MiRNA expression profile in GIST (gastrointestinal stromal tumor)
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE36087 | GEO | 2013/03/01
SECONDARY ACCESSION(S): PRJNA151739
REPOSITORIES: GEO
Similar Datasets
Project description:To clarify aberrantly expressed miRNAs affecting the biology of GIST, miRNA array was performed in 19 cases of GIST. A series of 19 GISTs specimens were analyzed using 3D-Gene Human miRNA Oligo chips containing 904 human miRNAs and 107 viral miRNAs anti-sense probes printed in duplicate spots (Toray, Kamakura, Japan).
2013-03-01 | E-GEOD-36087 | biostudies-arrayexpress
Project description:GIST is considered to invariably arise through gain-of-function KIT or PDGFRA mutation of the interstitial cells of Cajal (ICC). However, the genetic basis of the malignant progression of GIST is poorly understood. We analysed the expression levels of 54,613 probe sets in 32 surgical samples of untreated GIST of the stomach and small intestine with GeneChip Human Genome U133 Plus 2.0 arrays. Experiment Overall Design: Total RNA was extracted from 32 fresh frozen tumour specimens. We analysed the global gene exprssion profiles of these GIST cases in order to clarify the genomic basis behind the malignant progression of this tumor
2008-10-18 | E-GEOD-8167 | biostudies-arrayexpress
Project description:Gastrointestinal stromal tumor (GIST) is a common sarcoma of gastrointestinal tract (GIT) with high metastatic and recurrence rates, but the proteomic features are still less understood. Here we performed systematic quantitative proteome profiling of GIST from 13 patients classified into very low/low, intermediate and high risk subgroups. An extended cohort of GIST (n = 131) was used for immunohistochemical validation of proteins of interest. In total, 10064 proteins were quantified, covering 61% of the GIT transcriptome from The Human Protein Altas. Out of the 10064 quantified proteins, 4938 proteins were observed in all 13 cases with 518 proteins upregulated and 190 proteins downregulated in tumorous tissues independent of risk rating. Pathway analysis showed that the downregulated proteins were mostly enriched in metabolic pathway, while the upregulated proteins mainly belonged to spliceosome pathway. In addition, 131 proteins showed differentially expressed patterns among GIST subgroups with statistical significance. The 13 GIST cases were classified into 3 subgroups perfectly based on the expression of these proteins. The molecular phenotypes of oncoproteins, tumor suppressors, phosphatase and kinases were summarized, and some important molecules were observed. Immunohistochemical analysis of two phosphatases PTPN1 (n = 117) and PPP2CB (n=113) revealed that the GIST patients with high PTPN1 had low chances of developing metastasis, and the expression of PPP2CB was likely to be associated with GIST risk. Collectively, this work provides valuable information for understanding the inherent biology and evolution of GIST.
2019-01-29 | PXD011299 |
Project description:To identify mRNA profiles in GIST and CAFs, we performed RNA sequencing analysis (RNA-seq) using GIST cell lines, GIST-T1 and GIST882, and CAFs.
2020-01-14 | GSE143547 | GEO
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.
2015-01-08 | GSE64762 | GEO
Project description:To clarify the microRNA (miRNA) expression signatures in gastrointestinal stromal tumors (GISTs), a series of 32 GIST specimens were analyzed using Agilent miRNA microarray V3. Unsupervised hierarchical clustering revealed that GISTs can be categorized into 2 groups according to the expression of a miRNA cluster encoded on chromosome 14q32.31. Total RNA was extracted from 32 fresh frozen GIST specimens obtained from surgical resections. Expression of 851 miRNAs was analyzed using Human miRNA Microarray V3 (Rel 12.0 G4470C; Agilent technologies, Santa Clara, CA, USA). Risk grade was assessed according to the risk definition system proposed by Fletcher et al. (Hum Pathol. 2002;33:459-65.)
2011-11-01 | E-GEOD-31741 | biostudies-arrayexpress
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
Project description:To clarify the microRNA (miRNA) expression signatures in gastrointestinal stromal tumors (GISTs), a series of 32 GIST specimens were analyzed using Agilent miRNA microarray V3. Unsupervised hierarchical clustering revealed that GISTs can be categorized into 2 groups according to the expression of a miRNA cluster encoded on chromosome 14q32.31.
2011-11-01 | GSE31741 | GEO
Project description:A growing body of literature has consolidated the important role of miRNA in a variety of biological processes, in cancer development, acting both as oncogenes and tumor suppressor genes, and in their ability to distinguish tumors according to their diagnostic and prognostic properties.To date, little is known, however, about differences in miRNA expression between KIT/PDGFRA mutant and KIT/PDGFRA WT GIST.
2016-10-03 | E-MTAB-4490 | biostudies-arrayexpress
Project description:GIST is considered to invariably arise through gain-of-function KIT or PDGFRA mutation of the interstitial cells of Cajal (ICC). However, the genetic basis of the malignant progression of GIST is poorly understood. We analysed the expression levels of 54,613 probe sets in 32 surgical samples of untreated GIST of the stomach and small intestine with GeneChip Human Genome U133 Plus 2.0 arrays. Keywords: gene expression array-based, count
2008-06-15 | GSE8167 | GEO