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accession-icon GSE6055
Gene Expression Profiling Reveals Unique Pathways Associated with Differential Severity of Lyme Arthritis
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Expression 430A Array (moe430a)

Description

The murine model of Lyme disease provides a unique opportunity to study the localized host response to similar stimulus, B. burgdorferi, in the joints of mice destined to develop severe arthritis (C3H) or mild disease (C57BL/6). Pathways associated with the response to infection and the development of Lyme arthritis were identified by global gene expression patterns using oligonucleotide microarrays. A robust induction of IFN responsive genes was observed in severely arthritic C3H mice at one week of infection, which was absent from mildly arthritic C57BL/6 mice. In contrast, infected C57BL/6 mice displayed a novel expression profile characterized by genes involved in epidermal differentiation and wound repair, which were decreased in the joints of C3H mice. These expression patterns were associated with disease state rather than inherent differences between C3H and C57BL/6 mice, as C57BL/6-IL10-/- mice infected with B. burgdorferi develop more severe arthritis that C57BL/6 mice and displayed an early gene expression profile similar to C3H mice. Gene expression profiles at two and four weeks post infection revealed a common response of all strains that was likely to be important for the host defense to B. burgdorferi and mediated by NF-kB-dependent signaling. The gene expression profiles identified in this study add to the current understanding of the host response to B. burgdorferi and identify two novel pathways that may be involved in regulating the severity of Lyme arthritis.

Publication Title

Gene expression profiling reveals unique pathways associated with differential severity of lyme arthritis.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE349
Resistant
  • organism-icon Homo sapiens
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U95 Version 2 Array (hgu95av2), Affymetrix Human Genome U95A Array (hgu95a)

Description

These patients proved resistant to docetaxel treatment, exhibiting residual tumor of 25% or greater remaining volume.

Publication Title

Gene expression profiling for the prediction of therapeutic response to docetaxel in patients with breast cancer.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE350
Sensitive
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U95 Version 2 Array (hgu95av2)

Description

These patients were sensitive to docetaxel treatment, exhibiting less than 25% residual tumor.

Publication Title

Gene expression profiling for the prediction of therapeutic response to docetaxel in patients with breast cancer.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE63986
Integrative Functional Characterization of Cancer-Testis Antigens Defines Obligate Participation in Multiple Hallmarks of Cancer
  • organism-icon Homo sapiens
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.1 ST Array (hugene11st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Comprehensive functional characterization of cancer-testis antigens defines obligate participation in multiple hallmarks of cancer.

Sample Metadata Fields

Cell line, Treatment

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accession-icon GSE63984
Expression data to identify putative transcriptional targets of ZNF165 in Triple Negative Breast Cancer (TNBC)
  • organism-icon Homo sapiens
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.1 ST Array (hugene11st)

Description

We found that the cancer testis antigen, ZNF165, is required for viability and can modulate TGF-induced gene expression in mesenchymal, Claudin-Low, TNBC. We employed the Affymetrix microarray platform to uncover transcriptionally modulated genes following ZNF165 depletion and TGF stimulation using the Claudin-low TNBC tumor-derived cell lines, SUM159 as a model. Our results provide insight into how ZNF165 globally modulates TGF signaling.

Publication Title

Comprehensive functional characterization of cancer-testis antigens defines obligate participation in multiple hallmarks of cancer.

Sample Metadata Fields

Treatment

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accession-icon SRP131095
Transcriptional changes after overexpression of proliferation drivers in human mammary epithelial cells.
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Genomics has provided a detailed structural description of the cancer genome. Identifying oncogenic drivers that work primarily through dosage changes is a current challenge. Unrestrained proliferation is a critical hallmark of human cancer. We constructed modular, barcoded libraries of human open reading frames (ORFs) and performed screens for proliferation regulators in multiple cell types. Approximately 10% of genes tested regulate proliferation, many performing in an unexpectedly highly tissue-specific manner. Proliferation drivers in a given cell type showed specific enrichment in SCNAs (somatic copy number changes) from cognate tumors and helped predict aneuploidy patterns in those tumors, implying that tissue type-specific genetic network architectures underlie SCNA selection in different cancers. In vivo screening confirmed these results. We report a substantial contribution to the catalog of SCNA-associated cancer drivers, identifying 147 amplified and 107 deleted genes as potential drivers, and derive new insights about the genetic network architecture of aneuploidy in tumors. KRTAPs are a class of human genes that promote proliferation in mammary epithelial cells (HMEC), but the mechanism is not understood. We performed RNAseq to study transcriptional changes associated with oeverxepression of KRTAPs and other oncogenes in hTERT-immortalized human mammary epithelial cells. GSEA analysis revealed the top enriched pathways upregulated by KRTAP expression are E2F-mediated regulation of DNA replication, G1-S specific transcription, cell cycle, translation and ribosome. KRTAP-induced mRNA changes are most closely related to those due to CCND1 expression, including induction of E2F1 transcription factor. Overall design: Analysis of whole transcriptome in HMEC overexpressing different human genes.

Publication Title

Profound Tissue Specificity in Proliferation Control Underlies Cancer Drivers and Aneuploidy Patterns.

Sample Metadata Fields

Specimen part, Disease, Subject

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accession-icon GSE6434
Docetaxel treatment of sensitve and resistant patients
  • organism-icon Homo sapiens
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U95 Version 2 Array (hgu95av2), Affymetrix Human Genome U95A Array (hgu95a)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Patterns of resistance and incomplete response to docetaxel by gene expression profiling in breast cancer patients.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE133975
Reprogrammed alveolar macrophages after pneumonia recovery
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

Community-acquired pneumonia is a widespread disease with significant morbidity and mortality. Alveolar macrophages are tissue-resident lung cells that play a crucial role in innate immunity against bacteria causing pneumonia. We hypothesized that alveolar macrophages display adaptive characteristics after resolution of bacterial pneumonia. We studied mice one to six months after self-limiting lung infection due to Streptococcus pneumoniae, the most common cause of bacterial pneumonia. Among the myeloid cells recovered from the lung, only alveolar macrophages showed long-term modifications of their surface marker phenotype. The remodeling of alveolar macrophages was: (i) long-lasting (still observed 6 months post infection), (ii) regionally localized (only observed in the affected lobe after lobar pneumonia), and (iii) associated with a macrophage-dependent enhanced lung protection to another pneumococcal serotype. Metabolomic and transcriptomic profiling revealed that alveolar macrophages of mice which recovered from pneumonia had new baseline activities and altered responses to infection. Thus, the enhanced lung protection after mild and self-limiting respiratory infection includes a profound remodeling of alveolar macrophages that is long-lasting, compartmentalized, and manifest across surface receptors, metabolites, and both resting and stimulated transcriptomes.

Publication Title

Pneumonia recovery reprograms the alveolar macrophage pool.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE81294
Lung gene expression
  • organism-icon Homo sapiens
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2), Affymetrix Multispecies miRNA-3 Array (mirna3)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

miR-155 in the progression of lung fibrosis in systemic sclerosis.

Sample Metadata Fields

Specimen part, Disease

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accession-icon GSE81292
Expression of mRNA from lung tissue from Systemic Sclerosis patients with interstitial lung disease (SSc-ILD) and healthy controls (HC)
  • organism-icon Homo sapiens
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

Objective: MicroRNAs (miRNAs) control key elements of mRNA stability and likely contribute to the dysregulated lung gene expression observed in systemic sclerosis associated interstitial lung disease (SSc-ILD). We analyzed the miRNA gene expression of tissue and cells from SSc-ILD patients. A chronic lung fibrotic murine model was used.

Publication Title

miR-155 in the progression of lung fibrosis in systemic sclerosis.

Sample Metadata Fields

Specimen part, Disease

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)

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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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