Androgen receptor splice variants might be associated with castration resistance in prostate cancer as well as resistance to hormonal therapies including abiraterone and enzalutamide. New data demonstrate that splice variants can form dimers with each other as well as with the full-length androgen receptor, and that dimerization is required for androgen-independent transcriptional activation of target genes.
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E.S.A. has served as a paid consultant/advisor for Astellas, Dendreon, Essa, Janssen, Medivation and Sanofi; he has received research funding from Dendreon, Exelixis, Genentech, Janssen, Johnson & Johnson, Novartis, Sanofi and Tokai; he is a co-inventor of a technology that has been licensed to Tokai. J.L. has served as a paid consultant/advisor for Astellas, has been a speaker for Gilead and Sanofi, has received research funding from Astellas, Mirati, Orion, Sanofi and Tokai; he is also co-inventor of a technology that has been licensed to Tokai. Relevant disclosures have been reviewed and approved by Johns Hopkins University in accordance with its conflict of interest policies.
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Antonarakis, E., Luo, J. AR splice variant dimerization—clinical implications. Nat Rev Urol 12, 431–433 (2015). https://doi.org/10.1038/nrurol.2015.184
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DOI: https://doi.org/10.1038/nrurol.2015.184
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