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Direct Evidence for Epithelial-Mesenchymal Transitions in Breast Cancer

¹ Department of Molecular Genetics; ² Human Cancer Genetics Program, Comprehensive Cancer Center; ³ Department of Molecular Virology, Immunology, and Medical Genetics, College of Medicine; ⁴ Division of Epidemiology and Biostatistics, School of Public Health; and ⁵ Department of Veterinary Biosciences, The Ohio State University; ⁶ Center for Childhood Cancer, Columbus Children's Research Institute, Columbus, Ohio; and ⁷ Genomic Medicine Institute, Cleveland Clinic Lerner Research Institute and Department of Genetics, Case Western Reserve University School of Medicine, Cleveland, Ohio

Requests for reprints: Gustavo Leone, Departments of Molecular Genetics and Molecular Virology, Immunology, and Medical Genetics, Human Cancer Genetics Program, The Ohio State University, 808 Biomedical Research Tower, 460 West 12th Avenue, Columbus, OH 43210. Phone: 614-688-4567; Fax: 614-688-4181; E-mail: gustavo.leone{at}osumc.edu, or Michael C. Ostrowski, Department of Molecular and Cellular Biochemistry, Human Cancer Genetics Program, The Ohio State University, 810 Biomedical Research Tower, 420 West 12th Avenue, Columbus, OH 43210. Phone: 614-688-3824; Fax: 614-688-4181; E-mail: michael.ostrowski{at}osumc.edu.

Key Words: epithelial-mesenchymal transitions • c-myc • mammary tumor • LacZ • breast cancer

We developed stromal- and epithelial-specific cre-transgenic mice to directly visualize epithelial-mesenchymal transition (EMT) during cancer progression in vivo. Using three different oncogene-driven mouse mammary tumor models and cell-fate mapping strategies, we show in vivo evidence for the existence of EMT in breast cancer and show that myc can specifically elicit this process. Hierarchical cluster analysis of genome-wide loss of heterozygosity reveals that the incidence of EMT in invasive human breast carcinomas is rare, but when it occurs it is associated with the amplification of MYC. These data provide the first direct evidence for EMT in breast cancer and suggest that its development is favored by myc-initiated events. [Cancer Res 2008;68(3):937–45]