Balk Lab Group 112018350x235Dr. Steven Balk's lab developed methods to analyze advanced metastatic PCa through the use of bone marrow biopsies and showed that one mechanism for disease progression after androgen deprivation therapy was through mutations in the androgen receptor (AR). These mutations occur specifically in patients treated with an AR antagonist, flutamide, and are the result of strong selective pressure exerted by this drug. In subsequent studies his lab has further established a critical role for AR in PCa that relapses after androgen deprivation therapy, and identified mechanisms that mediate AR reactivation (including enhanced androgen synthesis by tumor cells). These results have led directly to successful clinical trials with translational as well as clinical endpoints. An additional current focus is mechanisms of progression from low grade to high grade prostate cancer, which will have an impact on management of low grade disease. In conjunction with these research efforts, he has directed the establishment of a prostate cancer tissue bank and correlative clinical database.

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Recent Publications

SOX9 drives WNT pathway activation in prostate cancer.

ErbB2 Signaling Increases Androgen Receptor Expression in Abiraterone-Resistant Prostate Cancer.

Lysine-specific demethylase 1 has dual functions as a major regulator of androgen receptor transcriptional activity.

Abiraterone treatment in castration-resistant prostate cancer selects for progesterone responsive mutant androgen receptors.

Tyrosine kinase BMX phosphorylates phosphotyrosine-primed motif mediating the activation of multiple receptor tyrosine kinases.

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