My laboratory focuses on the molecular understanding of the highly variable phenotypic spectrum of prostate cancer. We take clinical observations and generate hypotheses that are initially tested in prostate cancer cell lines and then validated in patient specimens from hospital-based and large population-based cohorts. We use multiple approaches including epidemiology and molecular biology. Our primary areas of broad interest are the genetic epidemiology of prostate cancer, resistance mechanisms to therapy, non-coding RNAs and their role in prostate cancer, and hormone transporters.
- Statin Use at the Time of Initiation of Androgen Deprivation Therapy and Time to Progression in Patients With Hormone-Sensitive Prostate Cancer. Harshman LC, Wang X, Nakabayashi M, Xie W, Valenca L, Werner L, Yu Y, Kantoff AM, Sweeney CJ, Mucci LA, Pomerantz M, Lee GS, Kantoff PW. JAMA Oncol. 2015 Jul;1(4):495-504. doi: 10.1001/jamaoncol.2015.0829. Erratum in: JAMA Oncol. 2015 Jul;1(4):544.
- PLZF, a tumor suppressor genetically lost in metastatic castration-resistant prostate cancer, is a mediator of resistance to androgen deprivation therapy. Hsieh CL, Botta G, Gao S, Li T, Van Allen EM, Treacy DJ, Cai C, He HH, Sweeney CJ, Brown M, Balk SP, Nelson PS, Garraway LA, Kantoff PW. Cancer Res. 2015 May 15;75(10):1944-8. doi: 10.1158/0008-5472.CAN-14-3602. Epub 2015 Mar 25.