Linear regressive analysis using prostate-specific antigen doubling time for predicting tumor biology and clinical outcome in prostate cancer
Article first published online: 29 JUN 2006
Copyright © 1993 American Cancer Society
Volume 72, Issue 9, pages 2638–2643, 1 November 1993
How to Cite
D'amico, A. V. and Hanks, G. E. (1993), Linear regressive analysis using prostate-specific antigen doubling time for predicting tumor biology and clinical outcome in prostate cancer. Cancer, 72: 2638–2643. doi: 10.1002/1097-0142(19931101)72:9<2638::AID-CNCR2820720919>3.0.CO;2-N
- Issue published online: 29 JUN 2006
- Article first published online: 29 JUN 2006
- Manuscript Accepted: 28 MAY 1993
- prostate cancer;
- prostate-specific antigen;
- tumor doubling time;
- outcome prediction
Background. This study was undertaken to calculate the prostate-specific antigen doubling time (PSA-DT) of prostate cancers recurrent after external beam radiation therapy and to investigate if a correlation exists between the PSA-DT and the clinical behavior of prostate cancer as a possible reflection of the tumor doubling time.
Methods. Twenty-two patients treated with external beam radiation between October 1985 and October 1990 for clinical stages B1, B2, and C (T2a, T2b, T3) prostate cancer experienced PSA elevation as their only sign of failure. Serial PSA determinations are available before initiation of any secondary treatment and these have been used to calculate PSA-DT.
Results. The results of this study reveal that the PSA-DT is a constant (r ± 0.98). Mathematically, this means the PSA value is growing exponentially and may represent tumor growth in the exponential phase. Second, the PSA-DT was found to be linearly correlated (r = 0.86) with the interval to clinical relapse after PSA failure. Graphically, the slope of this correlation is equal to the number of PSA-DT (4.5 with 95% confidence interval [3.6]) required before clinical disease manifests after PSA failure. Using this relationship, one can delineate those patients with aggressive tumor biology (PSA-DT < 3.8 months) who require immediate therapeutic intervention versus a relatively indolent tumor biology (PSA-DT ± 3.8 months) who can be spared the morbidity and expense of androgen deprivation therapy until clinical recurrence manifests. Furthermore, in the pretreatment setting, observation rather than treatment may be indicated for patients with PSA-DT for 18 months or more, because the disease may not become clinically apparent during the patient's lifetime.
Conclusion. PSA-DT after radiation therapy may reflect the tumor doubling time and has implications in the posttherapy setting regarding the optimal time of intervention with androgen deprivation and in the pretreatment setting regarding the necessity for treatment rather than observation.