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Danio rerio

ABSTRACT: Comparative oncogenomic analysis of copy number alterations in human and zebrafish tumors enables cancer driver discovery

PROVIDER: PRJNA167812 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR503018.fastq.gz	Fastqsanger.gz
	SRR503019.fastq.gz	Fastqsanger.gz
	SRR503020.fastq.gz	Fastqsanger.gz
	SRR503021.fastq.gz	Fastqsanger.gz
	SRR503022.fastq.gz	Fastqsanger.gz

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Comparative genomic hybridization of human GBM tumor vs. normal human DNA induced in mice

Project description:Highly rearranged and mutated cancer genomes present major challenges in the identification of pathogenetic events driving the cancer process. Here, we engineered lymphoma-prone mice with chromosomal instability to assess the utility of mouse models in cancer gene discovery and the extent of cross-species overlap in cancer-associated copy number aberrations. Integrating with targeted re-sequencing, our comparative oncogenomic studies efficiently identified FBXW7 and PTEN as commonly deleted or mutated tumor suppressors in human T-cell acute lymphoblastic leukemia/lymphoma (T-ALL). More generally, the murine cancers acquire widespread recurrent clonal amplifications and deletions targeting loci syntenic to alterations present in not only human T-ALL but also diverse tumors of hematopoietic, mesenchymal and epithelial types. These results thus support the view that murine and human tumors experience common biological processes driven by orthologous genetic events as they evolve towards a malignant phenotype. The highly concordant nature of genomic events encourages the use of genome unstable murine cancer models in the discovery of biologically relevant driver events in human cancer. Experiment Overall Design: 38 human GBM samples were analyzed. Normal Human DNA was used as reference. Some samples were hybridized with dye-swap replica.

2008-06-15 | E-GEOD-7602 | biostudies-arrayexpress

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