Abstract
This study aimed to first elucidate prostate-specific antigen (PSA) kinetics in prostate cancer patients treated with carbon ion radiotherapy (CIRT). From 2010 to 2015, 131 patients with prostate adenocarcinoma treated with CIRT (57.6 Gy relative biological effectiveness (RBE) in 16 fractions) alone were recruited. PSA was measured at 1, 2, 3, 6, 9, 12, 15, 18, 21, 24, 30, 36, 42, 48, 54, and 60 months post-CIRT. PSA bounce was defined as PSA increase over a cutoff followed by spontaneous decrease to or below the pre-bounce nadir. PSA failure was determined using the Phoenix criteria (nadir + 2.0 ng/mL). As a result, non-failure-associated temporary increase in PSA exhibited two distinct patterns, namely a classical bounce and a surge at one month. PSA bounce of ≥0.2 ng/mL was observed in 55.7% of the patients. Bounce amplitude was <2.0 ng/mL in 97.6% of cases. Bounce occurred significantly earlier than PSA failure. Younger age was a significant predictor of bounce occurrence. Bounce positivity was a significant predictor of favorable 5-year PSA failure-free survival. Meanwhile, a PSA surge of ≥0.2 ng/mL was observed in 67.9% of patients. Surge amplitude was significantly larger than bounce amplitude. Larger prostate volume was a significant predictor of PSA surge occurrence. PSA surge positivity did not significantly predict PSA failure. In summary, PSA bounce was distinguishable from PSA failure with regard to timing of occurrence and amplitude (earlier and lower for bounce, respectively). These data are useful for post-CIRT surveillance of prostate cancer patients.
Highlights
Radiotherapy plays a pivotal role in the management of prostate cancer [1]
Lower, respectively, for the datainsight may provide a clinical surveillance insight on post-treatment bounce should carefully outshould from failure especially within
We discovered a novel prostate-specific antigen (PSA) kinetics, that is, surge, that warrants further
Summary
Carbon ion radiotherapy (CIRT) has potential as a definitive radiotherapy modality for localized prostate cancer [2]. Prostate-specific antigen (PSA) is the gold standard biomarker for post-treatment surveillance of prostate cancer patients [3,4]. PSA levels fluctuate and temporarily increase in some patients, a phenomenon called the PSA bounce [7]. This bounce causes severe anxiety for prostate cancer patients and clinicians [8], and may even lead to unnecessary salvage treatment in cases that meet the definition of PSA failure [9]. We analyzed post-treatment PSA kinetics in prostate cancer patients treated with
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