Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Distinctive gene expression patterns in gastrointestinal stromal tumors identified with cDNA arrays

ABSTRACT: Gastrointestinal stromal tumors (GIST) are phenotypically and clinically heterogeneous mesenchymal tumors. Using the cDNA array technique, we analyzed the gene expression profiles of 22 GIST and 7 non-neoplastic gastrointestinal smooth muscle specimens, in order to detect molecular differences between GIST and non-neoplastic tissue, and to detect differences between GIST of various phenotypic and clinical subgroups. As a result, we found 796 differentially expressed genes and ESTs between GIST and smooth muscle tissue, including promising new candidate genes for the pathogenesis of GIST. Furthermore, we identified differences in gene expression between GIST of different site, size, and immunohistochemical expression of CD34 and SMA. Our data show that alterations in gene expression are associated with morphologically and clinically detectable features of GIST and provide new aspects for the understanding of these tumors. Keywords = Gastrointestinal Stromal Tumor (GIST) Keywords: other

ORGANISM(S): Homo sapiens

PROVIDER: GSE112 | GEO | 2003/04/10

SECONDARY ACCESSION(S): PRJNA84483

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Distinctive gene expression patterns in gastrointestinal stromal tumors identified with cDNA arrays

Project description:Gastrointestinal stromal tumors (GIST) are phenotypically and clinically heterogeneous mesenchymal tumors. Using the cDNA array technique, we analyzed the gene expression profiles of 22 GIST and 7 non-neoplastic gastrointestinal smooth muscle specimens, in order to detect molecular differences between GIST and non-neoplastic tissue, and to detect differences between GIST of various phenotypic and clinical subgroups. As a result, we found 796 differentially expressed genes and ESTs between GIST and smooth muscle tissue, including promising new candidate genes for the pathogenesis of GIST. Furthermore, we identified differences in gene expression between GIST of different site, size, and immunohistochemical expression of CD34 and SMA. Our data show that alterations in gene expression are associated with morphologically and clinically detectable features of GIST and provide new aspects for the understanding of these tumors. Keywords = Gastrointestinal Stromal Tumor (GIST)

2003-04-10 | E-GEOD-112 | biostudies-arrayexpress

MiRNAs array after SH3BP2 silencing in Gastrointestinal stromal tumor cells

Project description:Silencing of the adaptor SH3BP2 impairs Gastrointestinal stromal tumors growth through miRNAs We dissected SH3BP2 pathway in Gastrointestinal Stromal Tumor cells (GIST) performing a miRNA array in SH3BP2-silenced GIST cells

2022-09-23 | GSE213777 | GEO

Array CGH analysis of human gastrointestinal stromal tumors

Project description:Gastrointestinal stromal tumors (GISTs) are the most important mesenchymal tumors of the gastrointestinal tract. The vast majority of GISTs exhibit activating mutations of KIT or PDGFRA, but epigenetic alteration of GISTs is largely unknown. In this study, we aimed to clarify the involvement of DNA methylation in GIST malignancy. A total of 25 GIST specimens were studied using Human Genome CGH Microarray Kit 105A (G4412A, Agilent). Levels of LINE-1 methylation were analyzed using bisulfite-pyrosequencing. LINE-1 hypomethylation was correlated with risk grade, and high-risk GISTs exhibited lower levels of LINE-1 methylation than low- or intermediate-risk GISTs. Array CGH analysis revealed a significant correlation between LINE-1 hypomethylation and chromosomal aberrations. Our data suggest that LINE-1 hypomethylation correlates with the aggressiveness of GISTs. Hypomethylation may increase the malignant potential of GISTs by inducing accumulation of chromosomal aberrations. A total of 25 surgically obtained human gastrointestinal stromal tumors (GISTs) was analyzed using Agilent CGH microarray. Copy number aberration was compared with clinicopathological features and DNA methylation status.

2010-06-20 | E-GEOD-22185 | biostudies-arrayexpress

Gene expression signatures in gastrointestinal stromal tumors (GISTs)

Project description:To analyze the gene expression signatures in gastrointestinal stromal tumors (GISTs), a series of 14 GIST specimens were analyzed using Agilent Whole Human Genome Microarray (4x44K, G4112F).

2011-11-01 | GSE31802 | GEO

miRNA profiling analysis in high-risk intestinal GIST

Project description:Prognosis in Gastrointestinal Stromal Tumors (GIST) depends on clinical and pathological parameters that may be little objective, thus it is necessary to have other molecular biomarkers in the management of the disease.

2020-09-25 | GSE156715 | GEO

Distinct gene expression profiles between overt GIST and miniGIST

Project description:In contrast to the paucity of clinic GIST (Gastrointestinal stromal tumor; 0.0014 % happening rate), there is a more than twenty thousand times higher rate for miniGISTs, about ~30% of human population could be identified to have miniGISTs. Exploring the molecular differences between miniGISTs and overt GISTs will help us to understand the transformation mechanisms along with GIST progression, but C-kit and PDGFRA mutations analysis failed to identify the differences between these two groups. Conclusion: miniGISTs have significant distinct gene expression profile with overt GISTs by both unsupervised and supervised analysis. Our finding indicated that c-kit and DOG1 expression are the very early events in the genesis of miniGIST and overt GIST, and miniGIST is a molecular distinct group with overt GIST.

2014-12-25 | GSE52666 | GEO

Murine model of gastrointestinal stromal tumors harboring a germline Kit K641E oncogenic mutant

Project description:Gastrointestinal stromal tumors (GIST) are thought to derive from the interstitial cells of Cajal (ICC) or an ICC precursor. Oncogenic mutations of the receptor tyrosine kinase KIT are present in most GIST. KIT K642E was originally identified in sporadic GIST and later found in the germ line of a familial GIST. A mouse model of harboring a germline Kit K641E mutant was created to model familial GIST. The expression profile was investigated in the gastric antrum in the knock-in Kit K641E murine GIST model by microarray.

2009-09-25 | GSE12931 | GEO

Project description:Study of new mechanisms in Gastrointestinal stromal tumors (GIST)

| PRJNA748541 | ENA

Small RNA expression signatures of gastrointestinal stromal tumors: associations to imatinib resistance and patient outcome

Project description:We performed miRNA expression profiling in a series of fresh-frozen neoadjuvantly imatinib treated gastrointestinal stromal tumors (GIST), using a microarray approach. Significant differentially expressed miRNAs among imatinib-resistant and imatinib-sensitive groups were identified using SAM analysis.

2013-04-10 | GSE45901 | GEO

Kinome Profiling of Gastrointestinal Stromal Tumors Using Multiplexed Inhibitor Beads and Mass Spectrometry Identifies Wee1 as a Candidate Therapeutic Target

Project description:Purpose: Management of gastrointestinal stromal tumor (GIST) has been revolutionized by the identification of activating mutations in KIT and PDGFRA and the clinical application of receptor tyrosine kinase (RTK) inhibitors in the advanced disease setting. Stratification of GIST into molecularly defined subsets provides insight into clinical behavior and response to approved targeted therapies. Although these RTK inhibitors are effective in the majority of GIST, resistance to these agents remains a significant clinical obstacle. Development of effective treatment strategies for refractory GIST requires identification of novel targets to provide additional therapeutic options. Global kinome profiling has the potential to identify critical signaling networks and reveal protein kinases that are essential in GIST. Experimental Design: Using Multiplexed Inhibitor Beads and Mass Spectrometry paired with a super-SILAC kinome standard, we explored the majority of the kinome in GIST specimens from three GIST subtypes (KIT-mutant, PDGFRA-mutant and succinate dehydrogenase-deficient GIST) to identify novel kinase targets. In vitro and in vivo studies were performed to evaluate the utility of targeting the identified kinases in GIST. Results: Kinome profiling revealed distinct signatures in three GIST subtypes. PDGFRA-mutant GIST had elevated tumor associated macrophage (TAM) kinases and immunohistochemical analysis confirmed increased TAMs present in these tumors. Kinome profiling with loss-of-function assays revealed a significant role for G2-M tyrosine kinase, Wee1, in GIST survival. In vitro and in vivo studies revealed significant efficacy of MK-1775 (Wee1 inhibitor) in combination with avapritinib in both KIT and PDGFRA-mutant GIST cell lines, as well as notable efficacy of MK-1775 as a single agent in the PDGFRA-mutant line. Conclusions: These studies provide strong preclinical justification for the use of MK-1775 in GIST.

2021-09-09 | PXD020720 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

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