Expression data from peripheral blood in pancreatic ductal adenocarcinoma (PDAC) patients
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Octavio Caba
PROVIDER: E-GEOD-49641 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:Analysis of expression profile of peripheral blood from pancreatic ductal adenocarcinoma patients RNA expression profile of peripheral blood from pancreatic ductal adenocarcinoma patients Total RNA was isolated from peripheral blood. 36 patients with unresectable PDAC were recruited. The diagnosis of PDAC was based on clinical evaluation and imaging studies, which were histologically confirmed by surgery or imaging-guided biopsy. 14 gender, age, and habits matched healthy controls were also included. A total of 1000 ng of total RNA was processed using Illumina TotalPrep RNA Amplification Kit. Hybridization of human samples was performed on Illumina Human-HT12 Version 4.
2015-11-04 | E-GEOD-74629 | biostudies-arrayexpress
Project description:CLP1 was the first mammalian RNA kinase to be identified. However, determining its in vivo function has been elusive. Here we generated kinase-dead Clp1 (Clp1K/K) mice that show a progressive loss of spinal motor neurons associated with axonal degeneration in the peripheral nerves and denervation of neuromuscular junctions, resulting in impaired motor function, muscle weakness, paralysis and fatal respiratory failure. Transgenic rescue experiments show that CLP1 functions in motor neurons. Mechanistically, loss of CLP1 activity results in accumulation of a novel set of small RNA fragments, derived from aberrant processing of tyrosine pre-transfer RNA. These tRNA fragments sensitize cells to oxidative-stress-induced p53 (also known as TRP53) activation and p53-dependent cell death. Genetic inactivation of p53 rescues Clp1K/K mice from the motor neuron loss, muscle denervation and respiratory failure. Our experiments uncover a mechanistic link between tRNA processing, formation of a new RNA species and progressive loss of lower motor neurons regulated by p53. RNA was extracted from spinal cord of 3 Clp1 knock-out mice and 3 wild type mice (15 days old, male, all samples age and sex matched) and submitted to differential splicing analysis using Affymetrix Exon microarrays. Differential splicing analysis was performed between the Clp1 KO and WT samles employing a custom CDF, that was based on a complete re-alignment of oligonucleotide probes to the genome and transcriptome (Ensembl 52, ASTD 1.1; further information on http://bioinfo.i-med.ac.at).
2013-03-12 | E-GEOD-35924 | biostudies-arrayexpress
Project description:Glucocorticoids (GC) are pivotal in the treatment of childhood acute lymphoblastic leukaemia (ALL) but resistance is a continuing clinical problem with the underlying mechanisms still unclear. An isobaric tag proteomic approach was used to compare protein profiles of the B lineage ALL GC-sensitive cell line, PreB 697, and its GC-resistant sub-line, R3F9, before and after dexamethasone exposure. Two transcription factors involved in B- cell differentiation, PAX5 and IRF4, were differentially regulated in the PreB 697 compared to the R3F9 cell line in response to GC. PAX5 basal protein expression was less in R3F9 compared to its GC-sensitive parent and was confirmed to be lower in other GC-resistant sub-lines of Pre B697 and was associated with a decreased expression of the PAX5 transcriptional target, CD19. Gene set enrichment analysis of microarray data from the cell lines showed that increasing GC-resistance was associated with differentiation from preB-II to an immature B-lymphocytes stage. GC resistant sub lines were shown to have a higher levels of p-JNK compared to the parent line and JNK inhibition caused re-sensitisation to GC. Reduced CD19 levels accompanying GC resistance was also apparent in some clinical samples, with high levels of MRD persisting after GC containing induction chemotherapy. Thus, quantitative proteomic analysis reveals a role for PAX5 and maturation as a recurrent mechanism underlying glucocorticoid resistance in ALL and identifies JNK inhibitors as a possible re-sensitising therapy. Gene expresion profiling of GC-sensitive and resistant precursor B-ALL cells. Gene set enrichment analysis (GSEA) was used to analyse the state of differentiation of GC-resistant sub-lines and genes were ranked according to the correlation of gene expression with dexamethasone IC50 values for the individual sub-lines.
2015-09-02 | E-GEOD-63335 | biostudies-arrayexpress
Project description:Deregulation of cytokine- and growth factor signaling due to altered expression of endogenous regulators is well recognized in prostate and other cancers. Suppressor of cytokine signaling 2 (SOCS2) is a key regulator of growth hormone, IGF and prolactin signaling, that have been implicated in carcinogenesis. In this study we elucidate expression pattern and functional significance of SOCS2 in prostate cancer (PCa). Protein expression analysis employing tissue microarrays from two independent patient cohorts revealed significantly enhanced expression in tumor compared to benign tissue as well as association with Gleason score and disease progression. In vitro and in vivo assays uncovered the involvement of SOCS2 in the regulation of cell growth and apoptosis. Functionally, SOCS2 knockdown inhibited prostate cancer cell proliferation and xenograft growth in a CAM assay. Decreased cell growth after SOCS2 downregulation was associated with cell-cycle arrest and apoptosis. In addition, we prove for the first time that SOCS2 expression is significantly elevated upon androgenic stimulation in androgen receptor-positive cell lines, providing a possible mechanistic explanation for high SOCS2 levels in PCa tissue. Consequently, SOCS2 expression correlated with androgen receptor expression in malignant tissue of patients. Taken together, our study linked increased SOCS2 expression in PCa with a pro-proliferative role in vitro and in vivo. Prostate cancer cell lines LNCaP, DUCaP and VCaP cells were cultured in the absence or presence of R1881, an androgen in three independent experiments. Differential gene expression was determined by comparing R1881 treated samples with the corresponding controls (EtOH treated samples).
2013-12-03 | E-GEOD-50936 | biostudies-arrayexpress
Project description:The presence of some malignancies, such as cancer, impacts on peripheral blood mononuclear cells (PBMCs) gene expression profiling, suggesting the potential suitability of these genes as diagnostic and prognostic markers. The objective of this study was to identify new markers in peripheral blood that differentiate between PDAC patients and healthy controls as a means of facilitating fast detection of the disease.
2013-08-12 | GSE49641 | GEO
Project description:Transcriptomic profiling of peripheral immune cells can provide a wealth of information. Classical CD14++ CD16- monocytes were isolated from the peripheral blood of healthy volunteers and patients with pancreatic ductal adenocarcinoma and profiled for differential gene expression using Affymetrix human Genechips 2.1 U133. Differentially expressed genes were identified comparing gene expression profiles between healthy and PDAC.
2015-08-21 | E-GEOD-60601 | biostudies-arrayexpress
Project description:Glucocorticoids (GCs) are a central component in treating childhood acute lymphoblastic leukemia (chALL). They mainly act via regulating gene transcription. However, control of mRNA translation by GC has never been assessed systematically. In our research, T- and precursor B-ALL cells were cultured with and without GC for 6 hours and subjected to translational profiling, a technique combining sucrose gradient fractionation and microarray analysis of mRNA in different fractions. Analysis of GC regulation in different pools revealed no significant differences in regulation of mRNA translation by GC, suggesting no evidence for translational regulation by GC. Ribosome profiling by sucrose gradient fractionation followed by microarray analysis of RNA from 3 distinct pools representing free RNA (pool 1), RNA in small protein-RNA complexes or bound to single ribosomes (pool 2) and RNA from large protein-RNA complexes (polysomes, pool 3). See Material and Methods of the original article for a detailed description. Translational efficiency of genes was estimated by comparing the amount of a gene's mRNA in pool 3 with the total amount of mRNA of the gene (in all 3 pools). Translational regulation by GC was estimated by contrasting gene regulations in pool 3 with gene regulation between GC-treated and control samples in all 3 pools (depicted as transcriptional regulation). Moderated t-tests were used to assess significance for translational regulation.
2013-12-03 | E-GEOD-48680 | biostudies-arrayexpress
Project description:Background: The Epithelial Cell Adhesion Molecule (EpCAM) has been shown to be strongly expressed in human breast cancer and cancer stem cells and its overexpression has been supposed to support tumor progression and metastasis. However, effects of EpCAM overexpression on normal breast epithelial cells have never been studied before. Therefore, we analyzed effects of transient adenoviral overexpression of EpCAM on proliferation, migration and differentiation of primary human mammary epithelial cells (HMECs). METHODS: HMECs were transfected by an adenoviral system for transient overexpression of EpCAM. Thereafter, changes in cell proliferation and migration were studied using a real time measurement system. Target gene expression was evaluated by transcriptome analysis in proliferating and polarized HMEC cultures. A Chicken Chorioallantoic Membrane (CAM) xenograft model was used to study effects on in vivo growth of HMECs. RESULTS: EpCAM overexpression in HMECs did not significantly alter gene expression profile of proliferating or growth arrested cells. Proliferating HMECs displayed predominantly glycosylated EpCAM isoforms and were inhibited in cell proliferation and migration by upregulation of p27KIP1 and p53. HMECs with overexpression of EpCAM showed a down regulation of E-cadherin. Moreover, cells were more resistant to TGF-beta1 induced growth arrest and maintained longer capacities to proliferate in vitro. EpCAM overexpressing HMECs xenografts in chicken embryos showed hyperplastic growth, lack of lumen formation and increased infiltrates of the chicken leukocytes. CONCLUSIONS: EpCAM revealed oncogenic features in normal human breast cells by, inducing resistance to TGF-beta1-mediated growth arrest and supporting a cell phenotype with longer proliferative capacities in vitro. EpCAM overexpression resulted in hyperplastic growth in vivo. Thus, we suggest that EpCAM acts as a prosurvival factor counteracting terminal differentiation processes in normal mammary glands. For each gene a representative transcript probe set was selected based on a score that combines average expression and variation of expression across all samples. Transcript probe sets with more than 4 probes were preferred. Differential expression analysis between EPCAM over-expressing and control cells (expressing GFP) was performed using a paired moderated t-test employing functions provided by Bioconductor's limma package. p-values were subsequently adjusted for multiple hypothesis testing using the method from Benjamini and Hochberg for a strong control of the false discovery rate.
2013-06-20 | E-GEOD-37172 | biostudies-arrayexpress
Project description:Extracellular vesicles (EVs) are produced and released by both healthy and malignant cells and bear markers indicative of ongoing biological processes. In the present study we utilized high resolution flow cytometry to detect EVs in the plasma of patients with pancreatic ductal adenocarcinoma (PDAC) and in the supernatants of PDAC and healthy control (HC) pancreatic organoid cultures. Using ultrafiltration and size exclusion chromatography, PDAC and HC pancreatic organoid EVs were isolated for mass spectrometry analysis. Proteomic and functional analysis showed a striking distinction in that EV proteins profiled in pancreatic cancer organoids were involved in vesicular transport and tumorigenesis while EV proteins in healthy organoids were involved in cellular homeostasis. Thus, the most abundant proteins identified in either case represented non-overlapping cellular programs. Tumor-promoting candidates LAMA5, SCDB1 and TENA were consistently upregulated in PDAC EVs. Validation of specific markers for PDAC EVs versus healthy pancreatic EVs will provide the biomarkers and enhanced sensitivity necessary to monitor early disease or disease progression, with or without treatment. Moreover, disease-associated changes in EV protein profiles provide an opportunity to investigate alterations in cellular programming with disease progression.
2022-04-04 | PXD030325 | Pride
Project description:We employed high-throughput gene expression profiling to understand gene expression differences between habits-associated tongue cancers and non-habits tongue cancers. Expression data from 22 tumors were used to identify a set of 18 differentially expressed genes that can, with high precision, distinguish the two etiologically diverse oral tumors. Results from the study provide insights into molecular carcinogenesis of tongue cancers without a history of tobacco and alcohol use. We used RNA from 22 samples that included 10 tumor biopsies from habits-associated cancers and 12 from non-habits associated cancers.
2013-11-05 | E-GEOD-42023 | biostudies-arrayexpress