Affymetrix SNP array data for colon cancer samples
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE62875 | GEO | 2014/12/01
SECONDARY ACCESSION(S): PRJNA265875
REPOSITORIES: GEO
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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
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.
2009-04-16 | GSE14960 | 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:This study used tumour and paired normal samples from 28 Sézary Syndrome (SS) patients to define recurrent regions of chromosomal aberrations. Our data identified recurrent losses of 17p13.2-p11.2 and 10p12.1-q26.3 occurring in 71 and 68% of cases respectively; common gains were detected for 17p11.2-q25.3 (64%) and chromosome 8/8q (50%). Moreover, we identified novel genomic lesions recurring in more than 30% of tumours: loss of 9q13-q21.33 and gain of 10p15.3-10p12.2. In the Sézary Syndrome cases analysed, we could find several small and few large Uniparental Disomies involving interstitial or telomeric regions of LOH occurring mainly for chromosome 10 and to a lesser extent for chromosome 9 and 17. In the attempt to correlate Copy Number data and clinical parameters we find a relationship between complex pattern of chromosomal aberrations, involving at least three recurrent Copy Number alterations, and shorter survival. Integrating mapping and transcriptional data we were able to identify a total of 113 deregulated transcripts in aberrant chromosomal regions that included cancer related genes such as members of the NF-kB pathway (BAG4, BTRC, NKIRAS2, PSMD3, TRAF2) that might explain its constitutive activation in CTCL. Matching this list of genes with those discriminating patients with different survival times we identify several common candidates that might exert critical roles in Sézary Syndrome, like BUB3 and PIP5K1B.
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Project description:This study aimed to generate a new panel of comprehensively, genomically characterized high-grade serous ovarian carcinoma (HGSOC) cell line and xenograft models. Multidimensional genomic data were generated and compared between cell lines/xenografts and the tumours they were derived from, indicating the cell lines/xenografts are highly similar to their patient-matched tumours. Cell line/xenograft data were also compared to TCGA ovarian tumours to show the cell lines are good models of clinical HGSOC. Affymetrix SNP 6 arrays were performed according to the manufacturer's instructions on genomic DNA extracted from i) tumour cells purified from ovarian tumour ascites, ii) established cell lines, iii) patient derived xenografts, and iv) lymphoblast lines. Evaluation of the similarity in copy number/methylation/gene expression/mutational profiles of cell lines/tumours/xenografts was performed.
2016-08-11 | E-GEOD-71522 | biostudies-arrayexpress
Project description:Preeclampsia is a heterogeneous and complex disease caused by multiple factors, including heredity and environment. However, the underlying mechanism remains elusive due to diverse races, geography, and other factors. Previous findings have revealed that there is a tendency for preeclampsia to run in families. To define genetic factors associated with preeclampsia, we performed a genome-wide analysis of preeclampsia samples from 10 preeclampsia cases and 10 healthy age- and gravidity-matched normotensive pregnant women. We identified 27 aberrant copy number variations related to preeclampsia, including 22 deletions and 5 duplications. These differential copy number variant regions involved 27 differential genes, including SPATA6L, PPP2R3B, PREX2, IL1RAPL1, OR52N1, OR52N5, CHSY1, DPP6, KRTAP9-7, LPA, NTRK1, BTNL3, TBC1D3F, TBC1D3, LOC440434 , EYA2, APOBEC3A_B, APOBEC3A, APOBEC3B, FHIT, EXT1, PRR14, FBRS, LMF1, MALT1, BCAS1, and MIR4756. These findings suggest that these differential genes may be associated with the pathogenesis of preeclampsia and require further investigation.
2022-01-01 | GSE192614 | GEO
Project description:Affymetrix SNP arrays were performed according to the manufacturer's directions on DNA extracted from fresh frozen tissues. To obtain a profile of copy number alterations in RMS, we studied 65 samples in 60 RMS cases. Other data of 38 samples are deposited in GSE41263: GSM1528059 GSM1528057 GSM1528061 GSM1528058 GSM1528054 GSM1528060 GSM1012723 GSM1012722 GSM1012746 GSM1528055 GSM1528056 GSM1530028 GSM1012751 GSM1012724 GSM1012726 GSM1012747 GSM1012725 GSM1012716 GSM1012735 GSM1012713 GSM1012736 GSM1012737 GSM1012738 GSM1012730 GSM1012739 GSM1012740 GSM1012750 GSM1012717 GSM1012718 GSM1012719 GSM1012741 GSM1012732 GSM1012715 GSM1012720 GSM1012742 GSM1012721 GSM1012743 GSM1012744
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Project description:Pediatric patients with de novo acute myeloid leukemia. To define genomic architecture, we performed genome-wide copy number abberation analysis in 460 paired diagnostic-remission bone marrow aspirates.
2017-04-10 | GSE95496 | GEO
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.
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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.
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