Abstract
The complexity of genomic aberrations in most human tumors hampers delineation of the genes that drive the tumorigenic process. In this issue of Cell, and demonstrate that cognate mouse tumor models recapitulate these genetic alterations with unexpected fidelity. These results indicate that cross-species genomic analysis is a powerful strategy to identify the responsible genes and assess their oncogenic capacity in the appropriate genetic context.
MeSH terms
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Adaptor Proteins, Signal Transducing / genetics
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Animals
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Carcinoma, Hepatocellular / genetics
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Cell Cycle Proteins
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Genomics
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Humans
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Inhibitor of Apoptosis Proteins / genetics
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Liver Neoplasms / genetics
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Melanoma / genetics
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Mice
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Nuclear Proteins / genetics
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Oncogenes*
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Phosphoproteins / genetics
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Species Specificity
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Trans-Activators / genetics
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Transcription Factors
Substances
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Adaptor Proteins, Signal Transducing
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Cell Cycle Proteins
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Inhibitor of Apoptosis Proteins
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NEDD9 protein, human
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Nuclear Proteins
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Phosphoproteins
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Trans-Activators
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Transcription Factors
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YY1AP1 protein, human