Ontology highlight
ABSTRACT:
PROVIDER: PRJNA214971 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Copy number data from five primary human glioblastomas (frozen surgical resection)
| PRJNA214974 | ENA
Project description:We have employed a laser capture microdissection technique and single nucleotide polymorphism arrays to characterize genomic alterations associated with the development of glioblastomas. Combined analysis of LOH and copy number revealed that more than half of the identified 254 LOH loci showed no copy number alteration, indicating the presence of copy-number neutral LOH Keywords: DNA copy number, Loss of heterozygosity Affymetrix 50K SNP mapping arrays were used to profile 14 primary glioblastomas (GBMs) with matched blood DNA samples. Loss of heterozygosity (LOH) and copy number abnormality (CNA) profiles were derived from each tumour-blood pair.
2009-03-01 | E-GEOD-10922 | biostudies-arrayexpress
Project description:We have employed a laser capture microdissection technique and single nucleotide polymorphism arrays to characterize genomic alterations associated with the development of glioblastomas. Combined analysis of LOH and copy number revealed that more than half of the identified 254 LOH loci showed no copy number alteration, indicating the presence of copy-number neutral LOH Keywords: DNA copy number, Loss of heterozygosity
2009-03-01 | GSE10922 | GEO
Project description:Copy number analyses of regionally separated biopsies from primary and metastatic lesions of five colorectal cancers
2014-06-16 | GSE58512 | GEO
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:Glioblastoma multiforme shows multiple chromosomal aberrations, the impact of which on gene expression remains unclear. To investigate this relationship and to identify putative initiating genomic events, we integrated a paired copy number and gene expression survey in glioblastoma using whole human genome arrays. Loci of recurrent copy number alterations were combined with gene expression profiles obtained on the same tumor samples. We identified a set of 406 ‘cis-acting DNA targeted genes’ corresponding to genomic aberrations with direct copy-number-driving changes in gene expression, defined as genes with either significantly concordant or correlated changes in DNA copy number and expression. Functional annotation revealed that these genes participate in key processes of cancer cell biology, providing insights into the genetic mechanisms driving glioblastoma. The robustness of the gene selection was validated on an external microarray data set including 81 glioblastomas and 23 non-neoplastic brain samples. The integration of array CGH and gene expression data highlights a robust ‘cis-acting DNA targeted genes’ signature that may be critical for glioblastoma progression, with two tumor suppressor genes PCDH9 and STARD13 that could be involved in tumor invasiveness and resistance to etoposide. Keywords: Glioblastoma Multiforme, array CGH, microarray, data integration
2008-10-30 | GSE10878 | GEO
Project description:Expression data from five primary human glioblastomas (frozen surgical resection) and one non-neoplastic adult brain (frozen autopsy tissue)
| PRJNA214968 | ENA
Project description:Glioblastoma is an incurable brain cancer characterized by high genetic and pathological heterogeneity. Here we mapped active chromatin landscapes with gene expression, whole-exomes, copy number profiles, and DNA methylomes across 44 glioblastoma stem cell (GSCs) models, 50 primary glioblastomas, and 10 neural stem cells (NSCs) with the goal of identifying essential super enhancer (SE)-associated genes and the core transcription factors that establish them and glioblastoma identity. Glioblastomas segregate with two dominant enhancer profiles that coopt unique developmental transcription factor regulatory programs to enforce tumor identity. From group specific enhancer profiles, we inferred core transcription factors that define subgroup identity. These transcription factors show higher activity in glioblastomas versus normal neural stem cells, are associated with poor clinical outcomes, and are required for glioblastoma growth in vitro and in vivo. Given challenges with genetically-defined targeted therapies for glioblastoma, we propose targeting underlying transcriptional identity may serve as an important therapeutic strategy.
2019-03-18 | GSE119755 | GEO
Project description:Copy number data from paired primary and relapse ovarian tumours
| PRJNA169072 | ENA
Project description:Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Characterization of DNA copy number changes in 54 glial brain tumors using a cDNA microarray-based comparative genomic hybridization method. Tumors: 54 fresh-frozen glioma specimens subjected to standard WHO classification. Specimens included astrocytic [3 juvenile pilocytic astrocytomas, 1 low-grade astrocytic glioma, 3 anaplastic astrocytomas, 31 glioblastomas (of these 3 secondary glioblastomas and 2 gliosarcomas)], oligodendroglial [5 oligodendrogliomas, 3 anaplastic oligodendrogliomas], and 7 anaplastic oligoastrocytomas tumors. One tumor had been classified as glioneuronal neoplasm. Human male and female genomic reference DNA was purchased from Promega (Promega, Madison, WI). The results provide insights into molecular genetic changes associated with gliomagenesis. Keywords: other
2005-05-27 | GSE1991 | GEO