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Molecular Biology, Pathobiology, and Genetics |
1 Max-Delbrück Center for Molecular Medicine; 2 Institute of Pathology of the Medical Faculty; 3 Institute of Pharmacology and Toxicology of the Medical Faculty; and 4 Department of Hematology, Oncology and Tumorimmunology, Robert-Rössle Cancer Center and Helios Clinics at the Max Delbrück Center for Molecular Medicine, Charité, Humboldt University Berlin, Berlin, Germany; 5 Institute of Human Genetics and Anthropology, Heinrich-Heine University of Düsseldorf, Düsseldorf, Germany; 6 Division of Clinical Epidemiology, German Cancer Research Center, Heidelberg, Germany; and 7 Center of Advanced European Studies and Research (Caesar), Bonn, Germany
Requests for reprints: Hans-Dieter Royer, Center of Advanced European Studies and Research (Caesar), Ludwig-Erhard Allee 2, D-53175 Bonn, Germany. Phone: 49-228-965-6168; Fax: 49-228-965-6112; E-mail: royer{at}caesar.de.
YB-1 protein levels are elevated in most human breast cancers, and high YB-1 levels have been correlated with drug resistance and poor clinical outcome. YB-1 is a stress-responsive, cell cycle–regulated transcription factor with additional functions in RNA metabolism and translation. In this study, we show in a novel transgenic mouse model that human hemagglutinin-tagged YB-1 provokes remarkably diverse breast carcinomas through the induction of genetic instability that emerges from mitotic failure and centrosome amplification. The increase of centrosome numbers proceeds during breast cancer development and explanted tumor cell cultures show the phenotype of ongoing numerical chromosomal instability. These data illustrate a mechanism that might contribute to human breast cancer development.
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