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GSE15766
Sus scrofa
5 Downloadable Samples
Affymetrix Porcine Genome Array (porcine)
Description
Anaplasma phagocytophilum infects a wide variety of host species and causes the diseases granulocytic anaplasmosis in humans, horses and dogs and tick-borne fever in ruminants. The objective of this research was to characterize differential gene expression in wild boar naturally infected with A. phagocytophilum by microarray hybridization using the GeneChip Porcine Genome Array
Publication Title
Gene expression profile suggests that pigs (Sus scrofa) are susceptible to Anaplasma phagocytophilum but control infection.
Sample Metadata Fields
Specimen part, Disease, Disease stage
View Samples- Homo sapiens
- 51 Downloadable Samples
- Affymetrix Human Exon 1.0 ST Array [probe set (exon) version (huex10st), Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)
Description
Limited access to large samples and independent replication cohorts precludes genome-wide association (GWA) studies of rare but complex traits. To localize candidate genes in an on-going study utilizing family-based GWA, a novel exploratory analysis was first tested on 1,774 major histocompatibility complex single nucleotide polymorphisms (SNPs) in 240 DNA samples from 80 children with primary liver transplantation (LTx), and their biological parents. Genotyping was performed using the Illumina HumHap550k SNP BeadArray; the genotype calls for the 1813 SNPs in the MHC region are provided in the genotype_data.zip supplementary file linked to this series (see README file in the zip archive for more information).
Publication Title
Genetic variants in major histocompatibility complex-linked genes associate with pediatric liver transplant rejection.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 26 Downloadable Samples
- Affymetrix Human Exon 1.0 ST Array [probe set (exon) version (huex10st)
Description
The Affymetrix Human Exon 1.0 ST array was used to measure differential splicing patterns in archived RNA isolated from 26 of 80 children (11 Rejectors and 15 Non-Rejectors). The exon-level probe summaries reported in this series were computed using the Affymetrix Power Tools (APT) software and 'rma-sketch' normalization method.
Publication Title
Genetic variants in major histocompatibility complex-linked genes associate with pediatric liver transplant rejection.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 25 Downloadable Samples
Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)
Description
The Affymetrix Human Exon 1.0 ST array was used to measure differential splicing patterns in archived RNA isolated from 26 of 80 children (11 Rejectors and 15 Non-Rejectors). The gene-level probe summaries reported in this series were computed using the Affymetrix Power Tools (APT) software and 'rma-sketch' normalization method.
Publication Title
Genetic variants in major histocompatibility complex-linked genes associate with pediatric liver transplant rejection.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 132 Downloadable Samples
- Affymetrix Human Genome U219 Array (hgu219)
Description
A cross sectional study using data collected at the time of liver biopsy, the final eligibility assessment for participation in iWITH (NCT01638559), an immunosuppression withdrawal trial.
Publication Title
Evidence of Chronic Allograft Injury in Liver Biopsies From Long-term Pediatric Recipients of Liver Transplants.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 6 Downloadable Samples
IlluminaGenomeAnalyzerIIx
Description
Choline kinase alpha (CHKA) plays a crucial role in the regulation of membrane phospholipid synthesis and has oncogenic properties in vitro. We have analyzed the expression of CHKA in cell lines derived from pancreatic ductal adenocarcinoma (PDAC) and have found increased CHKA expression and a good correlation between protein expression and sensitivity to MN58b, a CHKA inhibitor that reduced cell growth through the induction of apoptosis. Accordingly, CHKA knockdown led to reduced drug sensitivity. In addition, we found that gemcitabine-resistant PDAC cells displayed enhanced sensitivity to CHKA inhibition and, in vitro, MN58b had synergistic effects with gemcitabine, 5-fluorouracil and oxaliplatin, three active drugs in the treatment of PDAC. Using tissue microarrays, CHKA was found to be overexpressed in 90% of pancreatic tumors. While cytoplasmic CHKA did not relate to survival, nuclear CHKA distribution was observed in 43% of samples and was associated with survival, especially among patients with well/moderately differentiated tumors. To identify the mechanisms involved in resistance to CHKA inhibitors, we cultured IMIM-PC-2 cells with continuous incremental concentrations of MN58b and isolated a subline with a 30-fold higher IC50. RNA-Seq analysis identified up-regulation of ABCB1 and ABCB4 multidrug resistance transporters and functional studies confirmed that their up-regulation is the main mechanism involved in resistance. Overall, our findings support the notion that CHKA inhibition merits further attention as a therapeutic option in patients with PDAC. Overall design: RNA profile from parental and MN58b-resistant IMIM-PC-2 were generated by deep sequencing were done in triplicates using illumina GAIIx
Publication Title
Choline Kinase Alpha (CHKα) as a Therapeutic Target in Pancreatic Ductal Adenocarcinoma: Expression, Predictive Value, and Sensitivity to Inhibitors.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 6 Downloadable Samples
- Illumina Genome Analyzer IIx
Description
Choline kinase a (CHKa) plays a crucial role in the regulation of membrane phospholipid synthesis and has oncogenic properties in vitro. We have analyzed the expression of CHKa in cell lines derived from pancreatic ductal adenocarcinoma (PDAC) and have found increased CHKa expression, associated with differentiation. CHKa protein expression was directly correlated with sensitivity to MN58b, a CHKa inhibitor that reduced cell growth through the induction of apoptosis. Accordingly, CHKa knockdown led to reduced drug sensitivity. In addition, we found that gemcitabine-resistant PDAC cells displayed enhanced sensitivity to CHKa inhibition and, in vitro, MN58b had additive or synergistic effects with gemcitabine, 5-fluorouracil, and oxaliplatin, three active drugs in the treatment of PDAC. Using tissue microarrays, CHKa was found to be overexpressed in 90% of pancreatic tumors. While cytoplasmic CHKa did not relate to survival, nuclear CHKa distribution was observed in 43% of samples and was associated with longer survival, especially among patients with well/moderately differentiated tumors. To identify the mechanisms involved in resistance to CHKa inhibitors, we cultured IMIM-PC-2 cells with increasingly higher concentrations of MN58b and isolated a subline with a 30-fold higher IC50. RNA-Seq analysis identified upregulation of ABCB1 and ABCB4 multidrug resistance transporters, and functional studies confirmed that their upregulation is the main mechanism involved in resistance. Overall, our findings support the notion that CHKa inhibition merits further attention as a therapeutic option in patients with PDAC and that expression levels may predict response. Overall design: RNAseq from parental (IMIM-PC2 cell line)) and MN58b-resistant cells by triplicate
Publication Title
Choline Kinase Alpha (CHKα) as a Therapeutic Target in Pancreatic Ductal Adenocarcinoma: Expression, Predictive Value, and Sensitivity to Inhibitors.
Sample Metadata Fields
Sex, Specimen part, Cell line, Subject
View Samples- Homo sapiens
- 10 Downloadable Samples
- Affymetrix Human Gene 2.0 ST Array (hugene20st)
Description
We examined the biological effects of a potent second-generation proteasome inhibitor, ixazomib, in T-cell lymphoma and Hodgkin lymphoma cell lines and human xenograft models. Ixazomib resulted in time- and dose-dependent cytotoxicity and apoptosis in all cell lines (IC50s <75nM). In vivo studies via SCID tumor xenografts showed significant inhibition of tumor growth (P<0.001) with significantly improved survival (P<0.001) in Jurkat and L540 models with ixazomib-treated mice versus controls. Through global transcriptome and network analyses, ixazomib-treated Jurkat and L540 cells showed significant overlap in biological functions involved in regulation of cell cycle, chromatin modification, and DNA repair processes with a lack of conservation observed in a relatively ixazomib-resistant cell line, L428. Moreover, the predicted activation and inhibition status of tumor suppressors and oncogenes strongly favored ixazomib inhibition of tumor progression. Most notably, ixazomib down-regulated protein levels of MYC and its target genes. Additionally, chromatin immunoprecipitation showed that histone H3 acetylation affected MYC levels and cell death response to ixazomib. Furthermore, inhibition of MYC with JQ1 resulted in synergistic cell death in L428, which was confirmed utilizing MYC knockout. Collectively, ixazomib down-regulated MYC and downstream substrates in TCL and HL, while resistance appeared mediated through MYC- and CHK1-dependent mechanisms.
Publication Title
Proteasomal Inhibition by Ixazomib Induces CHK1 and MYC-Dependent Cell Death in T-cell and Hodgkin Lymphoma.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Mus musculus
- 8 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
The adult human lung has a very limited capacity to regenerate functional alveoli. In contrast, adult mice have a remarkable capacity for neoalveolarization following either lung resection or injury. The molecular basis for this unique capability to regenerate lung tissue in mice is largely unknown. We examined the transcriptomic responses to single lung pneumonectomy in adult mice in order to elucidate prospective molecular signaling used in this species during lung regeneration. Unilateral left pneumonectomy or sham thoracotomy was performed under general anesthesia (n = 8 mice per group for each of the four time points). Total RNA was isolated from the remaining lung tissue at four time points post-surgery (6 hours, 1 day, 3 days, 7 days) and analyzed using microarray technology. The observed transcriptomic patterns revealed mesenchymal cell signaling, including up-regulation of genes previously associated with activated fibroblasts (Tnfrsf12a, Tnc, Eln, Col3A1), as well as modulation of Igf1-mediated signaling. The data set also revealed early down-regulation of pro-inflammatory cytokine transcripts, up-regulation of genes involved in T cell development and function, but few similarities to transcriptomic patterns observed during embryonic or post-natal lung development. Immunohistochemical analysis suggests that early fibroblast but not myofibroblast proliferation is important during lung regeneration and may explain the preponderance of mesenchymal-associated genes that are over-expressed in this model. This appears to differ from embryonic alveologenesis. These data suggest that modulation of mesenchymal cell signaling and proliferation may act in concert with immunomodulation to control inflammation during post-pneumonectomy lung regeneration in adult mice.
Publication Title
Global gene expression patterns in the post-pneumonectomy lung of adult mice.
Sample Metadata Fields
Sex, Treatment, Time
View Samples- Homo sapiens
- 12 Downloadable Samples
- Illumina human-6 v2.0 expression beadchip
Description
Employing MCT-1 oncogene mediated transformation of immortalized breast epithelial MCF10A cells; we characterized the largely reciprocal association of these two RBPs with target mRNAs and their influence on protein expression vis--vis cellular transformation. Using a ribonomics approach, we identified mRNAs from cancer-related pathways whose association with AUF1 and/or HuR were altered when comparing immortalized with transformed MCF10A cells.
Publication Title
Identification of transformation-related pathways in a breast epithelial cell model using a ribonomics approach.
Sample Metadata Fields
No sample metadata fields
View Samples