Ef165dd2-e7e4-4818-a502-ff7affdafd76 - samples
Ontology highlight
ABSTRACT:
PROVIDER: EGAD00001008380 | EGA |
REPOSITORIES: EGA
Similar Datasets
Project description:KCL SNP array samples for copy number analysis
| EGAD00001008379 | EGA
Project description:Genome-wide DNA copy number was studied to determine whether the Wilms' tumor samples generally show normal copy number variation comparing to the colon tumor samples We used custom Nimblegen microarrays to determine the genome-wide DNA copy number in human Wilms' Tumor samples
2011-08-29 | GSE29374 | GEO
Project description:Copy number profiling of CLL patient samples
| PRJEB97783 | ENA
Project description:DNA hypomethylation could lead to activation of alternate promoters in GBM. We profiled DNA methylation and H3K4me3 genome-wide, and also performed expression and copy number analysis on the same samples In this dataset, we include all array CGH copy number data obtained for five GBMs. We used estimated copy number to normalize sequencing-based methylation data.
2013-08-13 | GSE49808 | GEO
Project description:Chromosomal copy number variations (CNV) have been associated with various neurological and developmental disorders and chromosomal microarray (CMA) is a method of choice to diagnose Copy Number Gain/Loss syndromes. Recently, next-generation sequencing (NGS)-based low-coverage whole genome sequencing (LC-WGS) has been applied to detect Copy Number Gain/Loss syndromes. This dataset is intended to be used as a “Golden standard data set” for development of LC-WGS analysis method. It consists of patients (n=63) who have a mental delay and/or physical disability phenotype and normal (n=20) phenotype.
2018-09-29 | GSE120624 | GEO
Project description:High-grade serous ovarian cancer (HGSOC) is thought to originate from the fallopian tube (FT), highlighting the importance of studying molecular features across tumor samples. This dataset contains bulk RNA sequencing data from tumor samples of HGSOC patients. The data can be used for driver mutations and copy number alterations (CNAs) profiling and analysis of gene expression patterns, including regions relevant to HLA typing. This submission contains bulk RNA sequencing data associated with this study.
2026-04-07 | GSE301179 | 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:Chromosomal DNA copy number alterations are a hallmark of human malignancies, including hepatocellular carcinoma (HCC). However, which oncogenes or tumor suppressors located on regions with DNA copy number aberration may contribute to HCC initiation and progression still remain obscure. Here we performed a genome-wide DNA copy number analysis on human HCC samples to identify novel potential oncogenes or tumor suppressors with DNA copy number aberrations. Genome-wide DNA copy numbers analysis was performed with single nucleotide polymorphism micoarray. RT-PCR and immunohistochemical staining were employed to evaluate the NOXIN expression in HCC samples. Colony formation, cell cycle analysis and tumor xenograft assays were performed to assess the role of NOXIN in HCC cells. Reciprocal co-immunoprecipitation experiments were used to detect the interaction between NOXIN and DNA polymerase a primase. Genome-wide DNA copy number analysis on 43 paired HCC samples indentified the smallest DNA amplification region containing NOXIN, along with the elevated transcript. NOXIN overexpression was significantly associated with HCC tumor stage. Enforced NOXIN promoted cellular proliferation, colony formation, cell migration and in vivo tumorigenicity, whereas RNA interference against NOXIN can attenuate these effects. Interestingly, NOXIN overexpression can accelerate the G1-S transition of cell cycle progression through enhancing DNA synthesis in HCC cells, as indicated by bromodeoxyuridine incorporation. Furthermore, NOXIN can interact with DNA polymerase a, implying that NOXIN may promote de novo DNA synthesis via affiliating formation of DNA polymerase-primase complex. Affymetrix SNP arrays were performed according to the manufacturer's directions on DNA extracted from hepatocellular carcinoma and adjacent liver tissue samples.
2013-07-30 | GSE49317 | GEO
Project description:Copy number variation profiles comparing control female Dehong chicken blood DNA with 3 different chicken breeds (white Leghorn, Cobb broiler, and Dou chicken) blood DNA. Each test breed had one male and one female sample, for a total of 6 test DNA samples. The goal is to determine the global copy number variation profiles between chicken breeds.
2011-04-12 | GSE28526 | GEO
Project description:Non-small cell lung cancer (NSCLC) presents a notoriously genomically unstable cancer type, with numerous large scale and focal genomic aberrations resulting in gene copy number variations across the whole genome. The relations of these gene copy number changes to subsequent mRNA levels are only fragmentarily understood. The aim of this study was an integrated analysis of gene copy number changes and corresponding gene expression in a large clinically annotated NSCLC patient cohort. Fresh frozen tumor sample from 190 resected NSCLC patients were subjected to SNP arrays and gene expression array analysis resulting 39788 tested copy number/ RNA expression pairs. Correlation analysis using an externally centered correlation coefficient (ECCC) revealed that gene expression of 19058 genes was significantly influenced by gene copy number changes (FDR < 0.05). However, only 440 probe sets demonstrated high correlations (ECCC > 0.7) that were mostly due to few cases with high gene copy number gains. These gene copy number dependent genes were clustered in only few chromosomal hot spot regions and classical oncogenes (e.g. EGFR, MDM2, KRAS) are overrepresented among these genes. In a meta-analysis, including 1585 NSCLC patients, gene expression levels from 70 of 440 (16%) gene-copy-number-dependent genes were associated with survival. In conclusion, the genome-wide analysis indicates that gene copy number aberrations influence directly gene expression levels in a distinct subset of genes. The concrete illustration of these molecular relations help to interpret the impact of gene copy number changes and may serve as starting points to identify new cancer drivers in NSCLC.
2016-08-31 | GSE76730 | GEO