Freedom From a Detectable Ultrasensitive Prostate-specific Antigen at Two Years After Radical Prostatectomy Predicts a Favorable Clinical Outcome: Analysis of the SEARCH Database

被引:16
作者
Chang, Steven L. [1 ]
Freedland, Stephen J.
Terris, Martha K.
Aronson, William J.
Kane, Christopher J.
Amling, Christopher L.
Presti, Joseph C., Jr.
机构
[1] Stanford Univ, Dept Urol, Med Ctr, Stanford, CA 94305 USA
关键词
CANCER-SPECIFIC MORTALITY; SURROGATE END-POINT; DOUBLING TIME; BIOCHEMICAL RECURRENCE; PSA ASSAY; RADIATION-THERAPY; FAILURE; SERUM; TRIAL; RISK;
D O I
10.1016/j.urology.2009.06.089
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 ; 100201 ;
摘要
OBJECTIVES To assess the utility of kinetics for ultrasensitive prostate-specific antigen (uPSA) assays to identify men who are at risk of developing high-risk recurrent prostate cancer [prostate-specific antigen doubling time (PSADT) < 9 months] after radical prostatectomy. Previous studies demonstrate that a PSADT < 9 months after radical prostatectomy is associated with prostate cancer-specific mortality. Conventionally, PSADT has been calculated after biochemical failure (PSA >= 0.2 ng/mL). METHODS A review of the Shared Equal Access Regional Cancer Hospital database from 1988-2008 was performed to identify men with biochemical failure after radical prostatectomy and >= 2 uPSA values before failure (PSA >= 0.2 ng/mL) as well as >= 2 values after failure to calculate PSADT. These patients were stratified into low-risk (PSADT >= 9 months) and high-risk (PSADT < 9 months) cohorts. The following uPSA kinetics were analyzed for their ability to predict low-and high-risk cohorts: time to first detectable uPSA, time from uPSA to biochemical failure, uPSA velocity, uPSADT, uPSA exponential rise, and uPSA fluctuations. RESULTS The analysis included 89 low-and 26 high-risk men. Time to first detectable uPSA was inversely associated with the high-risk cohort (OR 0.96, 95% CI 0.92-0.99, P = .02) and characterized by a high sensitivity and negative predictive value at a threshold of 2 years after surgery. Other measures of uPSA kinetics showed no association with PSADT. CONCLUSIONS Time to first detectable uPSA identifies men with low-risk recurrence prostate cancer. Patients with an undetectable uPSA 2 years after surgery are unlikely to develop PSADT < 9 months after biochemical failure. UROLOGY 75: 439-446, 2010. Published by Elsevier Inc.
引用
收藏
页码:439 / 444
页数:6
相关论文
共 23 条
[1]  
Chan DW, 1999, CLIN CHEM, V45, P1863
[2]   Surrogate end point for prostate cancer-specific mortality after radical prostatectomy or radiation therapy [J].
D'Amico, AV ;
Moul, JW ;
Carroll, PR ;
Sun, L ;
Lubeck, D ;
Chen, MH .
JOURNAL OF THE NATIONAL CANCER INSTITUTE, 2003, 95 (18) :1376-1383
[3]   Time to biochemical failure and prostate-specific antigen doubling time as surrogates for prostate cancer-specific mortality: evidence from the TROG 96.01 randomised controlled trial [J].
Denham, James W. ;
Steigler, Allison ;
Wilcox, Chantelle ;
Lamb, David S. ;
Joseph, David ;
Atkinson, Chris ;
Matthews, John ;
Tai, Keen-Hun ;
Spry, Nigel A. ;
Christie, David ;
Gleeson, Paul S. ;
Greer, Peter B. ;
D'Este, Catherine .
LANCET ONCOLOGY, 2008, 9 (11) :1058-1068
[4]   Nonprostatic sources of prostate-specific antigen [J].
Diamandis, EP ;
Yu, H .
UROLOGIC CLINICS OF NORTH AMERICA, 1997, 24 (02) :275-+
[5]   Early detection of recurrent prostate cancer with an ultrasensitive chemiluminescent prostate-specific antigen assay [J].
Ellis, WJ ;
Vessella, RL ;
Noteboom, JL ;
Lange, PH ;
Wolfert, RL ;
Rittenhouse, HG .
UROLOGY, 1997, 50 (04) :573-579
[6]   Risk of prostate cancer-specific mortality following biochemical recurrence after radical prostatectomy [J].
Freedland, SJ ;
Humphreys, EB ;
Mangold, LA ;
Eisenberger, M ;
Dorey, FJ ;
Walsh, PC ;
Partin, AW .
JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION, 2005, 294 (04) :433-439
[7]  
Haese A, 2002, CLIN CHEM, V48, P944
[8]   CDNA CODING FOR THE ENTIRE HUMAN-PROSTATE SPECIFIC ANTIGEN SHOWS HIGH HOMOLOGIES TO THE HUMAN-TISSUE KALLIKREIN GENES [J].
HENTTU, P ;
VIHKO, P .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1989, 160 (02) :903-910
[9]  
Junker R, 1999, ANTICANCER RES, V19, P2625
[10]  
Morris DL, 1998, J CLIN LAB ANAL, V12, P65