Dr. 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.
Email Dr. Steven Balk
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.
Hematology & Oncology