Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Cancer Outlier Gene Profile Sets Elucidate Pathways and Patient-Specific Targets in Head and Neck Squamous Cell Carcinoma [Affymetrix HuEx1.0]

ABSTRACT: This study integrated Affymetrix SNPchip data for CNV estimation, Affymetrix HuEx1.0 data for gene expression estimation, and Illumina HumanMethylation27k BeadChip data for promoter methylation to estimate pathway activity Case:Control with HNSCC tumors and uvulopalatopharyngoplasty (UPPP) samples

ORGANISM(S): Homo sapiens

SUBMITTER: Michael Ochs

PROVIDER: E-GEOD-33205 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Cancer Outlier Gene Profile Sets Elucidate Pathways and Patient-Specific Targets in Head and Neck Squamous Cell Carcinoma

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-01-01 | E-GEOD-33232 | biostudies-arrayexpress

ZNF-mediated resistance to imatinib mesylate in gastrointestinal stromal tumor

Project description:siRNA knock-down of ZNF genes determined to impact gastrointestinal stromal tumor response to imatinib were used to determine functional significance of ZNFs and identify key targets related to imatinib resistance. exploratory array design to identify candidate effector genes for targeted study

2013-08-01 | E-GEOD-40080 | biostudies-arrayexpress

Gene expression from human B-lymphocytes (P493-6)

Project description:P493-6 contain a tet repressible MYC contruct. In the presense of tetracycline, MYC levels are great reduced and the cells cease to cycle. Gene expression was compared between high and low MYC expressing cells P493-6 cells were grown in both the presence and absence of tetracycline. RNA was extracted and gene expression analysis was performed using exon arrays

2011-09-18 | E-GEOD-32219 | biostudies-arrayexpress

Expression profile of melanoma cells following p300 HAT inhibition

Project description:Epigenetic events, including covalent post-translational modification of histones, have frequently been demonstrated to play critical roles in tumor development and progression. The transcriptional coactivator, p300/CBP, possesses both histone acetyltransferase (HAT) activity as well as scaffolding properties that directly influence transcriptional activation of targeted genes. We have used a recently reported small molecule inhibitor of p300 HAT activity, C646, to explore the specific contribution of p300/CBP HAT activity to tumor development and progression. We find that C646 inhibits the growth of lineage-specific tumor cell lines including human melanomas through direct transcriptional regulation of cell cycle regulatory proteins. Further evaluation of the p300 HAT transcriptome in human melanoma cells using comprehensive gene expression profiling reveals that p300 HAT activity globally promotes cell cycle progression, nucleosome assembly, and the DNA damage checkpoint through direct transcriptional regulatory mechanisms. Additionally, C646 promotes sensitivity to DNA damaging agents leading to enhanced apoptosis of melanoma cells following combination treatment with cisplatin. Together our data suggest that p300 HAT activity regulates critical growth regulatory pathways in tumors and may serve as a novel therapeutic target for melanoma and other malignancies by promoting cellular responses to DNA damaging agents. Keywords: p300, small molecule inhibitor, melanoma WM35 cells grown under normal culture conditions were treated for 6 and 24 hours with compound C646 to block p300 HAT activity. A vehicle control (DMSO) was included at each time point. RNA was extracted from all 4 samples using the Qiagen RNeasy kit. RNA quality check, labeling, hybridization, initial data processing and analysis was performed by the JHMI Microarray Core Facility. Affymetrix GeneChip Human Exon 1.0 ST Array was used for this study.

2013-08-01 | E-GEOD-45981 | biostudies-arrayexpress

miR-182 is Overexpressed in Head and Neck Squamous Cell Carcinomas Leading to Downregulation of Specific Transcripts

Project description:This study correlated miR expression with predicted targets to determine those miRs that both downregulated a subset of their predicted targets and showed differential expression in cancer samples compared to controls Case: Control with HNSCC tumors and uvulopalatopharyngoplasty (UPPP) samples

2013-01-01 | E-GEOD-34496 | biostudies-arrayexpress

Cancer Outlier Gene Profile Sets Elucidate Pathways and Patient-Specific Targets in Head and Neck Squamous Cell Carcinoma [Affymetrix SNP6]

Project description:This study integrated Affymetrix SNPchip data for CNV estimation, Affymetrix HuEx1.0 data for gene expression estimation, and Illumina HumanMethylation27k BeadChip data for promoter methylation to estimate pathway activity. Case:Control with HNSCC tumors and uvulopalatopharyngoplasty (UPPP) samples

2013-01-01 | E-GEOD-33229 | biostudies-arrayexpress

ECS-induced gene expression changes in mouse dentate gyrus

Project description:Neuronal activity-dependent gene expression plays important roles in neural plasticity. We use electroconvulsive stimulation (ECS) as an in vivo model for neuronal activation to identify genes that are regulated by neuronal activity. Dentate gyri (DG) were microdissected 4 hours after sham or ECS treatment for gene expression profiling. 4 total samples were analysed (2 for each condition). Averaged expression values between sham and ECS samples were pair-wise compared.

2011-08-31 | E-GEOD-30493 | biostudies-arrayexpress

Effect of myotonic dystrophy on pre-mRNA alternative splicing in skeletal muscle

Project description:Misregulated alternative splicing appears to be a major factor in the pathogenesis of myotonic dystrophy. The present study was done to further explore alternative splicing in this condition by doing exon-level analysis of mRNA from skeletal muscle of 8 subjects with type 1 myotonic dystrophy, 7 subjects with type 2 myotonic dystrophy, 8 disease controls (subjects with facioscapulohumeral muscular dystrophy), and 8 healthy controls . The ratios of signals from the various exons of a gene provided an index of altered exon inclusion/exclusion that was independent of the overall expression of that gene. There were numerous transcripts for which there was evidence of abnormal alternative splicing in subjects with myotonic dystrophy. For many of these transcripts, the abnormal splicing was confirmed by an independent RT-PCR approach. 31 subjects, one sample per subject, four groups: healthy subjects (n = 8), facioscapulohumeral dystrophy (n = 8), type 1 myotonic dystrophy (n = 8), type 2 myotonic dystrophy (n = 7)

2013-06-15 | E-GEOD-47968 | biostudies-arrayexpress

Gene Expression in Transformed Lymphocytes Reveals Phenotype-Modifying Pathways in Cystic Fibrosis

Project description:Heritable genetic variants modify cystic fibrosis (CF) clinical phenotypes, e.g., lung disease, age-of-onset of persistent Pseudomonas aeruginosa (P. aeruginosa), and meconium ileus (MI).Â Previous genome wide association studies (GWAS) have begun to inform the genetic architecture of CF phenotypes.Â Analyses of gene expression will complement GWAS, as demonstrated by analyses of gene expression in lymphoblastoid cell lines (LCLs) to identify disease-related pathophysiological processes for non-CF complex traits.Â In this study, global gene expression was measured in RNA from LCLs from 754 CF patients and analyzed for association with lung disease severity, age-of-onset of persistent P. aeruginosa pulmonary infection, and MI at birth.Â Each phenotype displayed distinct expression associations.Â Most pathways significantly associated with lung disease were related to membranes, vesicle traffic, and Golgi/endoplasmic reticulum (ER).Â Pathways containing HLA genes (Class I and II) were significantly associated with both lung and P. aeruginosa phenotypes, but they displayed qualitative differences between phenotypes.Â MI associated with pathways involving oxidative phosphorylation.Â The results support the concept that gene expression associated with heritable variation acts to modify phenotypes in CF. 754 samples were analyzed; 2 control samples were plated by Expression Analysis per plate and 1 pooled sample from the patient set was added to one well on each plate.

2016-05-19 | E-GEOD-60690 | biostudies-arrayexpress

Slu7 is essential for liver differentiation, metabolism and quiescence

Project description:The equilibrium between cellular differentiation and proliferation is fundamental for tissue homeostasis. This is particularly important for the liver, a highly differentiated organ with systemic metabolic functions still endowed with unparalleled regenerative potential. Hepatocellular de-differentiation and uncontrolled proliferation are at the basis of liver carcinogenesis. We have identified SLU7, a pre-mRNA splicing regulator inhibited in hepatocarcinoma as a pivotal gene for hepatocellular homeostasis. SLU7 knockdown in human liver cells and mouse liver resulted in profound changes in pre-mRNA splicing and gene expression, leading to impaired glucose and lipid metabolism, refractoriness to key metabolic hormones, and reversion to a fetal-like gene expression pattern. Hepatocellular proliferation and a switch to a tumor-like glycolytic phenotype were also observed. Mechanistically, SLU7 governed the splicing and/or expression of essential genes for hepatocellular differentiation like SRSF3 and HNF4a, and was identified as a critical factor in cAMP-regulated gene transcription. SLU7 is therefore central for hepatocyte identity and quiescence. The expression of the splicing factor SLU7 in the human hepatocellular carcinoma cell line PLC/PRF/5 was knocked down with specific siRNAs (siSlu7). An irrelevant siRNA (siGL2) was used as negative control. The RNAto perfrom the array analysis was extracted 48h after transfection.

2014-05-29 | E-GEOD-54090 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data