ETS gene fusions and PTEN loss are common events in prostate cancer, but their interactions are not well understood. A new study in mice suggests that overexpression of ETS in the setting of PTEN loss increases androgen receptor binding and restores androgen receptor transcriptional activity (pages 1023–1029).
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References
Tomlins, S.A. et al. Science 310, 644–648 (2005).
Baca, S.C. et al. Cell 153, 666–677 (2013).
Barbieri, C.E. et al. Nat. Genet. 44, 685–695 (2012).
Lin, C. et al. Cell 139, 1069–1083 (2009).
Rubin, M.A., Maher, C.A. & Chinnaiyan, A.M. J. Clin. Oncol. 29, 3659–3668 (2011).
Attard, G. et al. Cancer Res. 69, 2912–2918 (2009).
Reid, A.H.M. et al. Br. J. Cancer 102, 678–684 (2010).
Carver, B.S. et al. Cancer Cell 19, 575–586 (2011).
Chen, Y. et al. Nat Med. 19, 1023–1029 (2013).
Liu, W. et al. Nat. Med. 15, 559–565 (2009).
King, J.C. et al. Nat. Genet. 41, 524–526 (2009).
Baena, E. et al. Genes Dev. 27, 683–698 (2013).
Yu, J. et al. Cancer Cell 17, 443–454 (2010).
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Demichelis, F., Attard, G. A step toward functionally characterized prostate cancer molecular subtypes. Nat Med 19, 966–967 (2013). https://doi.org/10.1038/nm.3285
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DOI: https://doi.org/10.1038/nm.3285
