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    Expression of androgen receptor splice variants in clinical breast cancers

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    49
    Author
    Hickey, TE; Irvine, CM; Dvinge, H; Tarulli, GA; Hanson, AR; Ryan, NK; Pickering, MA; Birrell, SN; Hu, DG; Mackenzie, PI; ...
    Date
    2015-12-29
    Source Title
    Oncotarget
    Publisher
    IMPACT JOURNALS LLC
    University of Melbourne Author/s
    Tarulli, Gerard
    Affiliation
    School of BioSciences
    Metadata
    Show full item record
    Document Type
    Journal Article
    Citations
    Hickey, T. E., Irvine, C. M., Dvinge, H., Tarulli, G. A., Hanson, A. R., Ryan, N. K., Pickering, M. A., Birrell, S. N., Hu, D. G., Mackenzie, P. I., Russell, R., Caldas, C., Raj, G. V., Dehm, S. M., Plymate, S. R., Bradley, R. K., Tilley, W. D. & Selth, L. A. (2015). Expression of androgen receptor splice variants in clinical breast cancers. ONCOTARGET, 6 (42), pp.44728-44744. https://doi.org/10.18632/oncotarget.6296.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/260054
    DOI
    10.18632/oncotarget.6296
    Abstract
    The importance of androgen receptor (AR) signaling is increasingly being recognized in breast cancer, which has elicited clinical trials aimed at assessing the efficacy of androgen deprivation therapy (ADT) for metastatic disease. In prostate cancer, resistance to ADT is frequently associated with the emergence of androgen-independent splice variants of the AR (AR variants, AR-Vs) that lack the LBD and are constitutively active. Women with breast cancer may be prone to a similar phenomenon. Herein, we show that in addition to the prototypical transcript, the AR gene produces a diverse range of AR-V transcripts in primary breast tumors. The most frequently and highly expressed variant was AR-V7 (exons 1/2/3/CE3), which was detectable at the mRNA level in > 50% of all breast cancers and at the protein level in a subset of ERα-negative tumors. Functionally, AR-V7 is a constitutively active and ADT-resistant transcription factor that promotes growth and regulates a transcriptional program distinct from AR in ERα-negative breast cancer cells. Importantly, we provide ex vivo evidence that AR-V7 is upregulated by the AR antagonist enzalutamide in primary breast tumors. These findings have implications for treatment response in the ongoing clinical trials of ADT in breast cancer.

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