The androgen receptor (AR), a member of the steroid receptor subfamily of nuclear receptors, controls prostate cancer growth. Treatment of prostate cancer by prostactectomy or radiation can often eliminate cancer cells that remain confined within the prostate capsule. Treatment with luteinizing hormone-releasing hormone (LHRH) analogs and AR antagonists are commonly used to block the action of testicular androgens. Tumor cell growth is inhibited by androgen ablation therapy for a period of time but tumor regrowth occurs despite castrate levels of androgen.  Studies by our group and others have shown that during prostate cancer recurrence, AR is expressed, highly stable with or without androgen binding, localized to the nucleus and hypersensitive to low levels of dihydrotestosterone (DHT), a high affinity AR ligand. Although studies suggest involvement of the AR during prostate cancer recurrence, the mechanisms by which the AR orchestrates cellular proliferation and/or survival after castration remain ill defined. Further, stimulation of the ErbB/HER family of receptor tyrosine kinases through binding of extracellular growth factor ligands or mitogens and subsequent intracellular signal transduction activity, results in up regulation of cell-signaling cascades that favor cell survival and proliferation. Modulation of nuclear hormone receptor function has implicated kinase pathways activated in this growth factor response. Thus, links have been proposed between growth factor signaling, AR coactivators and AR transcriptional activity but the mechanisms by which growth factors influence AR activity are yet to be defined. 

My research project addresses the effects of AR protein down-regulation on cellular proliferation, expression of an androgen-regulated target gene, cell cycle progression and apoptosis in the CWR-R1 recurrent cancer cell line using self-complementary adeno-associated viral vectors (scAAV) expressing a potent AR-siRNA. Further, I am addressing the mechanisms by which EGF-mediated signaling increases AR transcriptional activity during prostate cancer recurrence in the absence or presence and low levels of androgen. 

Currently, I spend my time outside the lab in the Student Health Action Coalition (SHAC*) as a clinic interpreter and have recently become a Doula through the UNC Hospital Birth Partner Program. 
• SHAC (http://www.med.unc.edu/shac/index.html)