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Cross-species comparisons of cancer signaling

Nature Genetics volume 37, pages 7–8 (2005)Cite this article

Modeling of human cancer in genetically engineered mice and genome-wide measurements of mRNA expression have now been combined to accelerate the search for new molecularly targeted therapies against cancer. Looking forward, we propose a community-wide systematic effort to model and characterize an array of different cancer-related aberrant signaling pathways in several mouse models of cancer.

The mutations that cause cancer trigger thousands of perturbations in cell circuitry components, such as changes in gene expression levels. Even though tumorigenesis in mice does not fully parallel that in humans, is it possible that mouse models of cancer share 'conserved' changes that will allow cancer biologists to distinguish the crucial events from the multitude of secondary or adaptive changes? The signal coming from such a cross-species comparison would be analogous to the detection of conserved noncoding genomic regulatory regions by comparative genomics1. Three recent studies, reported in Cancer Cell2 and Nature Genetics3,4, including one by Alejandro Sweet-Cordero and colleagues on page 48 of this issue4, have detected different versions and strengths of cancer signaling conservation in gene expression data.

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Figure 1: Using mouse models to explore systematically the gene-expression changes associated with aberrant cancer signaling pathways across different tissue types.

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Authors and Affiliations

  1. Crump Institute for Molecular Imaging and the Department of Molecular and Medical Pharmacology,

    Thomas G Graeber & Charles L Sawyers

  2. Howard Hughes Medical Institute, and the Departments of Medicine, Molecular and Medical Pharmacology, and Urology at the David Geffen School of Medicine, University of California, Los Angeles, 90095, California, USA

    Thomas G Graeber & Charles L Sawyers

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  1. Thomas G Graeber
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Graeber, T., Sawyers, C. Cross-species comparisons of cancer signaling. Nat Genet 37, 7–8 (2005). https://doi.org/10.1038/ng0105-7

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