Synergistic response to oncogenic mutations defines gene class critical to cancer phenotype

Helene R. McMurray, Erik R. Sampson, George Compitello, Conan Kinsey, Laurel Newman, Bradley Smith, Shaw-Ree Chen, Lev Klebanov, Peter Salzman, Andrei Yakovlev and Hartmut Land ()
Additional contact information
Helene R. McMurray: Department of Biomedical Genetics,
Erik R. Sampson: Department of Biomedical Genetics,
George Compitello: Department of Biomedical Genetics,
Conan Kinsey: Department of Biomedical Genetics,
Laurel Newman: Department of Biomedical Genetics,
Bradley Smith: Department of Biomedical Genetics,
Shaw-Ree Chen: Department of Biomedical Genetics,
Lev Klebanov: Department of Biostatistics and Computational Biology,
Peter Salzman: Department of Biostatistics and Computational Biology,
Andrei Yakovlev: Department of Biostatistics and Computational Biology,
Hartmut Land: Department of Biomedical Genetics,

Nature, 2008, vol. 453, issue 7198, 1112-1116

Abstract: Cancer-inducing genes: Role of Ras/p53 synergy Oncogenes and/or the loss of tumour suppressor genes generally cooperate with each other in transforming cells into cancer cells. A new study identifies a list of genes synergistically regulated by the Ras oncogene and loss of the p53 tumour suppressor gene. Many of these genes are essential for tumour formation in vivo, whereas few of the genes regulated by either Ras or p53 alone are important. This establishes a new approach to finding genes important in tumorigenesis that may also represent novel targets for tumour therapy.

Date: 2008
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DOI: 10.1038/nature06973

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