Expression data from activated NK cells
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ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: martin villalba
PROVIDER: E-GEOD-50840 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:Natural Killer (NK) cells present natural cytotoxicity against tumor cells, although their activity is increased after activation. NK cell activation depends on a complex intracellular signaling process mediated by activating and inhibitory receptors and the functional outcome depends on the integration of the activating and inhibitory signals received. Soluble cytokines and/or ligands on target cells bind the NK cell receptors, and hence, influence the final NK cell response: attack versus ignorance. We used microarrays to detail the global programme of gene expression underlying NK cell activation by IL-2, a MHC-I-deficient target cell (K562)+IL-2 and an EBV-target cell (R69). PBLs from 4 different donors were activated by 100 U/ml IL-2; K562+IL-2 or R69 cells. After 5 days we obtained RNA and miRNA from naïve NK cells or from NK cells activated with the above mentioned stimuli, with more than 90% of purity. The 16 RNA samples were used to generate cDNA libraries that were hybridized on Human Gene 1.1ST arrays (Affymetrix) and analyzed with the Affymetrix Gene Chip Command Console Software v3.0 (AGCC 3.0, Affymetrix®) and the Expression Console Software v1.1 (Affymetrix®).
2014-09-09 | E-GEOD-50838 | biostudies-arrayexpress
Project description:Natural Killer (NK) cells present natural cytotoxicity against tumor cells, although their activity is increased after activation.NK cell activation depends on a complex intracellular signaling process mediated by activating and inhibitory receptors and the functional outcome depends on the integration of the activating and inhibitory signals received. Soluble cytokines and/or ligands on target cells bind the NK cell receptors, and hence, influence the final NK cell response: attack versus ignorance. We used microarrays to detail the global programme of gene expression underlying NK cell activation by IL-2, a MHC-I-deficient target cell (K562)+IL-2 and an EBV-target cell (R69). PBLs from 4 different donors were activated by 100 U/ml IL-2; K562+IL-2 or R69 cells. After 5 days we obtained RNA and miRNA from naïve NK cells or from NK cells activated with the above mentioned stimuli, with more than 90% of purity. The 16 RNA samples were used to generate cDNA libraries that were hybridized on Human Gene 1.1ST arrays (Affymetrix) and analyzed with the Affymetrix Gene Chip Command Console Software v3.0 (AGCC 3.0, Affymetrix®) and the Expression Console Software v1.1 (Affymetrix®).
2014-09-09 | E-GEOD-50839 | biostudies-arrayexpress
Project description:Background and aims: Liver transplantation (LT) is the most radical treatment for hepatocellular carcinoma (HCC) with high rates of long-term survival, but tumor recurrence after LT is an unresolved problem. The aim of our study was to identify predictive markers for tumor recurrence after liver transplantation. Methods: In a retrospective single-center study, we included all patients with LT for HCC in our institution (01/2007-12/2012). Beside demographic data, we analyzed course, bridging therapies, Serum-AFP, time point of tumor recurrence, as well as the correlation of imaging and histopathology of our recipients. Additionally, we performed a microarray analysis to identify different miRNA profiles of patients with and without HCC recurrence after LT. Single assay stem-loop real-time PCR (Q-RT-PCR) was used for validation of the results. Results: During the study period, we performed 92 LT in patients with HCC (22 women, 70 men). Twenty-two (23.9%) patients developed a recurrent HCC after LT. Our subgroup with tumor recurrence after LT, presented with a mean disease-free survival of 10 months (3-55 months) and an overall survival of 25.5 months (4-77 months). Milan criteria, AFP levels and pathologic grading had an influence on the tumor recurrence. Performing miRNA analysis, we could identify significant upregulation of 8 miRNAs and downregulation of another 5 miRNAs in patients with tumor recurrence. Consecutively, array data were successfully validated using Q-RT-PCR. Multivariate Cox regression, ROC analysis and Kaplan-Meier showed that a score consisting of two miRNAs and Milan criteria are an independent predictor for tumor recurrence-free survival. Conclusions: Despite careful selection of patients, an early recurrence of HCC after LT cannot be avoided completely. Reliable prognostic markers related to tumor biology are still missing. Analysis and validation of specific miRNAs combined with radiological parameters might lead to a promising strategy for the prediction of tumor recurrence, but prospective studies have to follow. 8 macrodissected hepatocellular carcinoma (recurrent HCC) and 10 macrodissected hepatocellular carcinoma (non-recurrent HCC).
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Project description:The human and mouse aryl hydrocarbon receptor (hAHR and mAHRb) share limited (58%) transactivation domain sequence identity. Compared to the mAHRb allele, the hAHR displays 10-fold lower relative affinity for prototypical ligands such as 2,3,7,8 tetrachlorodibenzo-p-dioxin (TCDD). However, in previous studies we have demonstrated that the hAHR can display a higher relative ligand binding affinity than the mAHRb for specific AHR ligands such as indirubin. Each receptor has also been shown to differentially recruit LXXLL co-activator-motif proteins and to utilize different TAD subdomains in gene transactivation. Using hepatocytes isolated from C57BL6/J mice (Ahrb/b) and AHRTtr transgenic mice which express hAHR protein specifically in hepatocytes, we investigated whether the hAHR and mAHRb differentially regulate genes. Microarray and quantitative-PCR analysis of Ahrb/b and AHRTtr primary-mouse hepatocytes treated with 10 nM TCDD revealed that a number of established AHR target genes such as Cyp1a1 and Cyp1b1 are significantly induced by both receptors. Remarkably, of the 1752 genes induced by mAHRb and 1186 genes induced by hAHR, only 265 genes (<10%) were significantly activated by both receptors in response to TCDD. Conversely of the 1100 and 779 genes significantly repressed in mAHRb and hAHR hepatocytes respectively, only 462 (<25%) genes were significantly repressed by both receptors in response to TCDD treatment. Genes identified as differentially expressed are known to be involved in a number of biological pathways, including cell proliferation and inflammatory response which suggests that compared to the mAHRb, the hAHR may play contrasting roles in TCDD-induced toxicity and endogenous AHR-mediated gene regulation. Experiment Overall Design: Isolated mouse hepatocytes from wild type and treated with 10nM TCDD for 6h were analyzed. 1 array per mouse (3 mice per treatment group) was used.GeneChip® Operating Software (Affymetrix) was utilized to preprocess CAB/CEL files generated from the 12 scanned microarrays which represented hepatocytes isolated from one mouse each. Data quality was initially assessed by checking the array image, B2 oligo performance, average background to noise ratios, poly-A controls, hybridization controls and the 3' to 5' probe-set ratios for control genes (e.g. Ã-actin or GAPDH). Microarray data was normalized using Probe Logarithmic Intensity Error Approximation PLIER-MM algorithm (Affymetrix Expression Console⢠Software 1.1). Normalized microarray data outputs from TCDD and control treated Ahrb/band AHRTtr hepatocytes were compared for differential expression using Significance Analysis of Microarrays (SAM, version 2.23A (Pan 2002; Tusher et al. 2001)) with 100 permutations, KNN-10.
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