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Prostate-Specific Antigen Nadir and Cancer-Specific Mortality Following Hormonal Therapy for Prostate-Specific Antigen Failure

From the Brigham and Women's Hospital, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA; Memorial Sloan-Kettering Cancer Center, New York, NY; University of Connecticut, Storrs, CT; Walter Reed Hospital, Bethesda, MD; University of California San Francisco, San Francisco, CA; and Duke University, Durham, NC

Address reprint requests to Alexandra Stewart, BM, MRCP, Radiation Oncology, L2, Brigham and Women's Hospital, 75 Francis St, Boston, MA 02115; e-mail: ajsintheus{at}yahoo.co.uk

PURPOSE: For men receiving androgen-suppression therapy (AST) for a rising postoperative or postradiation prostate-specific antigen (PSA), we evaluated whether a PSA nadir of more than 0.2 ng/mL was significantly associated with prostate cancer–specific mortality (PCSM).

PATIENTS AND METHODS: The study cohort comprised 747 men with rising PSA and negative bone scan after surgery (n = 486) or radiation therapy (n = 261) who were treated with AST. Cox regression was used to evaluate whether a significant association existed between the PSA nadir level after 8 months of AST and the time to PCSM, controlling for treatment and known prognostic factors.

RESULTS: The post-AST PSA nadir (p_Cox < .0001), the pre-AST PSA doubling time (DT) (p_Cox = .002), PSA level (P = .0001), and Gleason eight to 10 cancers (p_Cox = .01) were significantly associated with time to PCSM. The adjusted hazard ratio for PCSM was 20 (95% CI, 7 to 61; p_Cox < .0001), for men with a PSA nadir of more than 0.2 ng/mL as compared with all others. A PSA DT of less than 3 months was observed in 30% (224 of 747) of the study cohort. Of the 28 observed prostate cancer deaths, 21 (75%) occurred in men whose PSA nadir was more than 0.2 ng/mL and who had a PSA DT of less than 3 months.

CONCLUSION: A PSA nadir of more than 0.2 ng/mL after 8 months of AST given for postoperative or postradiation PSA failure is significantly associated with PCSM and is clinically significant because it accounted for 75% of the cancer deaths observed in this study.

Presented in part at the 41st Annual Meeting of the American Society of Clinical Oncology, Orlando, FL, May 13-17, 2005 (poster discussion). The authors state that this is an original work.

Authors' disclosures of potential conflicts of interest are found at the end of this article.

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