Tomlins et al. reply

Replying to: Carver, B. S. et al. Nature 457, 10.1038/nature07738 (2009)Carver et al. question our recent report that mice expressing ETV1 under the control of the probasin promoter (ARR2Pb) develop mouse prostatic intraepithelial neoplasia (mPIN). They report the generation of transgenic ARR2Pb-ERG...

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Bibliographic Details
Published in:	Nature (London) 2009-02, Vol.457 (7231), p.E2-E3
Main Authors:	Tomlins, Scott A, Laxman, Bharathi, Dhanasekaran, Saravana M, Helgeson, Beth E, Cao, Xuhong, Morris, David S, Menon, Anjana, Jing, Xiaojun, Cao, Qi, Han, Bo, Yu, Jindan, Wang, Lei, Montie, James E, Rubin, Mark A, Pienta, Kenneth J, Roulston, Diane, Shah, Rajal B, Varambally, Sooryanarayana, Mehra, Rohit, Chinnaiyan, Arul M
Format:	Article
Language:	eng
Subjects:	Development and progression DNA binding proteins Gene expression Genetic aspects Physiological aspects Prostate cancer Risk factors
Online Access:	Get full text
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Summary:	Replying to: Carver, B. S. et al. Nature 457, 10.1038/nature07738 (2009)Carver et al. question our recent report that mice expressing ETV1 under the control of the probasin promoter (ARR2Pb) develop mouse prostatic intraepithelial neoplasia (mPIN). They report the generation of transgenic ARR2Pb-ERG mice with no phenotypic differences from control mice. They propose that this demonstrates that ETS genetic rearrangements do not initiate prostate tumorigenesis and use data from human prostate cancer studies to propose that ETS rearrangements are associated with progression from PIN to prostate cancer. Although we and others have shown that ARR2Pb-ETV1 and ARR2Pb-ERG mice develop mPIN, we have consistently proposed that in human prostate cancer development, ETS rearrangements mediate the transition from PIN to cancer.
ISSN:	0028-0836 1476-4687