Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

12 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ZNF-mediated resistance to imatinib mesylate in gastrointestinal stromal tumor

ABSTRACT: 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

ORGANISM(S): Homo sapiens

SUBMITTER: Michael Ochs

PROVIDER: E-GEOD-40080 | 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 [Affymetrix HuEx1.0]

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-33205 | 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

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

Gene expression signatures in GIST-T1 cells transfected with siRNA targeting HOTAIR

Project description:To analyze the effect of HOTAIR depletion in a gastrointestinal stromal tumor (GIST) cells, RNAi-mediated knockdown of HOTAIR was carried out using GIST-T1 cells. Gene expression microarray analysis revealed that a number of reported HOTAIR target genes were upregulated by knockdown of HOTAIR. Moreover, we found that 1424 genes were upregulated by siHOT (>2-fold), and Gene Ontology analysis revealed enrichment of genes related to “nucleus”, “chromosome” and “membrane-bounded organelle.” For RNAi-mediated knockdown of HOTAIR, three different Stealth siRNAs against HOTAIR were generated by Invitrogen, after which a mixture of the three was used for transfection. GIST-T1 cells in 6-well plates were transfected with 100 pmol of Stealth siRNA (Invitrogen) or a Stealth RNAi Negative Control Medium GC (Invitrogen) using Lipofectamine2000 (Invitrogen). Total RNA was extracted 48 h after transfection.

2011-12-01 | E-GEOD-32064 | 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

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

Brd2 regulates gene expression and alternative splicing.

Project description:We analyzed a role of Brd2 protein in transcription and alternative splicing. 289 genes change alternative splicing after Brd2 knockdown and 1459 genes alter gene expression compared to cells treated with negative control siRNA. 6 samples (3 independent samples of cells treated with Brd2 siRNA, 3 samples of cells treated with negative control siRNA)

2013-12-03 | E-GEOD-39937 | biostudies-arrayexpress

The effect of imatinib therapy on tumor associated macrophages (TAMs) in human gastrointestinal stromal tumor (GIST)

Project description:The gene expression profile of TAMs microbead isolated from freshly obtained human GISTs were compared in tumors that were untreated, responding to imatinib (sensitive), or resistant to imatinib (resistant) The Affymetrix Human Genome U133A 2.0 platform was used TAMs were microbead isolated from 12 untreated, 5 sensitive, and 4 resistant tumors. Tumors were obtained freshly from the operating room from consenting patients using an IRB approved protocol. Tumors were digested using collagenase and TAMs isolated using microbead negative selection for KIT, CD3, and CD56 followed by positive selection for CD14.

2013-11-20 | E-GEOD-51697 | biostudies-arrayexpress

Combining transcriptome and proteome analysis to identify and characterize the RpoS regulon in Pseudomonas fluorescens

Project description:Background: Microorganisms are the major cause of food spoilage during storage, processing and distribution. Pseudomonas fluorescens is a typical spoilage bacterium that contributes to a large extent to the spoilage process of proteinaceous food. RpoS is considered an important global regulator involved in stress survival and virulence in many pathogens. Our previous work revealed that RpoS contributed to the spoilage activities of P. fluorescens by regulating resistance to different stress conditions, extracellular acylated homoserine lactone (AHL) levels, extracellular protease and total volatile basic nitrogen (TVB-N) production. However, RpoS-dependent genes in P. fluorescens remained undefined. Results: RNA-seq transcriptomics analysis combined with quantitative proteomics analysis basing on multiplexed isobaric tandem mass tag (TMT) labeling was performed for the P. fluorescens wild-type strain UK4 and its derivative carrying a rpoS mutation. A total of 375 differentially expressed genes (DEGs) and 212 differentially expressed proteins (DEPs) were identified in these two backgrounds. The DGEs were further verified by qRT-PCR tests, and the genes directly regulated by RpoS were confirmed by 5’-RACE-PCR sequencing. The combining transcriptome and proteome analysis revealed a role of this regulator in several cellular processes, including polysaccharide metabolism, intracellular secretion and extracellular structures, cell well biogenesis, stress responses, ammonia and biogenic amine production, which may contribute to biofilm formation, stress resistance and spoilage activities of P. fluorescens. Moreover, in this work we indeed observed that RpoS contributed to the production of the macrocolony biofilm’s matrix.

2019-11-12 | PXD010845 | Pride

Expression Data from Gastrointestinal Stromal Tumor (GIST) Cell Lines

Project description:Activating mutations in either KIT or PDGFRA are present in approximately 90% of gastrointestinal stromal tumors (GISTs). Although treatment with the KIT and PDGFR inhibitor imatinib can control advanced disease in about 80% of GIST patients, the beneficial effect is not durable. Here, we report that ligands from the FGF family reduced the effectiveness of imatinib in GIST cells, and FGF2 and FGFR1 are highly expressed in all primary GIST samples examined. The combination of KIT and FGFR inhibition showed increased growth inhibition in imatinib-sensitive GIST cell lines in the presence or absence of added FGF2 in vitro, and delayed tumor regrowth in vivo. In addition, inhibition of mitogen-activated protein kinase (MAPK) signaling by imatinib was not sustained in GIST cells. An extracellular signal-regulated kinase (ERK) rebound occurred through activation of FGF signaling, and was repressed by FGFR1 inhibition. Downregultation of Sprouty proteins played a role in the imatinib-induced feedback activation of FGF signaling in GIST cells. We used micorarrays to quantify the gene expression levels in GIST cell lines. Four GIST cell lines were split and cultured overnight. Cells were harvested for RNA extraction and hybridization on Affymetrix U133plus2 microarrays.

2015-01-08 | E-GEOD-64762 | 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