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accession-icon GSE50385
Expression data from human ependymoma
  • organism-icon Homo sapiens
  • sample-icon 56 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

We compared molecular characteristics of primary and recurrent pediatric ependymoma to identify sub-group specific differences.

Publication Title

Molecular sub-group-specific immunophenotypic changes are associated with outcome in recurrent posterior fossa ependymoma.

Sample Metadata Fields

Specimen part

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accession-icon GSE55628
Differentially expressed genes and chromosomal alterations in ovarian cancer cell lines sensitive or resistant to a Src-inihibitor, saracatinib
  • organism-icon Homo sapiens
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

We sought to detect predictive markers related to a Src kinase inhibitor (saracatinib) sensitivity in ovarian cancer. Cell proliferation assays assigned 18 ovarian cancer cell lines to sensitive or resistant to this drug.

Publication Title

PTTG1 Levels Are Predictive of Saracatinib Sensitivity in Ovarian Cancer Cell Lines.

Sample Metadata Fields

Specimen part

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accession-icon GSE30723
Gene Expression Profiles of human primary alveolar type II (ATII) cells and macrophages (AMs) after influenza virus infection
  • organism-icon Homo sapiens
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Abnormal function of genes is at the root of most cancers, but heritable cancer syndromes account for a very small minority of all tumors in humans and domestic animals. The majority of cancers are sporadic, that is, they are not heritable in the strictest sense. Instead, sporadic cancers occur due to interactions of unknown intrinsic (heritable) and environmental factors that lead to malignant transformation and uncontrolled growth. Identification of heritable risk factors in sporadic human cancers is difficult because individual genetic backgrounds are very heterogeneous. To this end, individual genetic backgrounds of purebred dogs are more homogeneous, and dog breeds show different predilection to develop specific cancers. Here, we used genomic screens based on gene expression profiling to identify sets of genes that may contribute to the development of canine hemangiosarcoma, a relatively common endothelial sarcoma. Specific genes in a single breed (Golden Retrievers) are modulated by (or with) heritable risk traits, showing functional features that appear to modulate tumor behavior. Our results suggest these methods are suitable to identify genes that will enhance our understanding of how these cancers happen, as well as possible treatment targets that will improve outcomes of both human and canine cancer patients.

Publication Title

Innate immune response to influenza A virus in differentiated human alveolar type II cells.

Sample Metadata Fields

Specimen part, Subject, Time

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accession-icon GSE86404
The Transcriptome of HIV-1 Infected Intestinal CD4+ T cells Exposed to Enteric Bacteria
  • organism-icon Homo sapiens
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.0 ST Array (hugene20st)

Description

The gastrointestinal tract is a major site of early HIV-1 replication and death of CD4+ T cells. As HIV-1 replicates in the gut, the protective epithelial barrier gets disrupted, leading to the entry of bacteria into the underlying tissue and the bloodstream, leading to inflammation and clinical complications even in HIV-1-infected patients taking antiviral drugs. Counteracting these pathogenic processes may require in-depth understanding of the molecular pathways that HIV-1 and microbes utilize to infect, functionally alter and/or kill CD4+ T cells. However, to date, the nature of the genes altered by relevant HIV-1 strains and bacteria in intestinal CD4+ T cells remains unclear.

Publication Title

The transcriptome of HIV-1 infected intestinal CD4+ T cells exposed to enteric bacteria.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE20715
Transcript analysis in response to ozone in mice deficient in TLR4
  • organism-icon Mus musculus
  • sample-icon 21 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Expression 430A Array (moe430a)

Description

We previously identified toll-like receptor 4 (Tlr4) as a candidate gene responsible for ozone (O3)-induced pulmonary hyperpermeability and inflammation. The objective of this study was to determine the mechanism through which TLR4 modulates O3-induced pulmonary responses and to utilize transcriptomics to determine TLR4 effector molecules. C3H/HeJ (HeJ; Tlr4 mutant) and C3H/HeOuJ (OuJ; Tlr4 normal), mice were exposed continuously to 0.3 ppm O3 or filtered air for 6, 24, 48 or 72 hr. Affymetrix Mouse430A_MOE gene arrays were used to analyze lung homogenates from HeJ and OuJ mice followed using a bioinformatic analysis. Inflammation was assessed by bronchoalveolar lavage and molecular analysis by ELISA, immunoblotting, and transcription factor activity. TLR4 signals through both the MYD88-dependent and independent pathways in OuJ mice, which involves MAP kinase activation, NF-kappaB, AP-1, and KC. Microarray analyses identifiedTLR4 responsive genes for strain and time in OuJ versus HeJ mice (p<0.05). One significantly upregulated cluster of genes in OuJ were the heat shock proteins (Hspa1b; Hsp70), Hsp90ab1). Furthermore, O3-induced expression of HSP70 protein was increased in OuJ compared to HeJ mice following 24-48 h O3. Moreover, BAL polymorphonuclear leukocytes (PMN) and total protein were significantly reduced in response to O3 in Hspa1a/Hspa1btm1Dix (Hsp70-/-) compared to Hsp70+/+ mice (p<0.05). TLR4 signaling (MYD88-dependent), ERK1/2, AP-1 activity, and KC protein content were also significantly reduced after O3 exposure in Hsp70-/- compared to Hsp70+/+ mice (p<0.05). These studies suggest that HSP70 is involved in the regulation of O3-induced lung inflammation through the TLR4 pathway and provide evidence that HSP70 is an endogenous in vivo TLR4 ligand.

Publication Title

Identification of candidate genes downstream of TLR4 signaling after ozone exposure in mice: a role for heat-shock protein 70.

Sample Metadata Fields

Sex, Specimen part, Treatment

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accession-icon GSE42708
Effect of Spot14 Overexpression on Gene Expression Profile of MMTV-Neu Mouse Tumors
  • organism-icon Mus musculus
  • sample-icon 22 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.1 ST Array (mogene11st)

Description

The objective of this study was to determine the effect of Thyroid Hormone Responsive Protein Spot14 (Spot14) overexpression on the gene expression profiles of tumors from MMTV-Neu mice. Hemizygous MMTV-Neu and MMTV-Spot14 mice were bred and 1 cm tumors from Neu control or Neu/Spot14 bitransgenic offspring were profiled using Affymetrix gene arrays. Tumors from Neu/Spot14 mice emerged significantly earlier than controls, but expressed many genes associated with lactogenic differentiation and were not highly metastatic. These results from the mouse model are consistent with observations from primary human breast tumors, which indicate that high Spot14 gene expression was directly correlated with a luminal subtype and a positive ER status. Overexpression of Spot14 in cultured mammary epithelial cells stimulated proliferation but not differentiation. Together, these data suggest that, in vivo, Spot14 is expressed in well-differentiated cells, and promotes the expansion of this population in the context of oncogenic signaling pathway activation.

Publication Title

Modulation of tumor fatty acids, through overexpression or loss of thyroid hormone responsive protein spot 14 is associated with altered growth and metastasis.

Sample Metadata Fields

Specimen part

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accession-icon GSE49116
Protective Role of IL6 in Vascular Remodeling in Schistosoma-Pulmonary Hypertension
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Protective role of IL-6 in vascular remodeling in Schistosoma pulmonary hypertension.

Sample Metadata Fields

Sex, Specimen part, Disease, Disease stage, Treatment

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accession-icon GSE36075
Estrogen receptor dynamics in diverse patient-derived luminal breast cancer xenografts
  • organism-icon Homo sapiens
  • sample-icon 19 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.1 ST Array (hugene11st)

Description

Primary breast cancer xenografts

Publication Title

No associated publication

Sample Metadata Fields

Treatment

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accession-icon GSE84649
Binary polycyclic aromatic hydrocarbon exposure alters the transcriptome inducing inflammation and inhibiting cell communication through p38 MAPK in lung cells
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

Low molecular weight polycyclic aromatic hydrocarbons (LMW PAHs) are generated by the incomplete combustion of organic material and are prevalent and ubiquitous in the environment, presenting a human health concern. While much is known about the high molecular weight genotoxic species of PAHs, there are insufficient studies for LMW PAHs and their impact on pulmonary health. Secondhand smoke, or environmental tobacco smoke (ETS), is a mixture of many PAHs, among other constituents. To study the effect of more than one PAH, we examined single PAH and a binary mixture on the dysregulation of gap junctional intercellular communication (GJIC), activation of mitogen activated protein kinases (MAPK), and induction of inflammation with a focus on the p38 MAPK pathway through transcriptomic analysis. A mouse non-tumorigenic alveolar type II cell line, C10, along with two normal, non-tumorigenic human bronchial epithelial cell lines, Beas2b and HBE1 cells, for human comparisons. Our findings in all cell lines indicate that 1-methylanthracene (1-MeA) and fluoranthene (Flthn), can dysregulated GJIC in a dose dependent manner and combining these two compounds lead to a similar effect on GJIC. MAPKs, particularly P38, are rapidly activated and the inhibition of this MAPK leads to a reversal of PAH dysregulation of GJIC. A toxicogenomic approach conducted using the C10 cells revealed inflammatory, metabolic, steroid synthesis, and oxidative pathways altered synergistically by a mixture of PAHs (1-MeA and Flthn), followed by qRT-PCR, ELISAs, and immunoblots validation. Our findings indicated LMW PAHs potential to induce pulmonary inflammation and emphasize the need for mixture exposure research to accurately estimate human exposure risk.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part, Cell line, Time

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accession-icon GSE57178
Gene Expression Profiles in Chronic Idiopathic Urticaria
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Lesions of chronic idiopathic urticaria (CIU) showed significant up-regulation of 506 genes and reduced expression of 51 genes.

Publication Title

Gene expression profiles in chronic idiopathic (spontaneous) urticaria.

Sample Metadata Fields

Specimen part, Subject

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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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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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