Distinct classes of chromosomal rearrangements create oncogenic ETS gene fusions in prostate cancer

Scott A. Tomlins, Bharathi Laxman, Saravana M. Dhanasekaran, Beth E. Helgeson, Xuhong Cao, David S. Morris, Anjana Menon, Xiaojun Jing, Qi Cao, Bo Han, Jindan Yu, Lei Wang, James E. Montie, Mark A. Rubin, Kenneth J. Pienta, Diane Roulston, Rajal B. Shah, Sooryanarayana Varambally, Rohit Mehra and Arul M. Chinnaiyan ()
Additional contact information
Scott A. Tomlins: Michigan Center for Translational Pathology
Bharathi Laxman: Michigan Center for Translational Pathology
Saravana M. Dhanasekaran: Michigan Center for Translational Pathology
Beth E. Helgeson: Michigan Center for Translational Pathology
Xuhong Cao: Michigan Center for Translational Pathology
David S. Morris: Department of Urology,
Anjana Menon: Michigan Center for Translational Pathology
Xiaojun Jing: Michigan Center for Translational Pathology
Qi Cao: Michigan Center for Translational Pathology
Bo Han: Michigan Center for Translational Pathology
Jindan Yu: Michigan Center for Translational Pathology
Lei Wang: Michigan Center for Translational Pathology
James E. Montie: Department of Urology,
Mark A. Rubin: Brigham and Women’s Hospital
Kenneth J. Pienta: Department of Urology,
Diane Roulston: Michigan Center for Translational Pathology
Rajal B. Shah: Michigan Center for Translational Pathology
Sooryanarayana Varambally: Michigan Center for Translational Pathology
Rohit Mehra: Michigan Center for Translational Pathology
Arul M. Chinnaiyan: Michigan Center for Translational Pathology

Nature, 2007, vol. 448, issue 7153, 595-599

Abstract: Distinct translocation mechanisms and additional translocation partners for ETS genes are found in prostate cancer. This study also provides the first functional evidence that ETS gene deregulation can promote cancer cell invasion in cell lines and pre-malignant prostate lesions in a transgenic mouse model.

Date: 2007
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DOI: 10.1038/nature06024

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