This SuperSeries is composed of the SubSeries listed below.
Integrative analysis reveals relationships of genetic and epigenetic alterations in osteosarcoma.
Sex, Age, Specimen part, Cell line
View SamplesOsteosarcomas are the most common primary malignant tumours of bone, and almost all conventional osteosarcomas are high-grade tumours showing complex genomic aberrations. We have integrated genome-wide genetic and epigenetic profiles from the EuroBoNeT panel of 19 human osteosarcoma cell lines based on microarray technologies. The cell lines showed complex patterns of DNA copy number changes, where copy number gains were significantly associated with gene-rich regions of the genome and losses with gene-poor areas. Integration of the datasets showed that the mRNA levels were regulated by either alterations in DNA copy number or DNA methylation. Using a recurrence threshold of 6/19 (> 30 %) cell lines, 348 genes were identified as having alterations of two data types (gain or hypo-methylation/over-expression, loss or hyper-methylation/under-expression). These genes are involved in embryonic skeletal system development and morphogenesis, as well as remodelling of extracellular matrix. Several genes were hyper-methylated and under-expressed compared to normal osteoblasts, and expression could be reactivated by demethylation using 5-Aza-2-deoxycytidine treatment for all four genes tested. Globally, there was as expected a significant positive association between gain and over-expression, loss and under-expression as well as hyper-methylation and under-expression, but gain was also associated with hyper-methylation and under-expression, suggesting that hyper-methylation may oppose the effects of increased copy number for some genes. Integrative analysis of genome-wide genetic and epigenetic alterations identified mechanistic dependencies and relationships between DNA copy number and DNA methylation in terms of regulating mRNA expression levels in osteosarcomas, contributing to better understanding of osteosarcoma biology.
Integrative analysis reveals relationships of genetic and epigenetic alterations in osteosarcoma.
Sex, Specimen part, Cell line
View SamplesAs part of a genomic profiling study of CRCs with MSI, we have performed genome-wide expression analyses of a consecutive patient series.
Multilevel genomics of colorectal cancers with microsatellite instability-clinical impact of JAK1 mutations and consensus molecular subtype 1.
Specimen part
View SamplesDiarrhea remains a major cause of death in children. Current diagnostic methods largely rely on stool culture and suffer from low sensitivity and inadequate specificity, often leading to inappropriate treatment. The objective of the present study was to use RNA sequencing (RNAseq) analysis to determine blood transcriptional profiles specific for several common pathogenic bacteria and viruses that cause diarrhea in children. We collected whole blood samples from children in Mexico having diarrhea associated with a single pathogen and without systemic complications. Our RNAseq data suggested that the blood signatures can differentiate children with diarrhea from healthy children either with or without bacterial colonization. Moreover, we detected different expression profiles from bacterial and viral infection, demonstrating for the first time the use of RNAseq to identify the etiology of infectious diarrhea. Overall design: 255 whole blood samples from 246 children including children with diarrhea caused by rotavirus (n=60 total; 5 repeated; 55 unique), E.coli (n=55), Salmonella (n=36), Shigella (n=37), adenovirus (n=8), norovirus (n=7), and control children (n=52 total; 4 repeated; 48 unique).
Shared and organism-specific host responses to childhood diarrheal diseases revealed by whole blood transcript profiling.
No sample metadata fields
View SamplesCo-expression of genes that physically cluster together is a common characteristic of eukaryotic transcriptomes. Identifying these groups of co-expressed genes is important to the functional annotation of genomes and understanding the evolutionary fates of the clustered genes.
Coordinated evolution of co-expressed gene clusters in the Drosophila transcriptome.
No sample metadata fields
View SamplesThe transcription factor Snail has been proposed to mediate epithelial-to-mesenchymal transition (EMT) and confer mesenchymal invasive phenotype to epithelial cancer cells
SNAIL-induced epithelial-to-mesenchymal transition produces concerted biophysical changes from altered cytoskeletal gene expression.
Specimen part, Cell line
View SamplesIncreasing evidence supports the existence of a subpopulation of cancer cells capable of self-renewal and differentiation into diverse cell lineages. These cancer stem-like or cancer-initiating cells (CICs) also demonstrate resistance to chemo- and radiotherapy and may function as a primary source of cancer recurrence. We report here on the isolation and in vitro propagation of multicellular ovarian cancer spheroids from a well-established ovarian cancer cell line (OVCAR-3). The spheroid-derived cells (SDCs) display self-renewal potential, the ability to produce differentiated progeny, and increased expression of genes previously associated with CICs. SDCs also demonstrate higher invasiveness, migration potential, and enhanced resistance to standard anticancer agents relative to parental OVCAR-3 cells. Furthermore, SDCs display up-regulation of genes associated with epithelial-to-mesenchymal transition (EMT), anticancer drug resistance and/or decreased susceptibility to apoptosis, as well as, down-regulation of genes typically associated with the epithelial cell phenotype and pro-apoptotic genes. Pathway and biological process enrichment analyses indicate significant differences between the SDCs and precursor OVCAR-3 cells in TGF-beta-dependent induction of EMT, regulation of lipid metabolism, NOTCH and Hedgehog signaling. Collectively, our results indicate that these SDCs will be a useful model for the study of ovarian CICs and for the development of novel CIC-targeted therapies.
Isolation and characterization of stem-like cells from a human ovarian cancer cell line.
Cell line
View SamplesPurpose: To identify the impact of 2''-FL supplementation on adaptive response following extensive intestinal resection. Methods: Transcriptomic profiles were obtained from mice undergoing ileocecal recection (8-10 week old male mice) and again at 8 weeks post-surgery. At the time of resection and again at 8 weeks post-op, small bowel samples were obtained from treatment and control animals and submitted for mRNA profiling. During these 8 weeks treatment animals (n=3) received 2''-FL supplementationion while controls (n=3) received only standard diet. Results: We observe enrichment in genes and pathways related to anti-microbial peptides, metabolism, and energy processing. Supplementation of 2''-FL increases energy availability and enhances the adaptive response. Overall design: Male C57BL/6 mice at 8 to 10 weeks of age were submitted to ileocecal recection. Following resection, half were supplemented with 2''-FL for 8 weeks; small bowels were obtained and submitted for mRNA profiling,
The human milk oligosaccharide 2'-fucosyllactose augments the adaptive response to extensive intestinal.
Sex, Specimen part, Cell line, Subject
View SamplesMicroarray analysis and quantitative real-time PCR revealed that TB40E infection of DCs led to changes of the gene expression pattern. A variety of pro-inflammatory cytokines and chemokines (CXCL10, CXCL11, CCL5), TLR3 and genes whose products function downstream of the TLR3 signalling pathway (e.g. IFN-, IFN-) were significantly upregulated.
Toll-like receptor 3 has no critical role during early immune response of human monocyte-derived dendritic cells after infection with the human cytomegalovirus strain TB40E.
Specimen part
View SamplesCoMet, a fully automated Computational Metabolomics method to predict changes in metabolite levels in cancer cells compared to normal references has been developed and applied to Jurkat T leukemia cells with the goal of testing the following hypothesis: up or down regulation in cancer cells of the expression of genes encoding for metabolic enzymes leads to changes in intracellular metabolite concentrations that contribute to disease progression. Nine metabolites predicted to be lowered in Jurkat cells with respect to normal lymphoblasts were examined: riboflavin, tryptamine, 3-sulfino-L-alanine, menaquinone, dehydroepiandrosterone, -hydroxystearic acid, hydroxyacetone, seleno-L-methionine and 5,6-dimethylbenzimidazole. All, alone or in combination, exhibited antiproliferative activity. Of eleven metabolites predicted to be increased or unchanged in Jurkat cells, only two (bilirubin and androsterone) exhibited significant antiproliferative activity. These results suggest that cancer cell metabolism may be regulated to reduce the intracellular concentration of certain antiproliferative metabolites, resulting in uninhibited cellular growth and have the implication that many other endogenous metabolites with important roles in carcinogenesis are awaiting discovery.
Identification of metabolites with anticancer properties by computational metabolomics.
No sample metadata fields
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