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Cancer-Specific Mortality After Surgery or Radiation for Patients With Clinically Localized Prostate Cancer Managed During the Prostate-Specific Antigen Era

Anthony V. D’Amico, Judd Moul, Peter R. Carroll, Leon Sun, Deborah Lubeck, Ming-Hui Chen

From the Department of Radiation Oncology, Brigham and Women’s Hospital and Dana-Farber Cancer Institute, Boston, MA; Department of Surgery and Urology Service, Center for Prostate Disease Research, Uniformed Service University and Walter Reed Army Medical Center, Rockville, MD; Department of Urology, University of California, San Francisco, CA; and Department of Statistics, University of Connecticut, Storrs, CT.

Address reprint requests to Anthony V. D’Amico, MD, PhD, Brigham and Women’s Hospital, Department of Radiation Oncology, 75 Francis St, L-2 Level, Boston, MA 02215; email: adamico{at}lroc.harvard.edu.

	ABSTRACT

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Purpose: To determine whether pretreatment risk groups shown to predict time to prostate cancer–specific mortality (PCSM) after treatment at a single institution retained that ability in a multi-institutional setting.

Patients and Methods: From 1988 to 2002, 7,316 patients treated in the United States at 44 institutions with either surgery (n = 4,946) or radiation (n = 2,370) for clinical stage T1c-2, N0 or NX, M0 prostate cancer made up the study cohort. A Cox regression analysis was performed to determine the ability of pretreatment risk groups to predict time to PCSM after treatment. The relative risk (RR) of PCSM and 95% confidence intervals (CIs) were calculated for the intermediate- and high-risk groups relative to the low-risk group.

Results: Estimates of non-PCSM 8 years after prostate-specific antigen (PSA) failure were 4% v 15% (surgery versus radiation; P_{log rank} = .002) compared with 13% v 18% (surgery versus radiation; P_{log rank} = .35) for patients whose age at the time of PSA failure was less than 70 as compared with 70 years, respectively. The RR of PCSM after treatment for surgery-managed patients with high- or intermediate-risk disease was 14.2 (95% CI, 5.0 to 23.4; P_Cox < .0001) and 4.9 (95% CI, 1.7 to 8.1; P_Cox = .0037), respectively. These values were 14.3 (95% CI, 5.2 to 24.0; P_Cox < .0001) and 5.6 (95% CI, 2.0 to 9.3; P_Cox = .0012) for radiation-managed patients.

Conclusion: This study provided evidence to support the prediction of time to PCSM after surgery or radiation on the basis of pretreatment risk groups for patients with clinically localized prostate cancer managed during the PSA era.

	INTRODUCTION

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THE INTRODUCTION of the serum prostate-specific antigen (PSA) test has changed the presentation of prostate cancer worldwide. Patients now present at a younger age and with lower-grade disease and are more likely to have organ-confined cancers found on pathologic evaluation of the radical prostatectomy specimen.¹ These more favorable clinical and pathologic findings have translated into longer time intervals to PSA failure after either surgical or radiotherapeutic management. Algorithms for predicting PSA outcome after radical prostatectomy (RP) or external-beam radiation therapy (RT) that are based on pretreatment clinical parameters have been validated.^2–4 However, given the competing causes of mortality that exist in men undergoing definitive treatment for localized prostate cancer, many men who sustain PSA failure will not live long enough to develop clinical evidence of distant disease, and far fewer will die from the disease. Although pretreatment risk-based staging systems predicting the end point of prostate cancer–specific mortality (PCSM)^5,6 have been published, none has been validated in the PSA era.

The purpose of this study was to assess whether a pretreatment risk-based staging system that has been shown to predict PCSM after RT delivered at a single institution can also predict PCSM after RP or RT using data gathered from patients treated at 44 institutions during the PSA era. RT and hormonal therapy are now the accepted standard treatments for patients with locally advanced prostate cancer because of the survival benefit shown in a randomized trial;⁷ therefore, the focus of this report in which RT was delivered as monotherapy will be on patients with clinically localized disease managed during the PSA era.

	PATIENTS AND METHODS

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Patient Selection and Treatment
Two multi-institutional databases containing baseline, treatment, and follow-up information on 7,316 men treated with either RP (n = 4,946) or RT (n = 2,370) between 1988 and 2002 at 44 institutions within the United States for clinical stage T1c-2, N0 (RP) or NX (RT), M0 prostate cancer (using the tumor-node-metastasis system of classification) comprised the data with which this study was performed. These two databases included patients from the Cancer of the Prostate Strategic Urologic Research Endeavor⁸ and the Center for Prostate Disease Research.⁹ The study was performed with permission from the human protection committees at each of the individual institutions. To be eligible for study entry, RP-managed patients were permitted to have received up to 3 months of neoadjuvant androgen suppression therapy (AST), given that the 5-year results of a randomized trial¹⁰ have shown no significant effect on cancer control from the addition of 3 months of neoadjuvant AST to RP. The median age of the RP- and RT-managed patients at the time of initial therapy was 63.5 (range, 34.3 to 98.8 years) and 71.3 years (range, 40.5 to 98.3 years), respectively. RP-managed (n = 75) and RT-managed (n = 277) patients with clinical stage T3 or T4 disease were excluded. In addition, any patient with clinical stage T1 or T2 disease who received adjuvant therapy was also excluded (n = 312). The pretreatment clinical characteristics of all patients stratified by the treatment received are shown in Table 1.

Follow-Up
The median follow-up for the entire study cohort of 4,946 and 2,370 RP- and RT-managed patients was 4.1 (range, 0.5 to 14.3 years) and 4.4 years (range, 0.8 to 14.3 years), respectively, using the first day of treatment as time zero. For those patients who sustained PSA failure, the median follow-up was 3.9 (range, 0.5 to 12.1 years) and 3.4 years (range, 0.4 to 12.0 years) for RP- and RT-managed patients, respectively, from the date of PSA failure. Before PSA failure, which was defined using the American Society for Therapeutic Radiology and Oncology consensus criteria,¹⁴ patients generally had a serum PSA measurement and DRE performed every 3 months for 2 years, then every 6 months for 3 additional years, and then annually thereafter. A total of 243 deaths occurred after PSA failure was sustained, 157 (102 after RT and 55 after RP) of which were from prostate cancer. No patient died as a result of prostate cancer before PSA failure. The determination of the cause of death was made using death certificates.

Statistical Methods
A Cox regression analysis¹⁵ was used to determine whether the pretreatment risk group (high or intermediate v low risk), initial therapy (RT v RP), or age at the time of PSA failure (continuous) predicted the time to non-PCSM after PSA failure. For the purpose of illustration, the Cox regression analysis was repeated, defining age at the time of PSA failure as a categorical variable (< 70 v 70 years) to assess whether patients younger than age 70 years selected for RT as compared with RP generally had a higher incidence of competing causes of non–prostate cancer mortality. For these three Cox regression analyses, time zero was defined as the date of PSA failure.

A Cox regression analysis¹⁵ was also performed to determine the ability of the pretreatment risk groups³ to predict time to PCSM after initial therapy. For the Cox regression analyses, time zero was defined as the day of RP or the last day of RT. The relative risk (RR) of PCSM with 95% confidence intervals (CIs) were calculated for each risk group; the value RR = 1.0 was assigned to the low-risk category. The RR was derived from the coefficients of the Cox model, and the 95% CIs were calculated using a bootstrapping technique¹⁶ with 2,000 replications.

Finally, a Cox regression analysis¹⁵ was also used to determine whether the presence of one, any two, or all three factors that defined intermediate risk affected the time to PCSM after initial therapy. For this analysis, patients with a PSA more than 10 to 20 ng/mL were selected as the baseline group.

For all analyses, the assumptions of the Cox model were tested and satisfied. Estimates of PCSM and non-PCSM were calculated using the cumulative incidence method.¹⁷ Comparisons of PCSM and non-PCSM were evaluated using a log-rank P value. The Bonferroni correction¹⁵ was used in the case of multiple comparisons to assess for clinical significance (ie, a significant P value was defined as P < .05/n, where n is the number of comparisons).

The risk groups were defined using the pretreatment serum PSA level, biopsy Gleason score, and 2002 AJCC tumor category. Specifically, low-risk patients had a PSA level of 10 ng/mL or less, a biopsy Gleason score of 6 or less, and 2002 AJCC category T1c or T2a disease. Intermediate-risk patients had a PSA of more than 10 ng/mL and not more than 20 ng/mL, a biopsy Gleason score of 7, or 2002 AJCC category T2b disease. Finally, high-risk patients had a PSA more than 20 ng/mL, a biopsy Gleason score of 8 to 10, or 2002 AJCC category T2c disease.

Plots of PCSM and non-PCSM are displayed stratified by the initial therapy (RP or RT), the patient’s age at the time of initial therapy (< 60, 60 to 64, 65 to 69, and 70 years), and the pretreatment risk group (low, intermediate, or high).

	RESULTS

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Rates of Competing Causes of Mortality After PSA Failure
As noted in Table 1, the pretreatment clinical characteristics were less favorable (P < .0001), and age at the time of initial therapy was more advanced (P < .0001) for RT-managed as compared with RP-managed patients. These differences were reflected in the increased observed death rate after PSA failure in the RT-managed cohort. Specifically, among RP- and RT-managed patients who experienced PSA failure, 8% and 17% have died, respectively. Age at the time of PSA failure (P_Cox = .001) and initial therapy (P_Cox =.03) were significant predictors of time to non-PCSM after PSA failure, whereas the pretreatment risk group was not (P_Cox = .58), as noted in Table 2. When the predictors of time to non-PCSM were analyzed using Cox regression for patients less than age 70 years at the time of PSA failure, men treated with RT had a shorter time to non-PCSM compared with RP-managed patients (P_Cox = .007), whereas initial therapy was not a significant predictor (P_Cox = .58) of time to non-PCSM in patients who were 70 years or older at the time of PSA failure. These findings are summarized in Table 2. To illustrate that RT-managed patients younger than age 70 years were generally less healthy than similarly aged RP-managed patients, Fig 1 displays the estimates of non-PCSM 8 years after PSA failure stratified by age at the time of PSA failure and initial therapy. Specifically, these rates were 4%_RP v 15%_RT (P_{log rank} = .002) compared with 13%_RP v 18%_RT (P_{log rank} = .35) for patients whose age at the time of PSA failure was younger than 70 years as compared with 70 years, respectively.

View larger version (16K): [in this window] [in a new window]   Fig 1. Non–prostate cancer–specific mortality after prostate-specific antigen (PSA) failure stratified by age at the time of PSA failure and initial therapy received. Pairwise P values (clinical significance15 defined as P < 0.05/6 or 0.008). All ages are in years. Surgery, age 70 versus radiation, age 70; P = .35. Surgery, age < 70 versus radiation, age < 70; P = .002. Surgery, age 70 versus surgery, age < 70; P = .002. Radiation, age 70 versus radiation, age < 70; P = .36. Radiation, age 70 versus surgery, age < 70; P < .0001. Radiation, age < 70 versus surgery, age 70; P = .93.

View larger version (14K): [in this window] [in a new window]   Fig 2. Prostate cancer–specific mortality after radical prostatectomy stratified by the pretreatment risk group. Pairwise P values (clinical significance15 defined as P < .05/3 or .017). Intermediate versus low: P = .001. High versus low: P < .0001. High versus intermediate: P < .0001.

View larger version (13K): [in this window] [in a new window]   Fig 3. Prostate cancer–specific mortality after radiation therapy stratified by the pretreatment risk group. Pairwise P values (clinical significance15 defined as P < .05/3 or .017). Intermediate versus low: P = .0003. High versus low: P < .0001. High versus intermediate: P < .0001.

View larger version (17K): [in this window] [in a new window]   Fig 4. Prostate cancer–and non–prostate cancer–specific mortality after radical prostatectomy stratified by age at the time of initial therapy and the pretreatment risk group. Blue, prostate cancer–specific mortality; red, non–prostate cancer–specific mortality.

View larger version (27K): [in this window] [in a new window]   Fig 5. Prostate cancer–and non–prostate cancer–specific mortality after radiation therapy stratified by age at the time of initial therapy and the pretreatment risk group. Blue, prostate cancer–specific mortality; red, non–prostate cancer–specific mortality.

View larger version (17K): [in this window] [in a new window]   Fig 6. Prostate cancer–specific mortality after radical prostatectomy for patients with 1, any 2, or all 3 factors that define intermediate risk. Pairwise P values (clinical significance15 defined as P < .05/10 or .005). Prostate-specific antigen (PSA) > 10 to 20 versus Gleason 7; P = .05. PSA > 10 to 20 versus T2b; P = .19; PSA > 10 to 20 versus any two factors; P = .09. PSA > 10 to 20 versus all three factors; P < .0001. Gleason 7 versus T2b; P = .39. Gleason 7 versus any two factors; P = .51. Gleason 7 versus all three factors; P = .005. T2b versus any two factors; P = .61. T2b versus all three factors; P = .003. Any two factors versus all three factors; P = .004.

View larger version (17K): [in this window] [in a new window]   Fig 7. Prostate cancer–specific mortality after radiation therapy for patients with one, any two, or all three factors that define intermediate risk. Pairwise P values (clinical significance15 defined as P < .05/10 or .005). Prostate-specific antigen (PSA) > 10 to 20 versus Gleason 7; P = .47. PSA > 10 to 20 versus T2b; P = .41. PSA > 10 to 20 versus any two factors; P = .10. PSA > 10 to 20 versus all three factors; P = .08. Gleason 7 versus T2b; P = .10. Gleason 7 versus any two factors; P = .30. Gleason 7 versus all three factors; P = .39. T2b versus any two factors; P = .03. T2b versus all three factors; P = .02. Any two factors versus all three factors; P = .73.

	DISCUSSION

TOP ABSTRACT INTRODUCTION PATIENTS AND METHODS RESULTS DISCUSSION REFERENCES

This study provided evidence to support the conjecture that not all men who sustain PSA failure subsequently die as a result of prostate cancer. In particular, within 8 years after PSA failure, estimates of non-PCSM ranged from 4% to 18% (Fig 1). As noted in Table 2, the numerical value of the mortality rate depended on both the age of the patient at the time of PSA failure (P_Cox = .001) and the initial therapy received (P_Cox = .03) for men who were younger than age 70 years at the time of PSA failure. This latter finding likely reflected the practice pattern in the United States during the study period that patients younger than age 70 years who were selected to undergo RT as opposed to RP were generally less healthy.

Nevertheless, despite the significant rates of non-PCSM after PSA failure, the results of this study that evaluated data obtained from 44 institutions during the PSA era supported a single institution report⁵ indicating that pretreatment risk groups³ initially derived to predict time to PSA failure after RP or RT could also stratify the time to PCSM after initial therapy. Specifically (Table 3), the RR of PCSM was approximately 14-fold or five-fold higher for patients in the high- or intermediate-risk groups, respectively, as compared with the low-risk group. This increase in the relative risk of PCSM with increasing risk group is illustrated in Figs 4 and 5, respectively, where the contributions from cancer-specific and competing causes to all causes of mortality are shown stratified by age at the time of initial therapy and the pretreatment risk group. In particular, for patients of all ages, PCSM increased with advancing risk group for both RP- and RT-managed patients. In addition, although the relative contribution of non-PCSM to all causes of mortality increased with advancing age as expected, high-risk prostate cancer remained a major cause of death for patients of all ages who were treated with RP or RT.

This study also noted that for patients in the intermediate-risk group who have one or any two of the factors that defined intermediate risk, estimates of PCSM were not significantly different after RP or RT. Patients with all three factors defining intermediate risk, however, had a time to PCSM after RP that was significantly shorter than patients whose definition of intermediate risk was based on a single (P_{log rank} .005) or any two factors (P_{log rank} = .004; Fig 6). This finding was not replicated for RT-managed patients (Fig 7). Prior investigators have shown a significant increase in PSA failure rates for patients in the intermediate-risk group with two or more of the three defining factors as compared with any single factor.¹⁹ Perhaps with further follow-up, PCSM profiles will more closely approximate the previously reported PSA failure profiles for patients with two or more of factors that define intermediate risk. At present, however, the data in this study only support the placement of the RP-managed patients who possess all three factors that define intermediate risk into the high-risk group.

Several points require further clarification. First, the pretreatment risk groups evaluated in this study represent one of two validated algorithms^2–4 for predicting time to PSA failure after RP or RT for patients with clinically localized prostate cancer. Nomograms that are based on pretreatment factors also have been validated for the prediction of time to PSA failure after RP in this patient population^2,4 and should be studied further to evaluate their ability to predict time to PCSM after RP or RT.

Second, prior studies have shown that by applying the percentage of positive prostate biopsy core information to the intermediate-risk group, a low- and high-risk group for defining time to PSA failure after RP or RT can be defined.^20–22 Therefore, additional studies will be necessary to assess whether adding the percentage of positive prostate biopsy core data to the intermediate-risk group will also succeed in stratifying the time to PCSM after RP or RT into low- and high-risk groups.

Third, the predictions of PCSM using the pretreatment risk groups in this study are only applicable to patients with clinically localized prostate cancer undergoing RP or RT therapy. Therefore, if future studies document a survival benefit for the addition of AST to RT for patients with clinically localized disease, as has been shown for patients with locally advanced prostate cancer,⁷ then the ability of the pretreatment risk groups to stratify time to PCSM after RT and AST would need to be evaluated in a future study. Finally, whether the specific treatment(s) individual patients received after PSA failure affected the time to PCSM remains unknown and requires clarification in future studies.

In conclusion, this study provided evidence to support the prediction of time to PCSM after RP or RT on the basis of pretreatment risk groups for patients with clinically localized prostate cancer managed during the PSA era.

	NOTES

 
Supported in part by the Department of Defense Center for Prostate Disease Research funded by the United States Army Medical Research and Material Command, Fort Detrick, MD. Cancer of the Prostate Strategic Urologic Research Endeavor is sponsored by TAP Pharmaceuticals Products Inc, Lake Forest, IL, and managed by the Urology Outcomes Research Group at the University of California, San Francisco, CA.

The opinions and assertions contained herein are the private views of the authors and are not to be construed as reflecting the views of the United States Army or Department of Defense.

	REFERENCES

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4. Graefen M, Karakiewicz PI, Cagiannos I, et al: A validation of two preoperative nomograms predicting recurrence following radical prostatectomy. Urol Oncol 7:141–146, 2002[CrossRef][Medline]

5. D’Amico AV, Cote K, Loffredo M, et al: Determinants of prostate cancer specific survival following radiation therapy for patients with clinically localized prostate cancer. J Clin Oncol 20:4567–4573, 2002[Abstract/Free Full Text]

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8. Lubeck DP, Litwin MS, Henning JM, et al: The CaPSURE database: A methodology for clinical practice and research in prostate cancer—CaPSURE Research Panel: Cancer of the Prostate Strategic Urologic Research Endeavor. Urology 48:773–777, 1996[CrossRef][Medline]

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16. Efron R, Tibsherani R. Introduction to the Bootstrap. New York, NY, Chapman and Hall, 1993

17. Gaynor JJ, Feur EJ, Tan CC, et al: On the use of cause-specific failure and conditional failure probabilities: Examples from clinical oncology data. J Am Stat Assoc 88:400–409, 1993[CrossRef]

18. National Center for Health Statistics, Washington, DC: National Vital Statistics report 50:1–120, 2002

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22. D’Amico AV, Schultz D, Silver B, et al: The clinical utility of the percent positive prostate biopsies in predicting biochemical outcome following external beam radiation therapy for patients with clinically localized prostate cancer. Int J Radiat Oncol Biol Phys 49:679–684, 2001[CrossRef][Medline]

Submitted January 13, 2003; accepted March 17, 2003.

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