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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Comparative genomic hybridization of 17 favourable histology Wilms tumour samples taken at immediate nephrectomy in order to identify changes in DNA copy number associated with clinical outcome

ABSTRACT: We have carried out microarray-based comparative genomic hybridisation (arrayCGH) on 17 Favourable histology Wilms tumour samples taken at immediate nephrectomy in order to identify changes in DNA copy number associated with clinical outcome. Tumour DNA was co-hybridised with normal female genomic DNA onto microarrays consisting of 2118 BAC clones with tiling-path coverage of chromosome 1. Data was normalised and quality-filtered, an adapted weights smoothing algorithm fitted, and changes in DNA copy number assessed for each clone.

ORGANISM(S): Homo sapiens

DISEASE(S): Wilms tumour

SUBMITTER: Anita Grigoriadis

PROVIDER: E-TABM-13 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Array CGH profiling of favourable histology Wilms tumours reveals novel gains and losses associated with relapse.

Natrajan R R Williams R D RD Hing S N SN Mackay A A Reis-Filho J S JS Fenwick K K Iravani M M Valgeirsson H H Grigoriadis A A Langford C F CF Dovey O O Gregory S G SG Weber B L BL Ashworth A A Grundy P E PE Pritchard-Jones K K Jones C C

The Journal of pathology 20060901 1

Despite the excellent survival of Wilms tumour patients treated with multimodality therapy, approximately 15% will suffer from tumour relapse, where response rates are markedly reduced. We have carried out microarray-based comparative genomic hybridisation on a series of 76 Wilms tumour samples, enriched for cases which recurred, to identify changes in DNA copy number associated with clinical outcome. Using 1Mb-spaced genome-wide BAC arrays, the most significantly different genomic changes betwe ...[more]

PMID: 16823893

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Comparative genomic hybridization of 100 favourable histology Wilms tumour samples taken at immediate nephrectomy in order to identify changes in DNA copy number associated with clinical outcome

Project description:We have carried out microarray-based comparative genomic hybridisation (arrayCGH) on 100 favourable histology Wilms tumour samples taken at immediate nephrectomy in order to identify changes in DNA copy number associated with clinical outcome. Tumour DNA was co-hybridised with normal female genomic DNA onto microarrays consisting of 4263 BAC clones with an approximate 1Mb spacing throughout the genome. Data was normalised and quality-filtered, an adapted weights smoothing algorithm fitted, and changes in DNA copy number assessed for each clone.

2006-05-11 | E-TABM-10 | biostudies-arrayexpress

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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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Comparative genomic hybridization of high grade gliomas arising in children and young people

Project description:As genome-scale technologies begin to unravel the complexity of the equivalent tumours in adults, detailed characterisation of high grade gliomas in children have until recently been lacking. In order to validate and extend investigations of the differences between paediatric and adult tumours, we carried out copy number profiling by array CGH using a 32K BAC platform on 63 formalin-fixed paraffin-embedded (FFPE) cases of high grade glioma arising in children and young people (<23 yrs).

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Comparative genomic hybridization of kidney samples from Wilms tumor patients to accurately map 1p13 breakpoints

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2009-04-15 | E-GEOD-11265 | biostudies-arrayexpress

TP53 mutational status is a potential marker for risk stratification in Wilms tumour with diffuse anaplasia

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-08-30 | E-GEOD-60940 | biostudies-arrayexpress

TP53 mutational status is a potential marker for risk stratification in Wilms tumour with diffuse anaplasia [aCGH]

Project description:The presence of diffuse anaplasia in Wilms tumours (DAWT) is associated with TP53 mutations and poor outcome. As patients receive intensified treatment, we sought to identify whether TP53 mutational status confers additional prognostic information. We studied 40 patients with DAWT with anaplasia in the tissue from which DNA was extracted and analysed for TP53 mutations and 17p loss. The majority of cases were profiled by copy number (n=32) and gene expression (n=36) arrays. TP53 mutational status was correlated with patient event-free and overall survival, genomic copy number instability and gene expression profiling. From the 40 cases, 22 (55%) had TP53 mutations (2 detected only after deep-sequencing), 20 of which also had 17p loss (91%); 18 (45%) cases had no detectable mutation but three had 17p loss. Tumours with TP53 mutations and/or 17p loss (n=25) had an increased risk of recurrence as a first event (p=0.03, hazard ratio (HR), 3.89; 95% confidence interval (CI), 1.26-16.0) and death (p=0.04, HR, 4.95; 95% CI, 1.36-31.7) compared to tumours lacking TP53 abnormalities. DAWT carrying TP53 mutations showed increased copy number alterations compared to those with wild-type, suggesting a more unstable genome (p=0.03). These tumours showed deregulation of genes associated with cell cycle and DNA repair biological processes. This study provides evidence that TP53 mutational analysis improves risk stratification in DAWT. This requires validation in an independent cohort before clinical use as a biomarker. 32 tumour samples were profiled by aCGH, in 2-colour hybridisations with common pooled unrelated normal genomic DNA in the reference channel. There were no replicates.

2014-08-30 | E-GEOD-60852 | biostudies-arrayexpress

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