Transcription profiling by array of human gastro-intestinal stromal tumors to validate prognostic signature
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ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Frederic Chibon
PROVIDER: E-MTAB-373 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:Gastrointestinal stromal tumors (GISTs) are the most common human sarcomas and typically locate in the stomach or small intestine. circular RNAs (circRNAs) were identified to plays vital roles in tumor oncogenesis and progression. To investigate the involvement of differentially expressing genes and circRNAs in GIST , transcriptomic analyses of differential expression genes and circRNAs were performed for discrimination of GISTs from normal tissues. The RNA samples were extracted from three GIST samples and three adjacent mucosa for microarray profiling and performed in Agilent-078298 human ceRNA array for gene and circRNAs expression profiling analysis. On average, we detected expression of 17,000 transcripts.Under the criteria fold change > 2 or < 0.5, we obtained a total of 5770 circRNAs and 1815 mRNAs were differentially expressed in GISTs. Hierarchy cluster analysis also indicated that the 6 samples were distributed into two clusters, 3 GIST samples in one cluster and 3 normal samples in another cluster. Then,qRT-PCR validation of the DEGs in GIST tissue and adjacent tissues.The results revealed that grouping was reasonable and the data can be directly applied to further analysis.
2019-05-21 | GSE131481 | GEO
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: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: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: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.
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Project description:Background: Recently a 76-gene prognostic signature able to predict distant metastases in lymph node-negative (N-) breast cancer patients was reported. The aims of this study conducted by TRANSBIG were to independently validate these results and to compare the outcome with clinical risk assessment. Materials and Methods: Gene expression profiling of frozen samples from 198 N- systemically untreated patients was performed at the Bordet Institute, blinded to clinical data and independent of Veridex. Genomic risk was defined by Veridex, blinded to clinical data. Survival analyses, done by an independent statistician, were performed with the genomic risk and adjusted for the clinical risk, defined by Adjuvant!Online. Results: The actual 5- and 10-year time to distant metastasis (TDM) were 98% (88%-100%) and 94% (83%-98%) respectively for the good profile group and 76% (68%- 82%) and 73% (65%-79%) for the poor profile group. The actual 5- and 10-year overall survival (OS) were 98% (88%-100%) and 87% (73%-94%) respectively for the good profile group and 84% (77%-89%) and 72% (63%-78%) for the poor profile group. We observed a strong time-dependency of this signature, leading to an adjusted HR of 13.58 (1.85-99.63) and 8.20 (1.10-60.90) at 5 years, and 5.11 (1.57-16.67) and 2.55 (1.07-6.10) at 10 years for TDM and OS respectively. Conclusion: This independent validation confirmed the performance of the 76-gene signature and adds to the growing evidence that gene expression signatures are of clinical relevance, especially for identifying patients at high risk of early distant metastases. Experiment Overall Design: dataset of microarray experiments from primary breast tumors used to validate the 76-gene signature (VERIDEX). No replicate, no reference sample.
2008-06-16 | E-GEOD-7390 | biostudies-arrayexpress
Project description:To explore mechanisms underlying wild-type GISTs, gene expression analysis was performed on 15 gastric GISTs.
2013-06-14 | GSE47911 | GEO
Project description:We provide an original multi-stage approach identifying a gene signature to assess the fibroblast polarization. Prototypic polarizations (inflammatory/fibrotic) were induced by seeded mouse embryonic fibroblasts (MEFs) with TNFα or TGFß1, respectively. The transcriptomic and proteomic profiles were obtained by RNA microarray and LC/MS-MS. Gene Ontology and pathways analysis were performed among the differentially expressed genes (DEGs) and proteins (DEPs). Balb/c mice underwent daily intradermal injections of HOCl (or PBS) as an experimental murine model of inflammation-mediated fibrosis in a time-dependent manner. As results, 1,456 and 2,215 DEGs, and 289 and 233 DEPs were respectively found in MEFs in response to TNFα or TGFß1, respectively. Among the most significant pathways, we combined 26 representative genes to encompass the proinflammatory and profibrotic polarizations of fibroblasts. Based on principal component analysis, this signature deciphered baseline state, proinflammatory polarization, and profibrotic polarization as accurately as did RNA microarray and LC/MS-MS. Then, we assessed the gene signature on dermal fibroblasts isolated from the experimental murine model. We observed a proinflammatory polarization at day 7, and a mixture of a proinflammatory and profibrotic polarizations at day 42 in line with histological findings. Our approach provides a small-size and convenient gene signature to assess murine fibroblast polarization.
2022-07-12 | PXD034078 | Pride
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:Endometrial stromal sarcomas (ESSs) are a genetically heterogeneous group of rare uterine neoplasms that are frequently driven by recurrent gene rearrangements. In conventional low-grade ESSs, JAZF1-SUZ12, PHF1-JAZF1, EPC1-PHF1 and MEAF6-PHF1 chimeric fusions have been reported in >50% of cases. The recently described t(10;17)(q22;p13) translocation yields YWHAE-FAM22A/B chimeric proteins that are associated with histologically high-grade and clinically more aggressive ESS. Integrating whole-transcriptome paired-end RNA sequencing with fluorescence in situ hybridization (FISH) and conventional cytogenetics, we identified MBTD1 (Malignant Brain Tumor Domain-containing 1) and CXorf67 (Chromosome X open reading frame 67) as the genes involved in the novel reciprocal t(X;17)(p11.2;q21.33) translocation in two independent low-grade ESS of classical histology. The presence of the MBTD1-CXorf67 fusion transcript was validated in both cases using RT-PCR followed by Sanger sequencing. A specific FISH assay to be used on paraffin tissues was developed to detect the novel t(X;17) translocation, and resulted in identification of an additional low-grade ESS case positive for the MBTD1-CXorf67 fusion among 14 uterine stromal tumours [9 ESSs and 5 undifferentiated endometrial sarcomas (UESs)] that were negative for JAZF1 and YWHAE rearrangements. Gene expression profiles of 3 ESSs with YWHAE- and 4 classical ESSs with JAZF1-rearrangements, and 4 UESs without known gene rearrangements, indicated clustering of tumours with MBTD1-CXorf67 fusion together with low-grade JAZF1-associated ESSs. The chimeric MBTD1-CXorf67 fusion identifies yet another cytogenetically distinct subgroup of low-grade ESS and offers the opportunity to shed light on the functions of two poorly characterized genes. Total RNA was extracted from 11 frozen tumor samples from 4 low-grade ESS cases, 4 UES cases and 3 high-grade ESS cases; Agilent One-Color technology.
2015-03-31 | E-GEOD-45783 | biostudies-arrayexpress