ETS rearrangements and prostate cancer initiation

Brett S. Carver (), Jennifer Tran (), Zhenbang Chen (), Arkaitz Carracedo-Perez (), Andrea Alimonti (), Caterina Nardella (), Anuradha Gopalan, Peter T. Scardino, Carlos Cordon-Cardo, William Gerald and Pier Paolo Pandolfi ()
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Brett S. Carver: Cancer Biology and Genetics Program, Sloan-Kettering Institute, Memorial Sloan-Kettering Cancer Center
Jennifer Tran: Cancer Biology and Genetics Program, Sloan-Kettering Institute, Memorial Sloan-Kettering Cancer Center
Zhenbang Chen: Cancer Biology and Genetics Program, Sloan-Kettering Institute, Memorial Sloan-Kettering Cancer Center
Arkaitz Carracedo-Perez: Cancer Biology and Genetics Program, Sloan-Kettering Institute, Memorial Sloan-Kettering Cancer Center
Andrea Alimonti: Cancer Biology and Genetics Program, Sloan-Kettering Institute, Memorial Sloan-Kettering Cancer Center
Caterina Nardella: Cancer Biology and Genetics Program, Sloan-Kettering Institute, Memorial Sloan-Kettering Cancer Center
Anuradha Gopalan: Memorial Sloan-Kettering Cancer Center
Peter T. Scardino: Memorial Sloan-Kettering Cancer Center
Carlos Cordon-Cardo: Columbia University
William Gerald: Memorial Sloan-Kettering Cancer Center
Pier Paolo Pandolfi: Cancer Biology and Genetics Program, Sloan-Kettering Institute, Memorial Sloan-Kettering Cancer Center

Nature, 2009, vol. 457, issue 7231, E1-E1

Abstract: Abstract Arising from: Tomlins et al. Nature 448, 595–599 (2007)10.1038/nature06024 ; Tomlins et al. reply The first recurrent translocation event in prostate cancer has been recently described1; it results in the translocation of an ETS (E26 transformation specific) transcription factor (ERG or ETV1) to the TMPRSS2 promoter region, which contains androgen responsive elements1. The TMPRSS2:ERG genetic rearrangement has been reported to occur in approximately 40% of primary prostate tumours (ETV1 genetic rearrangements occur at a much lower frequency), and it results in the aberrant androgen-regulated expression of ERG1,2,3. Tomlins et al.4 concluded that ETS genetic rearrangements are sufficient to initiate prostate neoplasia. However, here we show that ETS genetic rearrangements may in fact represent progression events rather than initiation events in prostate tumorigenesis. To this end, we demonstrate that the prostate-specific overexpression of ERG does not initiate prostate tumorigenesis.

Date: 2009
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DOI: 10.1038/nature07738

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