E-GEOD-22973
Ontology highlight
ABSTRACT:
PROVIDER: E-GEOD-22973 | ExpressionAtlas | 2020-04-03
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-GEOD-22973-analysis-methods.tsv | Tabular | |||
| E-GEOD-22973-atlasExperimentSummary.Rdata | Rdata | |||
| E-GEOD-22973-configuration.xml | Xml | |||
| E-GEOD-22973-percentile-ranks.tsv | Tabular | |||
| E-GEOD-22973.condensed-sdrf.tsv | Tabular |
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Project description:Gene expression profiling has demonstrated clinical utility as a predictive tool in clinical oncology. We have identified genes associated with invasion of pancreatic cancer, and with potential for identifying early recurrence. We used Affymetrix Human U133 Plus 2.0 microarrays to identify specific predictive profiles in pancreatic cancer, and the evolution of gene expression. We identified distinct classes of up-regulated genes during this process. Primary and metastatic pancreatic cancer cell lines (BxPC-3 and AsPC-1), were stimulated with with phorbol-12-myristate 13-acetate (PMA), a known inducer of invasion. Affymetrix gene expression microarray analysis was performed, comparing PMA stimulated BxPC-3 and AsPC-1 gene expression to unstimulated controls, and also PMA stimulated BxPC-3 verses stimulated AsPC-1 cell lines. Differential gene expression was identified using ArrayAssist bioinformatics software. Gene expression changes were confirmed using quantitative reverse transcription polymerase chain reaction (qRT-PCR) (Assays-on-demand, Taqman, ABI systems). Pathway Assist and GOstat were used to identify pathway and gene ontology changes.
2011-01-01 | E-GEOD-22973 | biostudies-arrayexpress
Project description:To investigate gene regulation in response to T cell activation. We then performed gene expression profiling analysis using data obtained from RNA-seq of cell lines stimulated by PMA and Ionomycin.
2022-12-28 | GSE221851 | GEO
Project description:As in other tumor types, progression of pancreatic cancer may require a functionally unique population of cancer stem cells. Although such cells have been identified in many invasive cancers, is not clear whether they emerge during early or late stages of tumorigenesis. Using mouse models and human pancreatic cancer cell lines, we investigated whether pre-invasive pancreatic neoplasia contains a subpopulation of cells with distinct morphologies and cancer stem cell like properties. Whole transcriptome anlaysis of AcTub Hi vs AcTub Low cells. Cells were labeled with an acetylated alpha tubulin antibody that recognized epitopes on the cell surface (AAT+). AcTub Hi vs Low cells were FACS sorted from the human pancreatic cancer cell lines CFPAC and AsPC1
2013-11-16 | GSE52406 | GEO
Project description:As in other tumor types, progression of pancreatic cancer may require a functionally unique population of cancer stem cells. Although such cells have been identified in many invasive cancers, is not clear whether they emerge during early or late stages of tumorigenesis. Using mouse models and human pancreatic cancer cell lines, we investigated whether pre-invasive pancreatic neoplasia contains a subpopulation of cells with distinct morphologies and cancer stem cell like properties. Whole transcriptome anlaysis of AcTub Hi vs AcTub Low cells. Cells were labeled with an acetylated alpha tubulin antibody that recognized epitopes on the cell surface (AAT+). AcTub Hi vs Low cells were FACS sorted from the human pancreatic cancer cell lines CFPAC and AsPC1 CFPAC and AsPC1 cells were labeling with AcTub (acetylated alpha tubulin antibody) and then FACS sorted based on high or low levels of AcTub, and microarray analyses were run on biological replicates.
2013-11-16 | E-GEOD-52406 | biostudies-arrayexpress
Project description:The goal of this experiment is to characterize the expression of two cell-line models of monocyte to macrophage transformation, U937 and THP-1. Either PMA (phorbol myristate acetate) and LPS (lipopolysaccharide) or VD3 (vitamin D3) and LPS were used as stimuli to induce differentiation. <br>The following protocol was used for both cell-lines: Cells from single replicates were cultured in parallel. At 0 hrs, cells were split into 6 aliquots with two aliquots in each of three treatment conditions; no treatment, 2 nM PMA or 66 nM Vitamin D3. At 24 hrs, one aliquot of cells from each treatment condition was stimulated with a spike-in of LPS to a final concentration of 100 ng/mL or given an equal amount of medium as a control. 18 hrs after LPS stimulation cells were harvested. <br>This RNA-seq experiment is being carried out as part of the Open Targets project to identify a gene expression signature of common immortalized cell lines/models. This signature will be used in combination with data from ChIP-seq experiments from the same cell lines against primary cells and tissues. The overall aim of the Open Targets Cell Line Epigenome project is to establish a systematic approach for the determination of human biological and disease relevance through the generation of transcriptomic and epigenomic data in cell lines of interest. Comparison of cell line mRNA expression and epigenome data with existing and newly generated reference data from human tissue and cell types will identify assay systems that will provide greater confidence in translating target biology and compound pharmacology to patients.
2016-10-22 | E-MTAB-5191 | biostudies-arrayexpress
Project description:Expression data from pancreatic cancer cell lines and non-neoplastic pancreatic cell line HPDE To identify genes epigenetically silenced and regulated in pancreatic cancer We compared the gene expression profiles of 6 pancreatic cancer cell lines (panc215, A32-1, A38-5, panc2.5, panc2.8, and panc3.014), to the non-neoplastic pancreas cell line, HPDE. We also compared the baseline gene expression of the pancreatic cancer cell lines to expression patterns after treatment with 5-aza-dC alone, TSA alone, and to a combination of 5-aza-dC/TSA.
2010-04-14 | E-GEOD-21163 | biostudies-arrayexpress
Project description:Purpose: Majority of pancreatic cancer (PDAC) patient deaths are associated to the metastatic progression of disease. To identify novel targeted-therapies, a complete understanding of transformation in genetic landscape in tumors during disease progression is needed. Widely in use, the artificially immortalized PDAC cell lines do not rightly represent the progression because of multiple donors and disparate genetic characteristics. To identify key genes underlying the progression of PDAC from localized disease to a metastatic form, we performed whole transcriptome RNA-Sequencing analysis of cell models representing localised to metaststic stage through paired-end deep sequencing Method: Mouse expressing a Cre-activated KrasG12D allele inserted into the endogenous Kras locus, and these mice were crossed with mice expressing Cre recombinase in pancreatic tissue by virtue of a PDX-1 promoter-driven transgene. Next a cross between K-rasG12D Pdx-Cre and p16-/- mice, transgenic K-rasG12D Pdx-Cre p16-/- mice were generated harboring tissue specific mutant Kras and p16 deletion resulting in an earlier appearance of PanIN lesions followed by rapid progression into highly invasive and metastatic pancreatic cancers. Results: Transgenic K-rasG12D Pdx-Cre p16-/- mice developed spontaneous- localized, invasive and metastatic pancreatic tumors and transcriptome of these cell models representing localized, invasive and metastatic pancreatic tumors were sequenced. Conclusions: Based on genetic analysis of a same-lineage genetic background cell models, this study identifies a novel molecular pathway underlying the progression of pancreatic cancer disease. This study shows that Intestine Specific Homeobox (ISX) gene is a novel biomarker unique to pancreatic cancer progression.
2019-06-20 | GSE116635 | GEO
Project description:MicroRNAs (miRNAs) are short single-stranded RNA molecules that have a critical role in the regulation of gene expression. Alterations in miRNA expression levels have been observed in multiple tumor types and there is clear evidence on their active involvement in cancer development. Here, a comprehensive miRNA expression profiling in 16 pancreatic cancer cell lines and four normal pancreatic samples provided a specific molecular signature for pancreatic cancer and enabled us to identify 72 differentially expressed miRNAs with approximately half of them being up- and half downregulated in cancer cells as compared to normal samples. Of these, miR-31 was selected for further functional analyses based on its interesting M-bM-^@M-^\on-offM-bM-^@M-^] type expression profile, i.e. very low or even absent expression in normal pancreas and in six of the pancreatic cancer samples but extremely high expression in the remaining ten cell lines. Quite unexpectedly, both the inhibition of miR-31 in AsPC-1 and HPAF-II pancreatic cancer cells with high endogenous expression and forced expression of miR-31 in MIA PaCa-2 with low endogenous levels led to reduced cell proliferation, migration and invasion. More importantly, in AsPC-1 cells further enhancement of miR-31 also resulted in reduced cell migration and invasion, implicating that the level of miR-31 is critical for these phenotypes. We also identified novel miR-31 target genes, APBB2 and RSBN1, that might contribute to cancer pathogenesis. This study highlights a specific miRNA expression pattern in pancreatic cancer and reveals that manipulation of miR-31 expression leads to reduced cell migration and invasion in pancreatic cancer. 16 pancreatic cancer cell lines and 4 normal pancreatic RNA samples were hybridized on Agilent vs1 miRNA microarrays. Pool of four normal samples was hybridized on each slide to allow normalization between slides.
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