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DNA copy number variation from human Wilms' Tumor samples

ABSTRACT: 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

ORGANISM(S): Homo sapiens

PROVIDER: GSE29374 | GEO | 2011/08/29

SECONDARY ACCESSION(S): PRJNA140217

REPOSITORIES: GEO

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DNA copy number variation from human Wilms' Tumor samples

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 We isolated genomic DNA from human Wilms' tumor tissues and hybridized to custom-designed Nimblegen microarrays (CHARM arrays).

2011-08-28 | E-GEOD-29374 | biostudies-arrayexpress

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Circulating miRNA in serum of Wilms tumor patients

Project description:Abstract: Background: MiRNA signatures in human sera have been reported for various tumor diseases. Here we generated miRNA profiles analyzing 1205 mature miRNA transcripts of serum samples of Wilms tumor patients, taken prior and after chemotherapy according to SIOP protocol 2001. Using a feature subset selection filter approach we identified a minimal number of miRNAs with a maximum contribution for the classification between treated and untreated patients and between patients and controls. Results: Analyzing 1205 mature miRNAs, we separated controls and Wilms tumor patients prior chemotherapy with an accuracy of 0.81. We obtained a similar accuracy (0.82) for the separation between controls and sera of Wilms tumor patients after preoperative chemotherapy. We identified 23 miRNAs that were differentially expressed in both comparisons. Subset selection improved the overall classification accuracy between controls and Wilms tumor patients prior and after chemotherapy to 0.94 and 0.91, respectively. Subset selection also allowed separating between Wilms tumor patients prior and after chemotherapy with an accuracy of 0.98. Conclusion: Our analysis identified serum based miRNA signatures that allowed separating between controls, untreated Wilms tumor patients, and Wilms tumor patients after chemotherapy with high accuracy for each of these comparisons.

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Comparative genomic hybridization of human perilobar nephrogenic rest and matching Wilms tumours to identify changes in DNA copy number associated with IGF-driven Wilms tumorigenesis

Project description:We have carried out microarray-based comparative genomic hybridisation (arrayCGH) on 50 perilobar nephrogenic rest and 25 matching Wilms tumours in order to identify changes in DNA copy number associated with IGF-driven Wilms tumorigenesis. All patient samples were formalin fixed-paraffin embedded archival material. Tumour DNA was co-hybridised with normal female genomic DNA onto 5.8K, 0.9Mb-spaced (E-MEXP-213) and/or a 16K, 100kb-spaced BAC array. Data was normalised and quality-filtered, an adapted weights smoothing algorithm fitted, and changes in DNA copy number assessed for each clone.

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Wilms' tumor 1 WT1(-KTS) isoform time course induction in U2OS cells

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Project description:Wilms tumor (WT) is the most common renal tumor in childhood. Among others, MYCN copy number gain and MYCN P44L and MAX R60Q mutations have been identified in WT. The proto-oncogene MYCN encodes a transcription factor that requires dimerization with MAX to activate transcription of numerous target genes. MYCN gain has been associated with adverse prognosis. The MYCN P44L and MAX R60Q mutations, located in either the transactivating or basic helix-loop-helix domain, respectively, are predicted to be damaging by different pathogenicity prediction tools. We screened a large cohort of unselected WTs and revealed frequencies of 3 % for MYCN P44L and 0.8 % for MAX R60Q, associated with a higher risk of relapse in the case of MYCN. Biochemical characterization identified a reduced transcriptional activation potential for MAX R60Q, while the MYCN P44L mutation did not change activation potential or protein stability. The protein interactome of N-MYC-P44L was likewise not altered as shown by mass spectrometric analyses of purified N-MYC complexes. Nevertheless, we could identify a number of novel N-MYC partner proteins, and several of these are known for their oncogenic potential. Correlated expression in WT samples suggests a role in WT oncogenesis and they expand the range of potential biomarkers for WT stratification and targeting, especially for high-risk WT.

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Project description:Copy number variations (CNVs), which represent a significant source of genetic diversity in mammals, are currently being associated with phenotypes of clinical relevance, mostly in humans and mice. Notwithstanding, little is known about the extent of CNV that contributes to genetic variation in farm animals, including pig. This Nimblegen experiment reports a genome-wide high resolution map of copy number variation in the porcine genome. After remapping the initial CNV sequences to the latest genome assembly (Sus scrofa v.9), 84 CNV regions (CNVRs) were identified among the genomes of 21 related porcine samples from Duroc breed. We used a set of NimbleGen CGH arrays that tile across the assayable portion of the pig genome with approximately 2.1 million probes, at a 502 bp average probe spacing (Sus scrofa pre assembly version 6). These CNVRs covered 2 Mb of the genome, and ranged in size from 4 to 352 kb (median size of 12 kb). Together, this analysis provides a useful resource to assist with the assessment of CNVs in the contexts of porcine variation, health and productive efficiency.

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