Article
Insertional mutagenesis in mice deficient for p15Ink4b, p16Ink4a, p21Cip1, and p27Kip1 reveals cancer gene interactions and correlations with tumor phenotypes.
Cancer research - 15 Jan 2010
Kool Jaap, Uren Anthony G, Martins Carla P, Sie Daoud, de Ridder Jeroen, Turner Geoffrey, van Uitert Miranda, Matentzoglu Konstantin, Lagcher Wendy, Krimpenfort Paul, Gadiot Jules, Pritchard Colin, Lenz Jack, Lund Anders H, Jonkers Jos, Rogers Jane, Adams David J, Wessels Lodewyk, Berns Anton, van Lohuizen Maarten
Abstract excerpt
The cyclin dependent kinase (CDK) inhibitors p15, p16, p21, and p27 are frequently deleted, silenced, or downregulated in many malignancies. Inactivation of CDK inhibitors predisposes mice to tumor development, showing that these genes function as tumor suppressors. Here, we describe high-throughput murine leukemia virus insertional mutagenesis screens in mice that are deficient for one or two CDK inhibitors. We...
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