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SUO 2018

SUO 2018: A Phase 3, Randomized, Double Blind, Placebo Controlled Study of Enzalutamide in Men with Nonmetastatic Castration-Resistant Prostate Cancer: Post Hoc Analysis of PROSPER by Prior Definitive Surgery

Phoenix, Arizona (UroToday.com) The PROSPER trial, published in the New England Journal of Medicine in June 2018, demonstrated that in med with non-metastatic castrate resistant prostate cancer with a rising PSA, treatment with enzalutamide led to a 71% lower risk of metastasis or death than placebo. Additionally, the median metastasis free survival was 36.6 months in the enzalutamide group versus 14.7 months in the placebo group. Furthermore, patients with non-metastatic castrate resistant disease have a high risk of developing metastatic disease. Goals of treatment in the non-metastatic space is to delay metastasis, delay additional systemic therapy, and prolong survival rates, among others.

In this multi-institutional post hoc analysis, men with non-metastatic castrate resistant disease, a PSA doubling time <10 months, PSA>2 continued androgen deprivation therapy and were randomized 2:1 to enzalutamide versus placebo. The goal of this analysis was to assess if previous definitive prostate treatment was associated with differences in survival or metastases in those treated with enzalutamide compared to placebo. In all patients, enzalutamide decreased the risk of metastasis or death by 71%. 28% of patients had previous definitive treatment (cryotherapy and prostatectomy). No differences were demonstrated in the risks of metastasis or death in those who received previous prostate treatment compared to those patients who did not.

In summary, enzalutamide treatment resulted in a statistically significant reduction risk of metastasis or death in patients who did and did not previously receive definitive treatment to the prostate.

This thought provoking post hoc analysis of PROSPER has interesting implications in prostate cancer biology. Continued investigations into prostate cancer genomics and tumor mutational load may uncover the etiology of these findings.

Presented By: Paul R. Sieber, MD

Written by: David B. Cahn, DO, MBS, Fox Chase Cancer Center, Philadelphia, PA, @dbcahn, at the 19th Annual Meeting of the Society of Urologic Oncology (SUO), November
28-30, 2018 – Phoenix, Arizona