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• W2080236468 abstract "Purpose/Objective: To assess the impact of PSA bounce and its association with biochemical failure (BF) and clinical failure (CF) in patients treated with brachytherapy and/or external beam radiotherapy (EBRT) with or without neoadjuvant androgen deprivation (AD). Materials/Methods: From 1987–2003, 2329 patients with clinical stage T1-T3 N0 M0 prostate cancer were treated at a single institution with conventional-dose (median 66.6 Gy) EBRT (n=1155), high-dose (median 75.6 Gy) adaptive EBRT (n=483), EBRT and high dose rate (HDR) brachytherapy boost (n=407), HDR brachytherapy alone (n=95), or permanent seed implant (n=189). 498 patients (21%) received neoadjuvant AD with RT (2% for conventional EBRT, 33% for adaptive EBRT, 51% for EBRT+HDR, 38% for brachytherapy alone). BF was scored using 3 rises, nadir + 2 ng/ml, and 3 ng/ml at or after nadir based on both current and absolute nadir methodologies. PSA bounce was defined as an increase followed by a decrease to the prior baseline or lower. The median number of PSA measurements after treatment was 8 and the median follow-up was 4.6 years (range = 0.4–15.9 years). Results: 288 patients (12%) experienced CF for a 10-year rate of 26%. PSA bounce at any time following RT of ≥ 0.1, ≥ 1.0, and ≥ 2.0 ng/ml occurred in 940 (40%), 178 (8%), and 59 patients (3%), respectively. Bounce after absolute nadir of ≥ 0.1, ≥ 1.0, and ≥ 2.0 ng/ml occurred in 421 (18%), 54 (2%), and 14 (0.6%), respectively. Of patients who experienced any PSA bounce, the median highest bounce peak and amplitude were 1.3 and 0.3 ng/ml, respectively. Use of AD was associated with a higher risk of bounce only for amplitude ≥ 0.1 ng/ml (45% for AD vs 39% for no AD, p=0.03). Use of AD was not associated with bounce of any higher amplitude (≥ 0.2 ng/ml: 32% for AD vs 31% for no AD; ≥ 1.0 ng/ml: 7% for AD vs 8% for no AD, p=0.78). Use of brachytherapy was associated with a higher risk of bounce ≥ 0.1 to ≥ 0.5 ng/ml (≥ 0.5 ng/ml: 19% for brachy vs 14% for no brachy, p<0.01). Use of brachytherapy was not associated with bounce of any higher amplitude (≥ 1.0 ng/ml: 9% for brachy vs 7% for no brachy, p=0.23). Bounce < 2.0 ng/ml showed no association with CF. For bounce ≥ 3.0 ng/ml, 23% demonstrated CF vs 12% without bounce of this amplitude (p=0.13). When examining EBRT alone patients (no brachy and no AD), 33% of those who experienced bounce ≥ 3.0 ng/ml developed CF vs 16% without a bounce of this amplitude (p=0.08). Bounces < 0.3 ng/ml were not more likely to be scored as BFs than non-bouncers for any of the BF definitions. However, bounces ≥ 1.0 ng/ml were more likely to be scored as BFs for all definitions based on current nadir (3 rises: 31% vs 21%, nadir+2: 46% vs 22%, 3 at/after nadir: 61% vs 25%) than those based on absolute nadir (3 rises: 20% vs 19%, nadir+2: 22% vs 22%, 3 at/after nadir: 25% vs 24%). Conclusions: PSA bounces appear to have minimal or no association with CF, especially with amplitude < 2.0 ng/ml. Bounces ≥ 1.0 ng/ml are rare following brachytherapy or neoadjuvant AD, occurring in only 9% of brachytherapy and 7% of AD patients. BF definitions based on absolute nadir are less sensitive to PSA bounces that occur after brachytherapy and/or AD." @default.
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• W2080236468 date "2005-10-01" @default.
• W2080236468 modified "2023-09-26" @default.
• W2080236468 title "Clinical Implication of PSA Bounce After Treatment of Prostate Cancer with Brachytherapy and/or External Beam Radiotherapy with or Without Androgen Deprivation" @default.
• W2080236468 doi "https://doi.org/10.1016/j.ijrobp.2005.07.516" @default.
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