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accession-icon GSE102972
Transcriptional response to a prime/boost vaccination of chickens with three vaccine variants based on HA DNA and Pichia-produced HA protein
  • organism-icon Gallus gallus
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Chicken Gene 1.1 ST Array (chigene11st)

Description

Broilers were immunized with three variants of subunit vaccines, based on the hemagglutinin (HA) DNA and Pichia-produced HA protein from H5N1 virus, in comparison to the control group, which was administered an empty vector (pCI). Gene expression changes in the spleens of chickens were investigated at 7 day post booster dose.

Publication Title

Transcriptional response to a prime/boost vaccination of chickens with three vaccine variants based on HA DNA and Pichia-produced HA protein.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE33753
Expression data from RU486 treated FVB wild-type and MMTV- PAX8PPARg mouse mammary tumors
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

To determine if RU-486 would be effective as a chemopreventive agent, microarrays were used to analyse global gene expression changes in wild-type vs. MMTV-PAX8PPARg mice to determine their differential response to RU486

Publication Title

The chemopreventive effect of mifepristone on mammary tumorigenesis is associated with an anti-invasive and anti-inflammatory gene signature.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE45804
Gene expression data from MCF-7 cells treated with Lacciac Acid A
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Lacciac Acid A was indentified as an inhibitor of DMNT1. MCF-7 cells were treated with Lacciac Acid A (200 uM) for 5 days. Changes in gene expression were identified by using Affymetrix Human gene ST1.0 arrays. We used microarrays to determine global changes in gene expression upon treatment with Lacciac Acid A an inhibitor of DMNT1.

Publication Title

Laccaic acid A is a direct, DNA-competitive inhibitor of DNA methyltransferase 1.

Sample Metadata Fields

Specimen part

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accession-icon GSE31954
Expression data from Sca-1 knockout mice
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

The role of Sca-1 on mammary tumorigenesis was assessed. Microarrays were used to analyse global gene expression changes in Sca-1 KO mice versus wild-type mice and determine the differential responses to MP and DMBA-induced Mammary carcinogenesis

Publication Title

Stem cell antigen-1 deficiency enhances the chemopreventive effect of peroxisome proliferator-activated receptorγ activation.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE27083
Expression data from MMTV-PDK1 transgenic mice
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The role of PDK1 on mammary tumorigenesis and its interaction with PPARdelta, was assessed. Transgenic mice were generated in which PDK1 was expressed in the mammary epithelium.

Publication Title

PPARδ activation acts cooperatively with 3-phosphoinositide-dependent protein kinase-1 to enhance mammary tumorigenesis.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE34109
Expression data from MMTV-PPARd mice, 1 week GW501516 treatment
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

The role of murine peroxisome proliferator-activated receptor-delta (PPARd) in mammary tumorigenesis was assessed. Microarrays were used to analyse global gene expression to determine changes in MMTV-PPARd transgenic mice versus wild-type mice and the effect of GW501516.

Publication Title

PPARδ induces estrogen receptor-positive mammary neoplasia through an inflammatory and metabolic phenotype linked to mTOR activation.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE23994
A molecular signature of normal breast epithelial and stromal cells from Li-Fraumeni syndrome mutation carriers
  • organism-icon Homo sapiens
  • sample-icon 19 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Specific changes in gene expression during cancer initiation should enable discovery of biomarkers for risk assessment, early detection and targets for chemoprevention. It has been previously demonstrated that altered mRNA and proteome signatures of morphologically normal cells bearing a single inherited hit in a tumor suppressor gene parallel many changes observed in the corresponding sporadic cancer. Here, we report on the global gene expression profile of morphologically normal, cultured primary breast epithelial and stromal cells from Li-Fraumeni syndrome (LFS) TP53 mutation carriers. Our analyses identified multiple changes in gene expression in both morphologically normal breast epithelial and stromal cells associated with TP53 haploinsufficiency, as well as interlocking pathways. Notably, a dysregulated p53 signaling pathway was readily detectable. Pharmacological intervention with the p53 rescue compounds CP-31398 and PRIMA-1 provided further evidence in support of the central role of p53 in affecting these changes in LFS cells and treatment for this cancer. Because loss of signaling mediated by TP53 is associated with the development and survival of many human tumors, identification of gene expression profiles in morphologically normal cells that carry one-hit p53 mutations may reveal novel biomarkers, enabling the discovery of potential targets for chemoprevention of sporadic tumors as well.

Publication Title

A molecular signature of normal breast epithelial and stromal cells from Li-Fraumeni syndrome mutation carriers.

Sample Metadata Fields

Specimen part

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accession-icon GSE11936
Induction of lipid oxidation gene expression by polyunsaturated fatty acids of marine origin in small intestine of mice
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Dietary polyunsaturated fatty acids (PUFA) act as potent natural hypolipidemics and are linked to many health benefits in humans and in animal models. Mice fed long-term a high fat diet, in which medium-chain alpha linoleic acid (ALA) was partially replaced by long-chain docosahexaenoic (DHA) and eicosapentaenoic (EPA) fatty acids, showed reduced accumulation of body fat and prevention of insulin resistance, besides increased mitochondrial beta-oxidation in white adipose tissue and decreased plasma lipids. ALA, EPA and DHA all belong to PUFA of n-3 series. The intestine is a gatekeeper organ for ingested lipids. To examine the potential contribution of the intestine in the beneficial effects of EPA and DHA, this study assessed gene expression changes using whole genome microarray analysis on small intestinal scrapings. The main biological process affected was lipid metabolism. Fatty acid uptake, peroxisomal and mitochondrial beta-oxidation, and omega-oxidation of fatty acids were all increased. Quantitative real time PCR and intestinal fatty acid oxidation measurements ([14C(U)]-palmitate) confirmed significant gene expression differences in a dose-dependent manner. Furthermore, no major changes in the expression of lipid metabolism genes were observed in colonic scrapings. In conclusion, we show that marine n-3 fatty acids regulate small intestinal gene expression patterns. Since this organ contributes significantly to whole organism energy use, this adaptation of the small intestine may contribute to the complex and observed beneficial physiological effects of these natural compounds under conditions that will normally lead to development of obesity and diabetes.

Publication Title

Induction of lipid oxidation by polyunsaturated fatty acids of marine origin in small intestine of mice fed a high-fat diet.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE1159
Expression profiles of acute myeloid leukemia patient samples
  • organism-icon Homo sapiens
  • sample-icon 291 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Expression profiles of acute myeloid leukemia patient samples.

Publication Title

Identification of genes with abnormal expression changes in acute myeloid leukemia.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE9476
Abnormal Expression Changes in AML
  • organism-icon Homo sapiens
  • sample-icon 64 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Acute myeloid leukemia (AML) is one of the most common and deadly forms of hematopoietic malignancies. We hypothesized that microarray studies could identify previously unrecognized expression changes that only occur only in AML blasts. We were particularly interested in those genes with increased expression in AML, believing that these genes may be potential therapeutic targets.

Publication Title

Identification of genes with abnormal expression changes in acute myeloid leukemia.

Sample Metadata Fields

Sex, Disease

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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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