Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: GSE20710
PROVIDER: PRJNA124905 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:In addition to KIT and PDGFRA mutations, sequential accumulation of other genetic events is involved in the development and progression of gastrointestinal stromal tumors (GISTs). Until recently, the significance of these other alterations has not been thoroughly investigated. The combination of gene expression profiling and high-resolution genomic copy number analysis offers a detailed molecular portrait of GISTs, providing an essential comprehensive knowledge necessary to guide the discovery of novel target genes involved in tumor development and progression. Fresh tissue specimens from 25 patients with GIST were collected and high-resolution genomic copy number analyses were performed using Affymetrix SNP array 6.0.
2010-08-27 | GSE20709 | GEO
Project description:Profiling of DNA copy number changes in human Leiomyosarcomas and Gastrointestinal Stromal Tumors using array CGH
2006-09-20 | E-MEXP-707 | biostudies-arrayexpress
Project description:In addition to KIT and PDGFRA mutations, sequential accumulation of other genetic events is involved in the development and progression of gastrointestinal stromal tumors (GISTs). Until recently, the significance of these other alterations has not been thoroughly investigated. The combination of gene expression profiling and high-resolution genomic copy number analysis offers a detailed molecular portrait of GISTs, providing an essential comprehensive knowledge necessary to guide the discovery of novel target genes involved in tumor development and progression. Fresh tissue specimens from 25 patients with GIST were collected and high-resolution genomic copy number analyses were performed using Affymetrix SNP array 6.0. GIST tumor samples from mutated (KIT or PDGFRA) or Wild Type patients were labeled for hybridization on Affymetrix microarrays. Copy number analysis of Affymetrix SNP6.0 arrays was performed for 25 GIST samples, then compared to gene expression data.
2010-08-27 | E-GEOD-20709 | biostudies-arrayexpress
Project description:In addition to KIT and PDGFRA mutations, sequential accumulation of other genetic events is involved in the development and progression of gastrointestinal stromal tumors (GISTs). Until recently, the significance of these other alterations has not been thoroughly investigated. The combination of gene expression profiling and high-resolution genomic copy number analysis offers a detailed molecular portrait of GISTs, providing an essential comprehensive knowledge necessary to guide the discovery of novel target genes involved in tumor development and progression. Fresh tissue specimens from 25 patients with GIST were collected and gene expression profiling was performed using Affymetrix U133Plus array.
2010-08-27 | GSE20708 | 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:Synchronous tumors are a rare disease and the underlying mechanism is seldom discussed. Here we present a case study of synchronous primary neoplasms detected in three distinct tissues: mantle cell lymphoma (MCL), clear cell renal cell carcinoma (ccRCC) and gastrointestinal stromal tumor (GIST). MCL is one form of B-cell non-Hodgkin’s lymphoma (NHL) that affects approximately 6% of NHL patients. GIST is thought to be derived from the Interstitial Cells of Cajal, a group of mesenchymal cells in the gastrointestinal tract involved in peristaltic motor activity. ccRCC tumor cells are the most common malignancy of kidney cancer and are characterized by enlarged cytoplasms. Genomic DNA from FFPE tumor sections and control DNA extracted from saliva were heat-fragmentated, labeled, hybridized and scanned following manufacturer’s recommendation for 244K arrays (Agilent). Raw data were background corrected and normalized in R. Nexus v4.1 (Biodiscovery) software was then used to call aberrant regions using Rank Segmentation algorithm from the processed data. Genes within aberrant regions can be indicated as copy number gain or loss accordingly. To identify significantly enriched canonical pathways, upstream and downstream genes for several cancer-related pathways were explored in Ingenuity knowledge base (Ingenuity Systems) and Genespring GX-10 (Agilent) with their copy number change status checked in Nexus. The analysis revealed high copy-number amplifications in gene regions related to an anti-apoptotic and cell-growth promoting pathway in all three cancers. Genomic DNA was isolated from mantle cell lymphoma (MCL), clear cell renal cell carcinoma (ccRCC) and gastrointestinal stromal tumor (GIST) FFPE tumor sections using the WaxFreeTM DNA Extraction Kit (TrimGen). Control DNA extracted from saliva was collected using a saliva self-collecting kit (Oragene). Heat-fragmentation, one-cycle target labeling, hybridization and scanning of the DNA were performed following manufacturer’s recommendation for 244K arrays (Agilent). The arrays were scanned by using the Agilent Scanner G2505B and Agilent Feature Extraction software v10.5 to produce raw data files. Raw data were background corrected and normalized in R. Nexus v4.1 (Biodiscovery) software was then used to call aberrant regions using Rank Segmentation algorithm from the processed data. Genes within aberrant regions can be indicated as copy number gain or loss accordingly.
2010-08-02 | E-GEOD-22905 | biostudies-arrayexpress
Project description:Soft tissue sarcomas are aggressive mesenchymal cancers that affect more than 10,600 new patients per year in the US, about 40% of whom will die of their disease. Soft tissue sarcomas exhibit remarkable histologic diversity, with more than 50 recognized subtypes, but our knowledge of their genomic alterations is limited. Here we describe the results of an integrative analysis of DNA sequence, copy number, and mRNA expression in 207 samples encompassing seven major subtypes. Genes mutated in more than 5% of samples within a subtype were KIT (in gastrointestinal stromal cell tumors, or GISTs), TP53 (pleomorphic liposarcomas), PIK3CA (myxoid/round-cell liposarcoma), and NF1 (both myxofibrosarcoma and pleomorphic liposarcoma). We show evidence that PIK3CA mutations, found in 18% of myxoid/round-cell liposarcomas, activate AKT in vivo and are associated with poor outcomes. Point mutations in the tumor suppressor gene NF1 were discovered in both myxofibrosarcomas and pleomorphic liposarcomas, while genomic deletions were observed in all subtypes at varying frequencies. Finally, we found that short hairpin RNA-based knockdown of a subset of genes that are amplified in dedifferentiated liposarcoma, including CDK4 and YEATS4, decreased cell proliferation. Our study yields the most detailed map of molecular alterations across diverse sarcoma subtypes to date and provides potential subtype-specific targets for therapy. Human soft-tissue sarcoma specimens were profiled on Affymetrix U133A arrays per manufacturer's instructions.
2010-07-05 | E-GEOD-21122 | biostudies-arrayexpress
Project description:HER2 gene amplification and protein overexpression (HER2+) define a clinically challenging subgroup of breast cancer with variable prognosis and response to therapy. Although gene expression profiling has identified an ERBB2 molecular subtype of breast cancer, it is clear that HER2+ tumors reside in all molecular subtypes and represent a genomically and biologically heterogeneous group. Genome-wide DNA copy number profiling, using BAC array comparative genomic hybridization (aCGH) were performed on 200 tumors with mixed clinical characteristics and amplification of HER2. Genomic Identification of Significant Targets in Cancer (GISTIC) was used to identify significant copy number aberrations (CNAs) in HER2+ tumors. This analysis sheds further light on the genomically complex and heterogeneous nature of HER2+ tumors in relation to other subgroups of breast cancer.
2010-04-14 | GSE21259 | GEO
Project description:Copy number analysis of primary esophageal squamous cell carcinoma (ESCC) from 40 patients in Japan. Integrative analysis of gene expression profiles and genomic alterations obtained from array-CGH and NGS provided us new insight into the pathogenesis of ESCC.
2013-09-01 | GSE47630 | GEO
Project description:131 patient-derived xenograft models were generated for non-small cell lung carcinoma and were profiled by analysis of gene copy number variation, whole exome sequence, methylome, transcriptome, proteome, and phospho(Tyr)-proteome. Proteome profiling resolved the known major histology subtypes and revealed 3 proteome subtypes (proteotypes) among adenocarcinoma and 2 in squamous cell carcinoma that were associated with distinct protein-phosphotyrosine signatures and patient survival. Proteomes of human tumor were discernible from murine stroma. Stromal proteomes were similar between histological subtypes, but two adenocarcinoma proteotypes had distinct stromal proteomes. Tumor and stromal proteotypes comprise signatures of targetable biological pathways suggesting that patient stratification by proteome profiling may be an actionable approach to precisely diagnose and treat cancer.
2021-11-24 | PXD016579 | Pride