Microarray analysis of beta-catenin regulated target genes in SW480 colon cancer cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Michele Cleary
PROVIDER: E-GEOD-53656 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:Transforming growth factor beta receptor 2 (Tgfbr2) was predicted as a causal gene for abdominal using a novel statistical method named LCMS (Schadt et al., 2005, Nature Genetics). In order to validate this prediction, we profiled the liver tissues of Tgfbr2 heterozygous knockout mice (Tgfbr2+/-) and their littermate wild-type (wt) controls to examine the gene expression signature as well as pathways/networks resulting from the single gene perturbation. 6 Tgfbr2+/- mice and 4 wt controls were profiled. Reference pool included RNA extracted from the liver of 6 wt control mice. Dye-swap was involved in the profiling.
2009-03-07 | E-GEOD-11994 | biostudies-arrayexpress
Project description:The genetics of complex disease produce alterations in molecular interactions of cellular pathways which collective effect may become clear through the organized structure of molecular networks. To characterize molecular systems associated with late-onset Alzheimer´s disease (LOAD), we constructed gene regulatory networks in hundreds of autopsied brain tissues from LOAD patients and non-demented subjects. We demonstrate that LOAD reconfigures specific portions of the molecular interaction structure, and via an integrative network-based approach we rank ordered these sub-networks (modules) for relevance to LOAD pathology, highlighting the immune/microglia module as the top ranking. Through a Bayesian inference approach we identified multiple key causal regulators for LOAD brains. Autopsied tissues from dorsolateral prefrontal cortex (PFC), visual cortex (VC) and cerebellum (CR) in brains of LOAD patients, and non-demented healthy controls, collected through the Harvard Brain Tissue Resource Center (HBTRC), were profiled on a custom-made Agilent 44K array (GPL4372_1). All subjects were diagnosed at intake and each brain underwent extensive LOAD-related pathology examination. Gene expression analyses were adjusted for age and sex, postmortem interval (PMI) in hours, sample pH and RNA integrity number (RIN). In the overall cohort of LOAD and non-demented brains the mean ± SD for sample PMI, pH and RIN were 17.8±8.3, 6.4±0.3 and 6.8±0.8, respectively. 230 samples with all PFC, VC, and CR tissue profiled were included for further multi-tissue analysis.
2013-04-25 | E-GEOD-44768 | biostudies-arrayexpress
Project description:The genetics of complex disease produce alterations in molecular interactions of cellular pathways which collective effect may become clear through the organized structure of molecular networks. To characterize molecular systems associated with late-onset Alzheimer´s disease (LOAD), we constructed gene regulatory networks in hundreds of autopsied brain tissues from LOAD patients and non-demented subjects. We demonstrate that LOAD reconfigures specific portions of the molecular interaction structure, and via an integrative network-based approach we rank ordered these sub-networks (modules) for relevance to LOAD pathology, highlighting the immune/microglia module as the top ranking. Through a Bayesian inference approach we identified multiple key causal regulators for LOAD brains. Autopsied tissues from dorsolateral prefrontal cortex (PFC), visual cortex (VC) and cerebellum (CR) in brains of LOAD patients, and non-demented healthy controls, collected through the Harvard Brain Tissue Resource Center (HBTRC), were profiled on a custom-made Agilent 44K array (GPL4372_1). All subjects were diagnosed at intake and each brain underwent extensive LOAD-related pathology examination. Gene expression analyses were adjusted for age and sex, postmortem interval (PMI) in hours, sample pH and RNA integrity number (RIN). In the overall cohort of LOAD and non-demented brains the mean ± SD for sample PMI, pH and RIN were 17.8±8.3, 6.4±0.3 and 6.8±0.8, respectively. 230 samples with all PFC, VC, and CR tissue profiled were included for further multi-tissue analysis.
2013-04-25 | E-GEOD-44771 | biostudies-arrayexpress
Project description:The genetics of complex disease produce alterations in molecular interactions of cellular pathways which collective effect may become clear through the organized structure of molecular networks. To characterize molecular systems associated with late-onset Alzheimer´s disease (LOAD), we constructed gene regulatory networks in hundreds of autopsied brain tissues from LOAD patients and non-demented subjects. We demonstrate that LOAD reconfigures specific portions of the molecular interaction structure, and via an integrative network-based approach we rank ordered these sub-networks (modules) for relevance to LOAD pathology, highlighting the immune/microglia module as the top ranking. Through a Bayesian inference approach we identified multiple key causal regulators for LOAD brains. Autopsied tissues from dorsolateral prefrontal cortex (PFC), visual cortex (VC) and cerebellum (CR) in brains of LOAD patients, and non-demented healthy controls, collected through the Harvard Brain Tissue Resource Center (HBTRC), were profiled on a custom-made Agilent 44K array (GPL4372_1). All subjects were diagnosed at intake and each brain underwent extensive LOAD-related pathology examination. Gene expression analyses were adjusted for age and sex, postmortem interval (PMI) in hours, sample pH and RNA integrity number (RIN). In the overall cohort of LOAD and non-demented brains the mean ± SD for sample PMI, pH and RIN were 17.8±8.3, 6.4±0.3 and 6.8±0.8, respectively. 230 samples with all PFC, VC, and CR tissue profiled were included for further multi-tissue analysis.
2013-04-25 | E-GEOD-44770 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series
2013-04-25 | E-GEOD-44772 | biostudies-arrayexpress
Project description:Dissecting the shared etiology of different diseases could benefit from a systematic search for associated molecules and their interactions. We investigated genome-wide disruptions in the co-regulation of genes in two neurodegenerative diseases, Alzheimer's or Huntington's disease (AD or HD), using expression profiles from postmortem prefrontal cortex samples of 624 demented patients and non-demented control individuals with matched genotype and clinical data. A meta-analysis based screen for changes in coordinate expression patterns revealed differentially co-expressed (DC) gene pairs that either gained or lost correlation in disease cases relative to the control group, with the former being dominant for both AD and HD. Integration of disruptions common to AD and HD with large-scale data on protein-protein and protein-DNA interactions yielded a 242-gene sub-network that was enriched for proteins involved in neuronal differentiation and genetic associations to brain structural changes and dementia in subjects aged over 70 years. Replication of the AD DC network in independent human and mouse cohorts lends confidence to the comprehensive view we offer on dysregulated brain molecular pathways in AD and HD. DLPFC (BA9) brain tissues of AD patients, HD patients and non-demented controls samples were obtained from Harvard Brain tissue resource center (HBTRC). The HBTRC samples were primarily of Caucasian ancestry, as only eight non-Caucasian outliers were identified, and therefore excluded for further analysis. Post-mortem interval (PMI) was 17.8+8.3 hours (mean ± standard deviation), sample pH was 6.4±0.3 and RNA integrity number (RIN) was 6.8±0.8 for the average sample in the overall cohort. Tissues were profiled on a custom-made Agilent 44K array (GPL4372). 624 individual DLPFC samples were profiled against a common DLPFC pool constructed from the same set of samples.
2014-07-31 | E-GEOD-33000 | biostudies-arrayexpress
Project description:The incidence of esophageal and junctional adenocarcinoma has increased 6 fold in the last 30 years and 5 year survival remains less than 14%. Most patients present with advanced disease and current staging is limited in its ability to predict survival. We aimed to generate and validate a molecular prognostic signature for esophageal adenocarcinoma. Gene expression profiling was performed and the resulting signatures correlated with clinical features for 91 snap frozen esophageal and junctional resection specimens. Gene expression profiles were obtained from 76/91 of the samples (82%). 119 genes were significantly associated with survival and 270 genes with the number of involved lymph nodes. Three genes were prognostic at the protein level in the external validation dataset. This three gene signature outperformed all the pathological features at predicting survival in this independent cohort (p<0.001). Total RNA isolated from human tissue sections was used to make fluorescently labeled cRNA that was hybridized to DNA oligonucleotide. Briefly, 4 µg of total RNA was used to synthesize dsDNA through reverse transcription. cRNA was produced by in vitro transcription and labeled postsynthetically with Cy3 or Cy5. Two populations of labeled cRNA, a reference population and an experimental population, were compared with each other by competitive hybridization to microarrays. Two hybridizations were done with each cRNA sample pair using a fluorescent dye reversal strategy. Human microarrays contained oligonucleotide probes corresponding to approximately 21,000 genes. All oligonucleotide probes on the microarrays were synthesized in situ with inkjet technology (Agilent Technologies, Palo Alto, CA). After hybridization, arrays were scanned and fluorescence intensities for each probe were recorded. Ratios of transcript abundance (experimental to control) were obtained following normalization and correction of the array intensity data. Gene expression data analysis was done with the Rosetta Resolver gene expression analysis software (version 7.0, Rosetta Biosoftware, Seattle, WA).
2010-06-01 | E-GEOD-19417 | biostudies-arrayexpress
Project description:To map the genetics of gene expression in metabolically relevant tissues and investigate the diversity of expression SNPs (eSNPs) in multiple tissues from the same individual, we collected four tissues from approximately 1,000 patients undergoing Roux-en-y gastric bypass and clinical traits associated with their weight loss and co-morbidities. We then performed high-throughput genotyping and gene expression profiling and carried out a genome-wide association analyses for more than one hundred thousand gene expression traits representing four metabolically relevant tissues; liver, omental adipose, subcutaneous adipose and stomach. We successfully identified 24,531 eSNPs corresponding to ~10,000 distinct genes. This represents the greatest number of eSNPs identified to our knowledge by any study to date and the first study to identify eSNPs from stomach tissue. We then demonstrate how these eSNPs provide a high quality disease map for each tissue in morbidly obese patients to not only inform genetic associations indentified in this cohort, but in previously published genome wide association studies as well. eSNPs and gene co-expression modules identification in morbidly obese patients represent a great resource that will aid in elucidating the key networks associated with morbid obesity, response to RYGB and disease as a whole. Keywords: Tissue profiling in a human cohort. Liver tissue was collected from patients at the time of RYGB surgery at Massachusetts General Hospital between 2000 and 2007. Samples were collected in RNAlater (Ambion/Applied Biosystems), stored at -80° and shipped to Rosetta Inpharmatics Gene Expression Laboratory Seattle, WA for extraction, amplification, labeling, and microarray processing. Samples processed ranged in size from 100-200mg. Total RNA extracted from liver was converted to fluorescently labeled cRNA that was hybridized to custom 44K DNA oligonucleotide microarrays manufactured by Agilent Technologies as described previously (Hughes et al. 2001; Schadt et al. 2008). Successful gene expression profiling results were collected from 651 liver samples.
2011-04-01 | E-GEOD-24293 | biostudies-arrayexpress
Project description:To map the genetics of gene expression in metabolically relevant tissues and investigate the diversity of expression SNPs (eSNPs) in multiple tissues from the same individual, we collected four tissues from approximately 1,000 patients undergoing Roux-en-y gastric bypass and clinical traits associated with their weight loss and co-morbidities. We then performed high-throughput genotyping and gene expression profiling and carried out a genome-wide association analyses for more than one hundred thousand gene expression traits representing four metabolically relevant tissues; liver, subcutaneous adipose, omental adipose and stomach. We successfully identified 24,531 eSNPs corresponding to ~10,000 distinct genes. This represents the greatest number of eSNPs identified to our knowledge by any study to date and the first study to identify eSNPs from stomach tissue. We then demonstrate how these eSNPs provide a high quality disease map for each tissue in morbidly obese patients to not only inform genetic associations indentified in this cohort, but in previously published genome wide association studies as well. eSNPs and gene co-expression modules identification in morbidly obese patients represent a great resource that will aid in elucidating the key networks associated with morbid obesity, response to RYGB and disease as a whole. Keywords: Tissue profiling in a human cohort. Subcutaneous adipose tissue was collected from patients at the time of RYGB surgery at Massachusetts General Hospital between 2000 and 2007. Samples were collected in RNAlater (Ambion/Applied Biosystems), stored at -80° and shipped to Rosetta Inpharmatics Gene Expression Laboratory Seattle, WA for extraction, amplification, labeling, and microarray processing. Samples processed ranged in size from 100-200mg. Total RNA extracted from subcutaneous adipose was converted to fluorescently labeled cRNA that was hybridized to custom 44K DNA oligonucleotide microarrays manufactured by Agilent Technologies as described previously (Hughes et al. 2001; Schadt et al. 2008). Successful gene expression profiling results were collected from 701 subcutaneous adipose samples.
2011-04-01 | E-GEOD-24297 | biostudies-arrayexpress
Project description:To map the genetics of gene expression in metabolically relevant tissues and investigate the diversity of expression SNPs (eSNPs) in multiple tissues from the same individual, we collected four tissues from approximately 1,000 patients undergoing Roux-en-y gastric bypass and clinical traits associated with their weight loss and co-morbidities. We then performed high-throughput genotyping and gene expression profiling and carried out a genome-wide association analyses for more than one hundred thousand gene expression traits representing four metabolically relevant tissues; liver, omental adipose, subcutaneous adipose and stomach. We successfully identified 24,531 eSNPs corresponding to ~10,000 distinct genes. This represents the greatest number of eSNPs identified to our knowledge by any study to date and the first study to identify eSNPs from stomach tissue. We then demonstrate how these eSNPs provide a high quality disease map for each tissue in morbidly obese patients to not only inform genetic associations indentified in this cohort, but in previously published genome wide association studies as well. eSNPs and gene co-expression modules identification in morbidly obese patients represent a great resource that will aid in elucidating the key networks associated with morbid obesity, response to RYGB and disease as a whole. Keywords: Tissue profiling in a human cohort. Omental adipose tissue was collected from patients at the time of RYGB surgery at Massachusetts General Hospital between 2000 and 2007. Samples were collected in RNAlater (Ambion/Applied Biosystems), stored at -80° and shipped to Rosetta Inpharmatics Gene Expression Laboratory Seattle, WA for extraction, amplification, labeling, and microarray processing. Samples processed ranged in size from 100-200mg. Total RNA extracted from omental adipose was converted to fluorescently labeled cRNA that was hybridized to custom 44K DNA oligonucleotide microarrays manufactured by Agilent Technologies as described previously (Hughes et al. 2001; Schadt et al. 2008). Successful gene expression profiling results were collected from 848 omental adipose samples.
2011-04-01 | E-GEOD-24294 | biostudies-arrayexpress