MiRNA expression signatures in gastrointestinal stromal tumors (GISTs)
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE31741 | GEO | 2011/11/01
SECONDARY ACCESSION(S): PRJNA145443
REPOSITORIES: GEO
Similar Datasets
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: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 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:Context: Gastrointestinal stromal tumors (GISTs) harboring mutations in the PDGFRA gene occur in only about 5–7% of patients. The most common PDGFRA mutation is exon 18 D842V, which is corre-lated with specific clinico-pathological features compared to the other PDGFRA mutated GISTs. Herein, we present a miRNA expression profile comparison of PDGFRA D842V mutant GISTs and PDGFRA with mutations other than D842V (non-D842V). miRNA expression profiling was carried out on 10 patients using a TLDA miRNA array. Then, miRNA expression was followed by bioinformatic analysis aimed at evaluating differential expression, pathway enrichment, and miRNA-mRNA networks. We highlighted 24 differentially expressed miRNAs between D842V and non-D842V GIST patients. Pathway enrichment analysis showed that deregulated miRNAs targeted genes that are mainly involved in the immune response pathways. The miRNA-mRNA networks highlighted a signature of miRNAs/mRNA that could explain the indolent behavior of the D842V mutated GIST. The results highlighted a different miRNA fingerprint in PDGFRA D842V GISTs compared to non-D842Vmutated patients, which could explain the different bio-logical behavior of this GIST subset.
2022-10-31 | GSE215402 | GEO
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
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.
2010-06-20 | GSE22185 | GEO
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:The anatomic site-dependent expression of hematopoietic progenitor cell antigen CD34 is a feature of gastrointestinal stromal tumours (GISTs). The basis for the differential CD34 expression is only incompletely understood. This study aimed at understanding the regulation of CD34 in GISTs and clarification of its site-dependent expression. Two sample sets of primary GISTs were interrogated including 52 fresh-frozen and 134 paraffin-embedded and formalin-fixed specimens. DNA methylation analysis was first performed by HumanMethylation450 BeadChip array in three cell lines, namely GIST-T1, GIST882 and GIST48b, that were derived from gastric and intestinal GISTs, and differentially methylated CpG sites were identified upstream of CD34. The methylation degree was further quantified by pyrosequencing and inversely correlated with CD34 mRNA and protein abundance. The gene's expression could be activated upon induction of DNA hypomethylation with 5-aza-2'-deoxycytidine in GIST-T1 and GIST882 cells. In patient samples, a strong inverse correlation of DNA methylation degree with immunohistochemically evaluated CD34 expression was documented. Both CD34 expression and DNA methylation levels were specific to the tumours' anatomic location and mutation status. A constant decrease in methylation levels was observed ranging from almost 100% hypermethylation in intestinal GISTs from duodenum to hypomethylation in rectum. CD34 was heavily methylated in gastric PDGFRA-mutant GISTs in comparison to hypomethylated KIT-mutant counterparts. Our results strongly suggest an epigenetic control of CD34 expression in GISTs by DNA methylation. Differential methylation and expression of CD34 in GISTs along the gastrointestinal tract axis and in tumours that harbour different gain-of-function mutations suggest the origin from different cell populations in the gastrointestinal tract.
2017-01-24 | GSE93963 | GEO
Project description:KIT, PDGFRA, NF1, and SDH mutations are alternate initiating events, fostering hyperplasia in gastrointestinal stromal tumors (GISTs), and additional genetic alterations are required for progression to malignancy. The most frequent secondary alteration, demonstrated in ~70% of GISTs, is chromosome 14q deletion. Here we report hemizygous or homozygous inactivating mutations of the chromosome 14q MAX gene in 16 of 76 GISTs (21%). We find MAX mutations in 17% and 50% of sporadic and NF1-syndromic GISTs, respectively, and we find loss of MAX protein expression in 48% and 90% of sporadic and NF1-syndromic GISTs, and in 3 of 8 micro GISTs, which are early GISTs. MAX genomic inactivation is associated with p16 silencing in the absence of p16 coding sequence deletion, and MAX induction restores p16 expression and inhibits GIST proliferation. Hence, MAX inactivation is a common event in GIST progression, fostering cell cycle activity in early GISTs.
2017-02-03 | GSE93077 | GEO
Project description:Gastrointestinal stromal tumors (GISTs) have an impaired gene expression. As microRNAs (miRNAs) are involved in post-transcriptional regulation of gene expression we performed the first high-throughput miRNA profiling of 15 paired GIST formalin-fixed and paraffin-embedded samples (tumor and adjacent normal tissue) using small RNA sequencing approach.
2017-03-30 | GSE89051 | GEO