Graff, R.Pettersson, A.Lis, R.Dupre, N.Jordahl, K.Nuttall, E.Rider, J.Fiorentino, M.Sesso, H.Kenfield, S.Loda, M.Giovannucci, E.Rosner, B.Nguyen, P.Sweeney, C.Mucci, L.2017-03-132017-03-132015Prostate, 2015; 75(9):897-9060270-41371097-0045http://hdl.handle.net/2440/103786Background. In the United States, half of men with prostate cancer harbor the androgenregulated gene fusion TMPRSS2:ERG. We hypothesized that men with TMPRSS2:ERG positive tumors are more responsive to androgen deprivation therapy (ADT). Methods. We studied a cohort of 239 men with prostate cancer from the Physicians’ Health Study and Health Professionals Follow-up Study who received ADT during their disease course. Fusion status was assessed on available tumor tissue by immunohistochemistry for ERG protein expression. We used Cox models to calculate hazard ratios (HRs) and 95% confidence intervals (CIs) for assessment of prostate cancer-specific mortality after ADT initiation.en© 2015 Wiley Periodicals, Inc.Transdisciplinary Prostate Cancer Partnership ToPCaPHumansProstatic NeoplasmsNeoplasms, Hormone-DependentOncogene Proteins, FusionImmunohistochemistryProportional Hazards ModelsSurvival AnalysisCohort StudiesFollow-Up StudiesProspective StudiesAgedMiddle AgedMaleNonsteroidal Anti-AndrogensSurveys and QuestionnairesJournal article003003942010.1002/pros.229730003542030000012-s2.0-84929999835187857Sweeney, C. [0000-0002-0398-6018]