Journal article
Expression of androgen receptor splice variants in clinical breast cancers
TE Hickey, CM Irvine, H Dvinge, GA Tarulli, AR Hanson, NK Ryan, MA Pickering, SN Birrell, DG Hu, PI Mackenzie, R Russell, C Caldas, GV Raj, SM Dehm, SR Plymate, RK Bradley, WD Tilley, LA Selth
Oncotarget | IMPACT JOURNALS LLC | Published : 2015
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-..
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Awarded by National Institutes of Health
Funding Acknowledgements
This work was supported by grants from: Susan G. Komen for the Cure (BCTR0601118; WDT and TEH); the National Breast Cancer Foundation of Australia (NC-12-21; WDT and TEH); the Prostate Cancer Foundation of Australia/Cancer Australia (Grant ID 1043482; WDT and LAS); the Ray and Shirl Norman Cancer Research Trust (WDT and LAS); the U.S. Department of Defense Prostate Cancer Research Program (Transformative Impact Award W81XWH-13-2-0093; SRP, SMD, WDT and LAS); the National Health and Medical Research Council of Australia (1008349); and a National Institutes of Health/National Cancer Institute P50 CA138293 career development award (RKB). LAS is supported by a Young Investigator Award from the Prostate Cancer Foundation (the Foundation 14 award; LAS) and TEH/HD by postdoctoral fellowships from the US Department of Defense Breast Cancer Research Program (W81XWH-11-1-0592 (TEH) and W81XWH-14-1-0044 (HD)).