodomain inhibition alone and in combination (RNAseq)
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

Three triple negative breast cancer cell lines (MDAMB231, SUM159, and HCC1806) were treated with small molecule inhibitors (JQ1, BET bromodomain inhibitor; GSK2801, BAZ2A/B bromodomain inhibitor) alone and in combination for 72 hours Overall design: 12 experimental samples

Publication Title

GSK2801, a BAZ2/BRD9 Bromodomain Inhibitor, Synergizes with BET Inhibitors to Induce Apoptosis in Triple-Negative Breast Cancer.

Sample Metadata Fields

Cell line, Treatment, Subject

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accession-icon SRP032280
MDA-MB-231 cell line transcriptome
  • organism-icon Homo sapiens
  • sample-icon 1 Downloadable Sample
  • Technology Badge IconIlluminaGenomeAnalyzerII

Description

RNAseq to determine baseline expression of kinome in MDA-MB-231 claudin-low breast cancer cell line

Publication Title

Dynamic reprogramming of the kinome in response to targeted MEK inhibition in triple-negative breast cancer.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP032344
SUM159PT cell line transcriptome
  • organism-icon Homo sapiens
  • sample-icon 1 Downloadable Sample
  • Technology Badge IconIlluminaGenomeAnalyzerII

Description

RNAseq of SUM159PT claudin-low breast cancer cell line to determine baseline kinome expression

Publication Title

Dynamic reprogramming of the kinome in response to targeted MEK inhibition in triple-negative breast cancer.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE38390
Expression data from leaves of GA-deficient and GA-insensitive transgenic poplar
  • organism-icon Populus tremula x populus alba
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Poplar Genome Array (poplar)

Description

We used whole-genome microarrays to identify differentially expressed genes in leaves of GA-deficient (35S::PcGA2ox) and/or GA-insensitive (35S::rgl1) transgenics as compared to WT poplar (717-1B4 genotype).

Publication Title

Roles of gibberellin catabolism and signaling in growth and physiological response to drought and short-day photoperiods in Populus trees.

Sample Metadata Fields

Specimen part

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accession-icon SRP044917
Discovery of biomarkers predictive of GSI response in triple negative breast cancer and adenoid cystic carcinoma
  • organism-icon Homo sapiens
  • sample-icon 27 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

Next generation sequencing was used to identify Notch mutations in a large collection of diverse solid tumors. NOTCH1 and NOTCH2 rearrangements leading to constitutive receptor activation were confined to triple negative breast cancers (TNBC, 6 of 66 tumors). TNBC cell lines with NOTCH1 rearrangements associated with high levels of activated NOTCH1 (N1-ICD) were sensitive to the gamma-secretase inhibitor (GSI) MRK-003, both alone and in combination with pacitaxel, in vitro and in vivo, whereas cell lines with NOTCH2 rearrangements were resistant to GSI. Immunohistochemical staining of N1-ICD in TNBC xenografts correlated with responsiveness, and expression levels of the direct Notch target gene HES4 correlated with outcome in TNBC patients. Activating NOTCH1 point mutations were also identified in other solid tumors, including adenoid cystic carcinoma (ACC). Notably, ACC primary tumor xenografts with activating NOTCH1 mutations and high N1-ICD levels were sensitive to GSI, whereas N1-ICD low tumors without NOTCH1 mutations were resistant. Overall design: Gene expression profiling for Notch-sensitive cancer cell lines using RNA-seq, each sample with triplicates

Publication Title

Discovery of biomarkers predictive of GSI response in triple-negative breast cancer and adenoid cystic carcinoma.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP007569
SuperSAGE evidence for CD14++CD16+ monocytes as a third monocyte subset
  • organism-icon Homo sapiens
  • sample-icon 3 Downloadable Samples
  • Technology Badge IconIlluminaGenomeAnalyzerIIx

Description

Monocytes are a heterogeneous cell population with subset-specific functions and phenotypes. The differential expression of CD14 and CD16 distinguishes classical CD14++CD16-, intermediate CD14++CD16+ and non-classical CD14+CD16++ monocytes. However, CD14++CD16+ monocytes remain the most poorly characterized subset so far. Therefore we analyzed the transcriptomes of the three monocyte subsets using SuperSAGE in combination with high-throughput sequencing. Analysis of 5,487,603 tags revealed unique identifiers of CD14++CD16+ monocytes, delineating these cells from the two other monocyte subsets. CD14++CD16+ monocytes were linked to antigen processing and presentation (e.g. CD74, HLA-DR, IFI30, CTSB), to inflammation and monocyte activation (e.g. TGFB1, AIF1, PTPN6), and to angiogenesis (e.g. TIE2, CD105). Therefore we provide genetic evidence for a distinct role of CD14++CD16+ monocytes in human immunity. Overall design: Human monocyte subsets (CD14++CD16-, CD14++CD16+, CD14+CD16++) were isolated from 12 healthy volunteers based on MACS technology. Total RNA from monocyte subsets was isolated and same aliquots from each donor and monocyte subset were matched for SuperSAGE. Three SuperSAGE libraries (CD14++CD16-, CD14++CD16+ and CD14+CD16++) were generated.

Publication Title

SuperSAGE evidence for CD14++CD16+ monocytes as a third monocyte subset.

Sample Metadata Fields

No sample metadata fields

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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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