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, Pier Paolo Pandolfi
Cancer Biology and Genetics Program, Sloan-Kettering Institute, Memorial Sloan-Kettering Cancer Center, New York, New York 10021, USA.
Nature 2009 Feb 12
The first recurrent translocation event in prostate cancer has been recently described; 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 elements. 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 ERG. Tomlins et al. 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.
Citation
Brett S Carver, Jennifer Tran, Zhenbang Chen, Arkaitz Carracedo-Perez, Andrea Alimonti, Caterina Nardella, Anuradha Gopalan, Peter T Scardino, Carlos Cordon-Cardo, William Gerald, Pier Paolo Pandolfi. ETS rearrangements and prostate cancer initiation. Nature. 2009 Feb 12;457(7231): E1; discussion E2-3
PMID: 19212347
View Full Text