Affymetrix 250K Nsp-tumor - samples
Ontology highlight
ABSTRACT:
PROVIDER: EGAD00010000682 | EGA |
REPOSITORIES: EGA
Similar Datasets
Project description:Data includes all available Affymetrix SNP data from a cohort of Pediatric malignant glioma samples, isolated from Formalin-fixed Paraffin embedded tissue. No clinical data is available. Copy number analysis of Affymetrix 250K Sty SNP arrays was performed for 28 pediatric malignant gliomas. The VN algorithm was used to generate the reference signal based on 48 Mapping 500k HapMap Trio Dataset template.
2011-11-23 | E-GEOD-25589 | biostudies-arrayexpress
Project description:glioma normal samples using 250K
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Project description:High-resolution genomic microarrays provides simultaneous detection of copy-number aberrations such as the known recurrent aberrations in Chronic Lymphocytic Leukemia_diagnostic sample_patient (del(11q), del(13q), del(17p) and trisomy 12), and copy-number neutral loss of heterozygosity. We screened 369 newly diagnosed Chronic Lymphocytic Leukemia_diagnostic sample_patient patient samples from a population-based cohort using 250K single nucleotide polymorphism-arrays.
2011-04-28 | GSE28030 | GEO
Project description:250k Sty, 250k Nsp, 250k Hind and 250k Xba Affymetrix SNP arrays for 50 leukemia remission samples used as controls for copy number analysis for GSE9109 and GSE9112. Keywords: Acute leukemia, BCR-ABL1, chronic myeloid leukemia, copy number analysis, loss-of-heterozygosity, genomics *** Due to privacy concerns, the primary SNP array data is no longer available with unrestricted access. Individuals wishing to obtain this data for research purposes may request access using the Web links below. ***
2009-09-02 | GSE9111 | GEO
Project description:Copy number analysis of 21 paediatric low-grade astrocytomas identified a discrete copy number gain of 1.9Mb in chromosome band 7q34. The gain was present in 12/14 cerebellar pilocytic astrocytomas. Subsequent analysis of tumour cDNA indentified a novel gene fusion between KIAA1549 and BRAF in these tumours. Copy number analysis of 21 paediatric low-grade astrocytomas using the Affymetrix GeneChip Human Mapping 250K Nsp Array. This study comprised 14 pilocytic astrocytomas, 4 diffuse astrocytomas, one pilomyxoid astrocytoma, one pilomyxoid glioma and one pleomorphic xanthoastrocytoma. Tumours were compared to the mean of two normal male DNA controls.
2010-04-09 | E-GEOD-14960 | biostudies-arrayexpress
Project description:Metabolomics was used to identify metabolic fingerprints of AKT1 activation or MYC overexpression in human prostate tumors. Genomics was used to determine how many of these tumors had a genetic aberration underlying signaling activation. Copy number analysis of Affymetrix 250K SNP arrays was performed for 59 human prostate tumors and 6 normal prostate samples.
2014-10-20 | E-GEOD-62218 | biostudies-arrayexpress
Project description:Data includes all available Affymetrix SNP data from a cohort of Pediatric malignant glioma samples, isolated from Formalin-fixed Paraffin embedded tissue. No clinical data is available.
2011-11-23 | GSE25589 | GEO
Project description:In the study of tumor genetics, formalin-fixed paraffin-embedded (FFPE) tumors are the most readily available tissue samples. While DNA derived from FFPE tissue has been validated for array comparative genomic hybridization (aCGH) application, the suitability of such fragmented DNA for single-nucleotide polymorphism (SNP) array analysis has not been well examined. Furthermore, whole-genome amplification (WGA) has been used in the study of small precursor lesions to produce sufficient amount of DNA for aCGH analysis. It is unclear whether the same approach can be extended to SNP analysis. In this study, we examined the utility and limitations of genotyping platform performed on whole-genome amplified DNA from FFPE tumor samples for both copy number and SNP analyses. We analyzed the results obtained using DNA derived from matched FFPE and frozen tissue samples on Affymetrix 250K Nsp SNP array. Two widely used WGA methods, Qiagen (isothermal protocol) and Sigma (thermocycling protocol), were used to determine how WGA methods affect the results. We found that the use of DNA derived from FFPE tumors (without or with WGA) for high-resolution SNP array application can produce a significant amount of false positive and false negative findings. While some of these misinterpretations appear to cluster in genomic regions with high or low GC contents, the majority appears to occur randomly. Only large-scale chromosome LOH (>10Mb) can be reliably detected from FFPE tumor DNA samples (without or with WGA) but not smaller LOH or copy number alterations. Our findings here indicate a need for caution in SNP array data interpretation when using FFPE tumor-derived DNA, particularly with WGA.
2011-08-15 | GSE27399 | GEO
Project description:In cancer, proto-oncogenes are often altered by genomic amplification. Recent studies have highlighted a role for PDGFRA as an oncogene in non-small cell lung cancer. To characterize 4q12 copy number status in NSCLC, both previously published (Weir et al. PMID 17982442) and unpublished Affymetrix 250K SNP array data for 733 NSCLC samples (628 primary samples, 105 cell lines) were evaluated for copy number aberrations. 4q12 amplifications overlapping the PDGFRA/KIT locus were observed in 31 (4.2%) NSCLC samples. SNP array and FISH analysis indicate that 4q12 is amplified in 3-7% of lung adenocarcinomas and 8-10% of lung squamous cell carcinomas. In addition, the NSCLC cell line NCI-H1703 exhibits focal amplification of PDGFRA and is dependent on PDGFRα activity for cell growth. Treatment of NCI-H1703 cells with PDGFRA-specific shRNAs or with the PDGFRα/KIT small molecule inhibitors imatinib or sunitinib leads to cell growth inhibition. However, these observations do not extend to NSCLC cell lines with lower-amplitude and broader gains of chromosome 4q. Together these observations implicate PDGFRA and KIT as potential oncogenes in NSCLC, but further study is needed to define the specific characteristics of those tumors that could respond to PDGFRα/KIT inhibitors.
2009-09-15 | GSE17429 | GEO
Project description:To identify genes in the chromosome 3p12 pathway to tumorigenesis in pancreatic cancer, we screened two expression platforms and then as a third platform interrogated pancreatic cancer tumor/normal samples for differential expression. Data from the third expression platform experiments are shown herein.
2011-07-01 | GSE22780 | GEO