Gene expression signatures in gastric gastrointestinal stromal tumors (GISTs)
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE47911 | GEO | 2013/06/14
SECONDARY ACCESSION(S): PRJNA208309
REPOSITORIES: GEO
Similar Datasets
Project description:To explore mechanisms underlying wild-type GISTs, gene expression analysis was performed on 15 gastric GISTs. 11 KIT-mutant, 1 PDGFRA-mutant and 3 wild-type GISTs
2013-06-14 | E-GEOD-47911 | biostudies-arrayexpress
Project description:To explore mechanisms underlying wild-type GISTs, array CGH was performed on 32 gastric GISTs (4 risk groups stratified by tumor size and mitotic counts comprised 8 cases each).
2013-06-14 | GSE47912 | GEO
Project description:To explore mechanisms underlying wild-type GISTs, array CGH was performed on 32 gastric GISTs (4 risk groups stratified by tumor size and mitotic counts comprised 8 cases each). 27 KIT-mutant, 1 PDGFRA-mutant and 4 wild-type GISTs
2013-06-14 | E-GEOD-47912 | 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: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
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:Abstract: Most GISTs require oncogenic activation of the KIT or PDGFRA receptor tyrosine kinase proteins, and the genomic mechanisms of oncogene activation are heterogeneous. Notably, the kinase mutation type correlates with both tumor biology and imatinib response. For example, GISTs with KIT exon 11 mutations are typically gastric and have excellent imatinib response, whereas those with KIT exon 9 mutations generally arise in the small bowel and are less responsive to imatinib. To identify genes that might contribute to these biological differences, we carried out gene expression profiling of 26 GISTs with known KIT and PDGFRA mutational status. Expression differences were then evaluated further by RNA in situ hybridization, immunohistochemistry, and immunoblotting. Unsupervised hierarchical clustering grouped tumors with similar mutations together, but the distinction between the different groups was not absolute. Differentially expressed genes included ezrin, p70S6K, and PKCs, which are known to have key roles in KIT or PDGFRA signaling, and which might therefore contribute to the distinctive clinicopathological features in GISTs with different mutation types. These gene products could serve as highly selective therapeutic targets in GISTs containing the KIT or PDGFRA mutational types with which they are associated. A disease state experiment design type is where the state of some disease such as infection, pathology, syndrome, etc is studied. Keywords: disease_state_design
2006-01-10 | GSE4001 | GEO
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). Total RNA was extracted from 32 fresh frozen GIST specimens obtained from surgical resections. Gene expression was analyzed using Agilent Whole Human Genome Microarray (4x44K, G4112F, 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-31802 | biostudies-arrayexpress
Project description:We performed microRNA expression profiling in a series of fresh-frozen neoadjuvantly imatinib-treated and non-treated gastrointestinal stromal tumors (GIST), using a microarray approach. Significant differentially expressed microRNAs among imatinib-treated and non-treated groups were identified using SAM analysis. Agilent microarray platform with probes matching 903 human microRNAs was used to determine miRNA expression profiles in 34 GISTs (19 imatinib-treated and 15 non-treated). Re-analysis of GSE45901 for 17 imatinib-treated GISTs. To validate the microarray platform, the expression levels of selected microRNAs were evaluated using qRT-PCR.
2015-08-01 | E-GEOD-63159 | biostudies-arrayexpress
Project description:Gastrointestinal stromal tumors (GISTs) comprise a biologically diverse group of neoplasms with respect to activating mutations in either KIT or PDGFRA genes, histology, anatomic site of origin, and clinical aggressiveness. In this study, we applied the high resolution array-based comparative genomic hybridization (array-CGH) technology to 66 primary GISTs (40 gastric and 26 non-gastric, 48 with KIT- and 18 with PDGFRA-mutations) for identification of novel high-level alterations and for characterization of genotype-related genomic changes. All cases had genomic imbalances with the highest occurrence of chromosome 14q (73%), 1p (62%), 22q (59%), 15q (38%) and 13q (29%) losses. Our data indicate that loss of chromosome 14 and/or 22 is an early change in GIST tumorigenesis irrespective of tumor genotype. Furthermore, DNA copy number changes showed a site dependent pattern. These included lower incidence of losses at 14q (87% vs. 35%), and higher frequency of losses at 1p (45%, vs. 85%) and 15q (17% vs. 69%) in non-gastric versus gastric site (p<0.001 for all). However, in the multivariate analysis with adjustment to tumor risk stratification, only the chromosome 14q loss site-dependent pattern of distribution retained its significance. These findings suggest that loss of chromosome 14q is a relatively late genetic event in the development of non-gastric GISTs, the lack of which is most likely substituted by the accumulation of chromosomes 1p/15q and other changes. The novel minimal overlapping regions of deletion at chromosome 1p (1p36.32-1p35.2, 1p34.1, and 1p22.1-1p21.3), 13q (13q14.11-q14.2 and 13q32.3-q33.1) and 15q23 were delineated, which point to chromosomal regions that may harbor genes relevant to the development of these neoplasms. Keywords: comparative genomic hybridization, genotype, site dependent changes
2006-11-08 | GSE5336 | GEO