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accession-icon GSE15221
Malaria primes the innate immune response due to IFNg induced enhancement of Toll-like receptor expression and function.
  • organism-icon Homo sapiens
  • sample-icon 28 Downloadable Samples
  • Technology Badge IconIllumina human-6 v2.0 expression beadchip

Description

Patients with febrile malaria were recruited in order to determine Peripheral Blood Mononuclear Cell (PBMC) gene expression during malaria. Blood was harvested from patients during the acute phase of the illness, and then patients were given a curative regimen of antimalarials. Three to four weeks after treatment, patients returned to the malaria clinic and blood was collected again, in order that each patient could serve as his or her own control. PBMC were isolated at the time of blood collection and forzen in RNA extraction buffer. At the end of the study, each patient was arrayed for ~47,000 transcripts, comparing gene expression at the end of therapy to that at the beginning. The goal was to determine which genes were altered as a result of disease at least 2 fold in a statistically significant manner and to assess if the genes involved could be related to Toll-like receptor signaling pathways. Approximately 60 genes involved in inflammation were confirmed by qPCR.

Publication Title

Malaria primes the innate immune response due to interferon-gamma induced enhancement of toll-like receptor expression and function.

Sample Metadata Fields

Sex, Age

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accession-icon GSE50794
GEMM CRC collection analysis
  • organism-icon Mus musculus
  • sample-icon 60 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

A collection of genetically engineered mouse models (GEMM) of colorectal cancer (CRC) were created, and primary tumors from these GEMMs were analyzed.

Publication Title

Cross-species analysis of genetically engineered mouse models of MAPK-driven colorectal cancer identifies hallmarks of the human disease.

Sample Metadata Fields

Specimen part

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accession-icon SRP186466
High-Fructose Corn Syrup Enhances Intestinal Tumor Growth in Mice
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Excessive consumption of beverages sweetened with high-fructose corn syrup (HFCS) is associated with obesity and with an increased risk of colorectal cancer. Whether HFCS contributes directly to tumorigenesis is unclear. We investigated the effects of daily oral administration of HFCS in APC mutant mice, which are predisposed to develop intestinal tumors. The HFCS-treated mice showed a dramatic increase in tumor size and tumor grade in the absence of obesity or metabolic syndrome. HFCS increased the levels of fructose and glucose in the intestinal lumen and serum, respectively, and the tumors absorbed both sugars. Within the tumors, fructose was converted to fructose-1-phosphate, leading to activation of glycolysis and increased synthesis of fatty acids that support tumor growth. These mouse studies support the hypothesis that the combination of dietary glucose and fructose, even at a moderate dose, can enhance tumorigenesis. Overall design: We investigated tumor and small intestines in APC mutant mice, which are predisposed to develop intestinal tumors.

Publication Title

High-fructose corn syrup enhances intestinal tumor growth in mice.

Sample Metadata Fields

Specimen part, Cell line, Treatment, Subject

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accession-icon GSE39557
Expression data from genetically engineered mouse models (GEMMs)
  • organism-icon Mus musculus
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

3 Cell lines from Apc, p53 (AP) GEMMs were compared to 12 cell lines from Apc, Kras, p53 (AKP) GEMMs.

Publication Title

Development of a colon cancer GEMM-derived orthotopic transplant model for drug discovery and validation.

Sample Metadata Fields

Sex, Cell line

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accession-icon SRP056597
High-fat diet enhances stemness and tumorigenicity of intestinal progenitors
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Little is known about how pro-obesity diets regulate tissue stem and progenitor cell function. Here we find that high fat diet (HFD)-induced obesity augments the numbers and function of Lgr5+ intestinal stem cells (ISCs) of the mammalian intestine. Like HFD, ex vivo treatment of intestinal organoid cultures with palmitic acid (PA), a constituent of the HFD, enhances the self-renewal potential of these organoid bodies. Mechanistically, HFD induces a robust peroxisome proliferator-activated receptor delta (PPAR-delta signature in intestinal stem and progenitor cells and pharmacologic activation of PPAR-delta recapitulates the effects that HFD has on these cells. Interestingly, HFD- and agonist-activated PPAR-delta signaling endows organoid-initiating capacity to non-stem cells and enforced PPAR-delta signaling permits these non-stem cells to form in vivo tumors upon loss of the tumor suppressor Apc. These findings highlight how diet-modulated PPAR-delta activation alters not only the function of intestinal stem and progenitor cells but also their capacity to initiate tumors. Overall design: mRNA profiles of intestinal stem cells (GFP-Hi) and progenitors (GFP-Low) from WT or HFD fed mice were generated by deep sequencing using HiSeq 2000.

Publication Title

High-fat diet enhances stemness and tumorigenicity of intestinal progenitors.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP093713
Transcriptome analysis of Cdc73 deletion in AML cells
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

The Polymerase Associated Factor (PAFc) complex is an epigenetic regulating complex that has been shown to to be important for Acute Myeloid Leukemias harboring an MLL chromosomal translocations, such as MLL-AF9 leukemias. This study describes the transcriptomic profiling of AML cells following genetic deletion of the PAFc subunit Cdc73. Overall design: Cdc73floxed cells were transformed to an AML using MLL-AF9 oncogene transduction. The cells were also transduced with a 4OHT inducible CreER. The cells were then treated for 24 or 48 hours with 4OHT to induce genetic excision of Cdc73 and polyA mRNA was isolated for sequencing of the transcriptome. Biological duplicates are labelled _1 and _2.

Publication Title

The PAF complex regulation of Prmt5 facilitates the progression and maintenance of MLL fusion leukemia.

Sample Metadata Fields

Cell line, Treatment, Subject, Time

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accession-icon GSE59426
Expression data from Arabidopsis wild type and ibr1 ibr3 ibr10 triple mutant seedlings root tip segments treated with indole-3-butyric acid (IBA)
  • organism-icon Arabidopsis thaliana
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

The root cap-specific conversion of the auxin precursor indole-3-butyric acid (IBA) into the main auxin indole-3-acetic acid (IAA) generates a local auxin source which subsequently modulates both the periodicity and intensity of auxin response oscillations in the root tip of Arabidopsis, and consequently fine-tunes the spatiotemporal patterning of lateral roots. To explore downstream components of this signaling process, we investigated the early transcriptional regulations happening in the root tip during IBA-to-IAA conversion in Col-0 and ibr1 ibr3 ibr10 triple mutant after 6 hours of IBA treatment.

Publication Title

Root Cap-Derived Auxin Pre-patterns the Longitudinal Axis of the Arabidopsis Root.

Sample Metadata Fields

Age, Specimen part, Treatment

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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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