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Charles R. Pound, MD; Alan W. Partin, MD, PhD; Mario A. Eisenberger, MD; Daniel W. Chan, PhD; Jay D. Pearson, PhD; Patrick C. Walsh, MD

JAMA. 1999;281:1591-1597.

ABSTRACT
Context  In men who develop an elevated serum prostate-specific antigen level (PSA) after having undergone a radical prostatectomy, the natural history of progression to distant metastases and death due to prostate cancer is unknown.

Objective  To characterize the time course of disease progression in men with biochemical recurrence after radical prostatectomy.

Design  A retrospective review of a large surgical series with median (SD) follow-up of 5.3 (3.7) years (range, 0.5-15 years) between April 1982 and April 1997.

Setting  An urban academic tertiary referral institution.

Patients  A total of 1997 men undergoing radical prostatectomy, by a single surgeon, for clinically localized prostate cancer. None received neoadjuvant therapy, and none had received adjuvant hormonal therapy prior to documented distant metastases.

Main Outcome Measures  After surgery, men were followed up with PSA assays and digital rectal examinations every 3 months for the first year, semiannually for the second year, and annually thereafter. A detectable serum PSA level of at least 0.2 ng/mL was evidence of biochemical recurrence. Distant metastases were diagnosed by radionuclide bone scan, chest radiograph, or other body imaging, which was performed at the time of biochemical recurrence and annually thereafter.

Results  The actuarial metastasis-free survival for all 1997 men was 82% (95% confidence interval, 76%-88%) at 15 years after surgery. Of the 1997 men, 315 (15%) developed biochemical PSA level elevation. Eleven of these underwent early hormone therapy after the recurrence and are not included in the study. Of the remaining 304 men, 103 (34%) developed metastatic disease within the study period. The median actuarial time to metastases was 8 years from the time of PSA level elevation. In survival analysis, time to biochemical progression (P<.001), Gleason score (P<.001), and PSA doubling time (P<.001) were predictive of the probability and time to the development of metastatic disease. An algorithm combining these parameters was constructed to stratify men into risk groups. Once men developed metastatic disease, the median actuarial time to death was 5 years. The time interval from surgery to the appearance of metastatic disease was predictive of time until death (P<.02).

Conclusions  Several clinical parameters help predict the outcomes of men with PSA elevation after radical prostatectomy. These data may be useful in the design of clinical trials, the identification of men for enrollment into experimental protocols, and counseling men regarding the timing of administration of adjuvant therapies.

INTRODUCTION

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Radical prostatectomy provides excellent cancer control in most men with clinically localized disease. However, approximately 35% of men will experience a detectable serum prostate-specific antigen (PSA) elevation within 10 years following surgery.^1-5 At this early sign of biochemical recurrence, patients want to know what this means, whether they will survive, and if not, how long they will have to live. Cancer-specific and metastasis-free survival rates following radical prostatectomy have been reported.^{2, 6-10} However, until now, the time course of progression to distant metastases or death due to prostate cancer in men with biochemical failure following radical prostatectomy has not been documented. This report characterizes the natural history of the disease in these men. This analysis provides information to men and their physicians considering systemic therapy, even in the setting of minimal elevation of PSA levels. It provides additional background data that are lacking in the proper design of some clinical trials.

METHODS

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A total of 1997 men had undergone radical prostatectomy for clinically localized prostate cancer by a single surgeon at The Johns Hopkins Hospital, Baltimore, Md, between April 1982 and April 1997. The Hybritech-Tandem R and E, San Diego, Calif, and the TOSOH PSA assays, (Hybritech/Beckman, San Francisco, Calif) were used at The Johns Hopkins Hospital. These assays have been demonstrated to be comparable in intralaboratory testing. Other comparable PSA assays may have been used at referring institutions. Pathologic diagnosis of prostate cancer was based on examination of prostate tissue. Histologic grading was performed using the Gleason system for the prostatectomy specimen. No man received neoadjuvant radiation or hormonal therapy. The method of pathologic analysis at our institution has been described.¹¹ Tumors were determined to be organ-confined, to penetrate the prostatic capsule without extension to the seminal vesicles, to involve the seminal vesicles without nodal disease, or to involve the pelvic lymph nodes.

After the operation, men were followed up, either at our institution or by referring physicians, with serum PSA levels and digital rectal examinations performed every 3 months for the first year, semiannually for the second year, and yearly thereafter. Isolated biochemical PSA elevation was defined as a serum PSA level of at least 0.2 ng/mL, which represents a measurable value above the level of detection for this assay. Radionuclide bone scans were performed either at our institution or by the referring physicians at the time of biochemical recurrence and on a yearly basis thereafter unless performed earlier for symptoms suggestive of distant metastasis. A positive bone scan result or other radiographic or histologic (lymph node biopsy) evidence of distant failure was used for the diagnosis of distant metastases.

Thirteen men who had received immediate adjuvant radiation therapy based on pathologic features and 11 men who had received adjuvant hormonal therapy prior to the development of metastatic disease were not included in the analysis of progression after PSA elevation. Therefore, adjuvant hormonal therapy had no impact on either the time to biochemical progression or the time to distant metastasis in this analysis. Men with a PSA elevation following surgery who received postoperative radiation to the prostatic bed and demonstrated a biochemical response for longer than 24 months were considered to have local recurrences only and cured by the combination of surgery and radiation, and thus were not included in this analysis. Conversely, 83 (27%) of 304 men who had a PSA level elevation and had received adjuvant radiation without a sustained biochemical response (not cured by adjuvant radiation) were considered to harbor distant metastatic disease and were included in this analysis.

Some men with documented metastatic disease had received a variety of experimental therapies for androgen-insensitive disease. No form of systemic therapy substantially prolonged survival in men with hormone-resistant prostate cancer. These therapies were not considered to have had a significant effect on the length of survival after the development of metastatic disease.¹²

Serum PSA level increases above 0.2 ng/mL demonstrated an exponential growth curve similar to that originally reported by Patel et al.¹³ By this manner, a correlation between the log of PSA levels and time was linear. Prostate-specific antigen doubling time (PSADT) was calculated by natural log of 2 (0.693) divided by the slope of the relationship between the log of PSA and time of PSA measurement for each patient. To determine the optimal PSADT cutoff for predicting metastatic disease progression for this cohort, several doubling-time calculation models were analyzed. Models that used all postoperative PSA values, only the first 2 values regardless of level,¹³ only the first 2 values after a level of 0.2 ng/mL was reached, and all PSA values within a 2-, 3-, and 5-year period following a documented PSA elevation were analyzed by recursive partitioning to determine the optimal PSADT cutoff level. The method of recursive partitioning involved calculating PSADT based on the PSA values in all of the above models and using sequential values of PSADT provided by each model as a trial cutoff level to determine the optimal separation of men based on their risk of developing metastatic disease. The PSADT values that were less than 0 (stable, nonincreasing, or decreasing PSA levels) were assigned a value equal to 0. The PSADT values that were exceptionally long (eg, >100 months) were assigned a value of 100 months for ease of calculations.

Patients who died were placed into 1 of 3 categories: dead with no evidence of disease (no previous history of a detectable PSA), dead with cancer (history of a detectable PSA, and elevated PSA with documented death due to another cause), and death due to cancer. Death due to prostate cancer was defined as death in any man with metastatic disease that showed any progression following treatment with hormonal therapy. No patient with metastatic disease died due to any cause other than prostate cancer and thus cancer-specific survival was the same as overall survival in men with metastatic disease for this series.

Statistical analyses were performed using the STATA 5.0 software package (Stata Corporation, College Station, Tex). Cox proportional hazards regression analysis was used to compare the models for calculating the PSADT. The PSADT method used was optimized to provide the best ² P value with the most number of men with PSA data. Analyses of actuarial survival were performed as described by Kaplan and Meier.¹⁴ Statistical significance of Kaplan-Meier actuarial survival curves was calculated using the Wilcoxon-Gehan statistic.

RESULTS

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The clinical TNM stages, the range of preoperative PSA levels, prostatectomy Gleason scores, and the pathologic stages of all 1997 men are detailed in Table 1. These men have been followed up for a mean (SD) of 5.3 (3.7) years (range, 0.5-15 years). Seventeen percent (344/1997) have been followed up for 10 or more years. Figure 1 depicts the actuarial metastasis-free likelihood following surgery for all 1997 men with a 15-year metastasis-free likelihood of 82% (95% confidence interval [CI], 76%-88%). Actuarial cancer-specific survival at 10 and 15 years following surgery was 94% (95% CI, 92%-96%) and 91% (95% CI, 87%-94%), respectively.

View this table: [in this window] [in a new window] Table 1. Disease Characteristics in 1997 Men Before Undergoing Anatomical Radical Prostatectomy

View larger version (10K): [in this window] [in a new window] Figure 1. Actuarial Likelihood of Metastasis-Free Survival in 1997 Men Treated With Radical Prostatectomy No man received early hormonal therapy prior to diagnosis of metastatic disease or symptomatic local recurrence.

Three hundred fifteen men (15%) have demonstrated biochemical recurrence. No man has experienced a distant or local recurrence with an undetectable serum PSA level. Eleven of these 315 men with biochemical recurrence underwent early hormonal therapy after PSA elevation and are not included in the analysis of progression to metastatic disease. Table 2 depicts the pathologic stage, Gleason score, follow-up, and year of PSA recurrence for the remaining 304 men.

View this table: [in this window] [in a new window] Table 2. Pathologic Gleason Score, Pathologic Stage, and Follow-up in the 304 Men Who Had Demonstrated Prostate-Specific Antigen (PSA) Recurrence After Anatomical Radical Prostatectomy

Various models for determining PSADT were compared using a Cox proportional hazards regression model (Table 3). Use of all PSA values within 2 years of initial documented PSA level elevation provided the optimal combination of statistical significance and number of evaluable men for this group. The median PSADT for this group of men (n=131) was 10 months. When used as a cutoff level for further comparison, a PSADT of greater than or less than 10 months provided the most statistically significant prediction (P<.001) of time to distant disease progression after PSA elevation.

View this table: [in this window] [in a new window] Table 3. Prostate-Specific Antigen Doubling Times and Calculation Methods*

The time from PSA elevation to the development of clinically evident metastasis is depicted by actuarial analysis in Figure 2. The significance of Gleason score on the risk of developing metastatic disease after PSA elevation is illustrated in Figure 3, A (P<.001). At the time of this report, of the 304 men with biochemical recurrence, 103 (34%) have developed distant metastases. The median actuarial time to development of metastases following PSA elevation was 8 years, and the 5-year metastasis-free rate was 63%. Figure 3, B demonstrates that the time to development of distant metastases was dependent on the time of the PSA elevation (2 or >2 years following surgery; P<.001). Figure 3, C demonstrates that a PSADT cutoff of 10 months predicted the likelihood of subsequent development of metastatic disease as well (P<.001). In men with Gleason score 6 or 7 tumors, substratification according to the presence of organ-confined disease or surgical margin status did not identify a subset of men with a significantly different time course to metastatic disease. When all 304 men were considered, pathologic stage stratified as organ-confined disease, capsular penetration with negative seminal vesicles and lymph nodes, or involvement of the seminal vesicles and/or pelvic lymph nodes was statistically significant in predicting time to metastatic disease (data not shown, P=.01).

View larger version (11K): [in this window] [in a new window] Figure 2. Actuarial Likelihood of Metastasis-Free Survival in 304 Men With Prostate-Specific Antigen (PSA) Elevation After Radical Prostectomy Times indicated are years from biochemical recurrence. None of the men received endocrine therapy prior to development of metastatic disease. None of the men received hormonal therapy prior to development of metastatic disease. Estimates are calculated at 3, 5, or 7 years from the time of the initial PSA elevation (metastatic disease free period), based on Gleason score in the surgical specimen, the time of initial biochemical recurrence (2 vs >2 years), and PSA doubling time (<10 vs 10 months).

View larger version (11K): [in this window] [in a new window] Figure 3. Actuarial Likelihood of Metastasis-Free Survival in 304 Men With Prostate-Specific (PSA) Antigen Elevation After Radical Prostatectomy A, Based on Gleason scores in the radical prostatectomy specimen (P<.001). B, Based on years until initial biochemical recurrence (P<.001). C, Based on prostate-specific antigen doubling time (PSADT) (P<.001).

We constructed an algorithm (Figure 4) to predict a man's likelihood of developing metastatic disease within various periods following initial biochemical recurrence. Unfortunately, when pathologic stage was used to further subcategorize the algorithm in Figure 4, the number of men within each category was not sufficient to obtain reasonable 95% CIs, and pathologic stage was not included in the algorithm for this reason. Using the prostatectomy Gleason score, the time of initial biochemical recurrence (2 vs >2 years), and PSADT (<10 vs 10 months) for men with Gleason score of less than 8, we estimated a man's likelihood of remaining free of clinically evident metastatic disease over various times (3, 5, and 7 years) without additional therapeutic intervention. The PSADT was not a statistically significant predictor for men with a Gleason score of greater than 7 when time to PSA elevation was known. This may be due to small numbers of men within each subset and requires further investigation. The periods indicate years from biochemical recurrence as opposed to years from surgery.

View larger version (32K): [in this window] [in a new window] Figure 4. Algorithm for Estimating a Man's Likelihood of Remaining Free of Metastatic Disease Estimates are calculated at 3, 5, or 7 years from the time of the initial prostate-specific antigen (PSA) elevation (metastatic-disease free period, based on Gleason score in the surgical specimen, the time of initial biochemical recurrence (2 vs >2 years), and prostrate-specific antigen doubling time (PSADT) (<10 vs 10 months). CI indicates confidence interval.

Forty-four (43%) of the 103 men with metastatic disease died due to prostate cancer. Again, no man with metastatic disease died due to any cause other than prostate cancer. The actuarial median time to death after development of metastatic disease was slightly less than 5 years (Figure 5). The only variable that reliably separated men based on time to death was the length of time from surgery until diagnosis of metastatic disease. Figure 6 demonstrates a significant difference in the time to death after development of distant disease between those men who developed metastatic disease within 1 to 3, 4 to 7, and 8 to 15 years following surgery (P=.02). Median survival for men developing metastases within the first 3 years after surgery was approximately 4 years from the diagnosis of metastatic disease. For men developing metastases between 4 and 7 years following surgery, median survival was approximately 5 years, and the median survival has not been reached in men developing metastases at 8 or more years following surgery. Gleason score, time to biochemical recurrence, PSADT, and serum PSA levels at diagnosis of metastases did not significantly influence time until death.

View larger version (14K): [in this window] [in a new window] Figure 5. Actuarial Likelihood of Death Due to Prostate Cancer in 104 Men Diagnosed as Having Metastases After Radical Prostatectomy The survival times indicated are years from the diagnosis of metastatic disease.

View larger version (19K): [in this window] [in a new window] Figure 6. Actuarial Likelihood of Death Due to Prostate Cancer in 104 Men Diagnosed as Having Metastases After Radical Prostatectomy Men are categorized according to the period after surgery in which the diagnosis of metastatic disease was made at 1 to 3 years, 4 to 7 years, or more than 8 years. The time of survival is indicated as years from diagnosis of metastatic disease.

COMMENT

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We are able to estimate a patient's probability of long-term cure after radical prostatectomy using pathologic stage as a surrogate end point. Both clinical and pathologic factors play a role in determining a patient's likelihood of having an undetectable serum PSA level at 10 to 15 years following surgery.^1-5 The most predictive of these factors include pretreatment PSA level, pathologic stage, and Gleason score; however, other microscopic features and biomarkers have also been suggested to identify patients at risk for failure following surgery.^1-5,15-17

Between 27% and 53% of men undergoing radical prostatectomy will have a detectable serum PSA elevation within 10 years following surgery.^1-5 Until now, there have been no reliable data concerning the timing and natural history of disease progression for men with an isolated PSA level elevation after radical prostatectomy. These findings should allow physicians and patients to make educated decisions about the progression of disease and need for treatment and to facilitate the design of clinical trials.

Twenty-three percent of the men who demonstrated biochemical recurrence in our series had an undetectable serum PSA level for at least 5 years, and a small percentage (4%) had an undetectable level for 10 years prior to biochemical recurrence (Table 2). In other series, PSA progression has been rare in men with an undetectable PSA level for 5 to 6 years after surgery.¹⁸ Our series demonstrates that with a larger number of patients and with yearly extended follow-up, men do continue to experience recurrence even 10 years and longer after surgery.

This analysis demonstrates that some men remain free of metastasis for an extended length of time after biochemical recurrence. The median actuarial time from biochemical recurrence until progression to metastases was 5 years (mean, 8 years). The metastasis-free rate of 63% for all men at 5 years after biochemical progression is similar to the 60% to 75% progression-free rates at 5 years after surgery in men with lymph node–positive disease treated solely by radical prostatectomy.^19-21

The risk of developing metastatic disease after biochemical recurrence was shown to correlate with pathologic Gleason scores. Men with tumors of Gleason scores less than 8 had a 73% chance of remaining free of progression at 5 years after biochemical recurrence compared with a 40% probability in men with higher grade tumors (Gleason score, 8-10). A similar correlation between risk of progression and tumor grade was also seen in men with lymph node–positive disease treated solely with radical prostatectomy.²⁰

The length of time after surgery prior to biochemical recurrence was important in determining the risk of eventual distant failure for men with lower (5, 6, and 7) and men with high (8, 9, and 10) Gleason scores (Figure 4). A similar observation was made previously by Partin et al²² in a report demonstrating that a high Gleason score and advanced pathologic stage were important in determining the likelihood of local or distant failure. Using a cutoff of 10 months, PSADT provided further substratification for men with a Gleason score of less than 8. Men with rapid PSA level elevation (<2 years), a Gleason score of 5 to 7, and a PSADT (>10 months) demonstrated a 76% probability of remaining free of metastatic disease for 5 years following initial PSA level elevation compared with men with a shorter PSADT (<10 months) who had only 35% chance of remaining free of metastatic disease for 5 years after biochemical recurrence. Although not as strong as Gleason score, time of biochemical recurrence, and PSADT, the pathologic stage did contribute to the likelihood of distant metastasis (P=.01). The PSADT has been suggested by Patel et al¹³ as a useful predictor of the type of eventual recurrence after radical prostatectomy. They measured the PSADT for a group of 77 men with biochemical recurrence following radical retropubic prostatectomy and found that shorter PSADTs (<6 months) were more indicative of distant disease when compared with local recurrence.

The overall 10- and 15-year metastasis-free survival rates in the present report were 87% and 82%, respectively. Zincke et al² previously reported 10- and 15-year metastasis-free rates of 82% and 76% in more than 3000 men undergoing radical prostatectomy. In a multi-institutional study, Gerber et al⁶ reported 10-year metastasis-free rates that varied directly with tumor grade (low, 87%; intermediate, 68%; and high, 52%). When patients in our series were divided into these same categories, the metastasis-free rates at 10 years were better than those reported for those who had the low-grade tumors (100%) and intermediate-grade tumors (91%) but were somewhat lower in the higher-grade tumors (43%). This lower rate for the high-grade tumors may be due to the lack of early hormonal therapy in our patients with high-grade disease. Although this issue was not specifically addressed by Gerber et al,⁶ more than one quarter of the men in the report from the Mayo Clinic received either early hormonal or radiation therapy.²

After the development of metastatic disease, the actuarial median time until death due to prostate cancer was slightly less than 5 years and dependent on the timing of progression to distant disease. Men who progressed to distant disease within 1 to 3 years following surgery died due to cancer at a higher rate than those men who developed metastases at 4 to 7 years or more than 8 years after surgery. Seventy-eight percent of the men who developed distant disease 8 years or more after surgery survived an additional 5 years. Time to original biochemical recurrence, serum PSA level at the time of diagnosis of metastatic disease, and Gleason score did not prove useful in stratifying risk of cancer-specific death. Data relating to the extent of disease on radionuclide bone scan, serum testosterone level, and performance status was not available in these men. These factors have also been shown to be important in determining overall survival in men with metastatic disease.^23-24

The 10- and 15-year cancer-specific survival rates of 94% and 91% for all 1997 men were similar to those reported in 2 recent analyses.^7-10 As was the case for metastasis-free survival, our rates of cancer-specific survival are higher than those reported by Gerber et al⁶ and Zincke et al²; this may due to patient selection.

None of the men in our study with metastatic disease died due to causes other than prostate cancer. This means that our cancer-specific death rate in men with metastatic disease is the same as the overall survival rate. The overall survival rate of 43% at 5 years was almost identical to that reported in men with minimal metastatic disease and good performance status in the National Cancer Institute Intergroup Study Number 0036 and other studies.^24-32

For men who experience an isolated biochemical recurrence, the algorithm in Figure 4 should provide a reasonable estimate of their probability of developing metastatic disease over the next 3, 5, or 7 years. This information should allow physicians and patients to make educated treatment decisions based on their risk of recurrence.^25-32

We anticipate that this algorithm should provide valuable information for the stratification of patients into different risk groups when designing and enrolling patients in investigational protocols. This analysis demonstrates that the duration of survival in these men is quite long and must be taken into account when determining the feasibility of proposed clinical trials.

CONCLUSION

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This report characterizes the natural history of disease progression to distant metastasis and death due to prostate cancer in men with a PSA elevation following radical prostatectomy. Radical prostatectomy was shown to provide excellent long-term cure rates with 82% metastasis-free survival at 15 years following surgery for all men in this study group. Of the men who did develop a PSA elevation, many remained free of metastatic disease for an extended period after initial biochemical recurrence without other forms of therapy. This has important implications in the selection of systemic therapies that are not curative and have no demonstrated impact on eventual outcome. The extended interval between biochemical recurrence and clinical metastatic disease emphasizes the need to design clinical trials to examine new treatment modalities in these men.

Factors that predicted the time course to the development of metastatic disease included the timing of initial PSA elevation, Gleason score, and PSADT. These factors were used to construct an algorithm that should be useful to the clinician in counseling patients about the time course and likelihood of eventual development of metastatic disease after initial biochemical recurrence.

AUTHOR INFORMATION

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Funding/Support: This study was supported by the Fund for Research and Progress in Prostate Cancer of the James Buchanan Brady Urological Institute, The Johns Hopkins Medical Institutions, Baltimore, Md, and the National Cancer Institute, Bethesda, Md, SPORE Grant, CA 58326.

Corresponding Author and Reprints: Alan W. Partin, MD, PhD, The James Buchanan Brady Urological Institute, The Johns Hopkins Hospital, 600 N Wolfe St, Baltimore, MD 21287-2101 (e-mail: apartin{at}jhmi.edu).

Author Affiliations: Departments of Urology, The James Buchanan Brady Urological Institute (Drs Pound, Partin, and Walsh), Oncology (Dr Eisenberger), and Pathology (Dr Chan), The Johns Hopkins Medical Institutions, Baltimore, Md; and Department of Epidemiology, Merck Research Laboratories, Blue Bell, Pa (Dr Pearson).

REFERENCES

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Prognostic factors in men with stage D1 prostate cancer: identification of patients less likely to have prolonged survival after radical prostatectomy. J Urol. 1994;152:1077-1081. ISI | PUBMED 21. Golimbu M, Provet J, Al-Askari S. Radical prostatectomy for stage D1 prostate cancer. Urology. 1987;30:427-435. PUBMED 22. Partin AW, Pearson JD, Landis PK, et al. Evaluation of serum prostate-specific antigen velocity after radical prostatectomy to distinguish local recurrence from distant metastases. Urology. 1994;43:649-659. FULL TEXT | ISI | PUBMED 23. Soloway MS. The importance of prognostic factors in advanced prostate cancer. Cancer. 1990;66(suppl 5):1017-1021. 24. Eisenberger MA, Blumenstein BB, Crawford ED, et al. Bilateral orchiectomy with or without flutamide for metastatic prostate cancer. N Engl J Med. 1998;339:1036-1042. FREE FULL TEXT 25. Byar DP. The Veterans Administration Cooperative Urological Research Group's studies of cancer of the prostate. Cancer. 1973;32:1126-1130. 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Prognostic Stratification in Patients Who Received Hormonal Therapy for Prostate-specific Antigen Recurrence after Radical Prostatectomy
Ide et al.
Jpn J Clin Oncol 2009;0:hyp133v1-hyp133.
ABSTRACT | FULL TEXT  

Review: Risk stratification in the hormonal treatment of patients with prostate cancer
Uhlman et al.
Therapeutic Advances in Medical Oncology 2009;1:79-94.
ABSTRACT  

Safety and Immunological Efficacy of a DNA Vaccine Encoding Prostatic Acid Phosphatase in Patients With Stage D0 Prostate Cancer
McNeel et al.
JCO 2009;27:4047-4054.
ABSTRACT | FULL TEXT  

A Phase II Trial of Calcitriol and Naproxen in Recurrent Prostate Cancer
SRINIVAS and FELDMAN
Anticancer Res 2009;29:3605-3610.
ABSTRACT | FULL TEXT  

Pretreatment Prostate-Specific Antigen (PSA) Velocity and Doubling Time Are Associated With Outcome but Neither Improves Prediction of Outcome Beyond Pretreatment PSA Alone in Patients Treated With Radical Prostatectomy
O'Brien et al.
JCO 2009;27:3591-3597.
ABSTRACT | FULL TEXT  

New Molecular Biomarkers for the Prognosis and Management of Prostate Cancer - The Post PSA Era
BICKERS and AUKIM-HASTIE
Anticancer Res 2009;29:3289-3298.
ABSTRACT | FULL TEXT  

Gleason Score and Lethal Prostate Cancer: Does 3 + 4 = 4 + 3?
Stark et al.
JCO 2009;27:3459-3464.
ABSTRACT | FULL TEXT  

Prostate-cancer screening.
Catalona et al.
NEJM 2009;361:202-203.
FULL TEXT  

Challenges in Clinical Prostate Cancer: Role of Imaging
Kelloff et al.
Am. J. Roentgenol. 2009;192:1455-1470.
ABSTRACT | FULL TEXT  

Patient Anxiety About Prostate Cancer Independently Predicts Early Initiation of Androgen Deprivation Therapy for Biochemical Cancer Recurrence in Older Men: A Prospective Cohort Study
Dale et al.
JCO 2009;27:1557-1563.
ABSTRACT | FULL TEXT  

A Simulation Study of Control Sampling Methods for Nested Case-Control Studies of Genetic and Molecular Biomarkers and Prostate Cancer Progression
Wang et al.
Cancer Epidemiol. Biomarkers Prev. 2009;18:706-711.
ABSTRACT | FULL TEXT  

Introducing Nanochemoprevention as a Novel Approach for Cancer Control: Proof of Principle with Green Tea Polyphenol Epigallocatechin-3-Gallate
Siddiqui et al.
Cancer Res. 2009;69:1712-1716.
ABSTRACT | FULL TEXT  

Disseminated Tumor Cells in Prostate Cancer Patients after Radical Prostatectomy and without Evidence of Disease Predicts Biochemical Recurrence
Morgan et al.
Clin. Cancer Res. 2009;15:677-683.
ABSTRACT | FULL TEXT  

Percentage of Tumor in Prostatectomy Specimens: A Study of American Veterans
Vollmer
Am J Clin Pathol 2009;131:86-91.
ABSTRACT | FULL TEXT  

Role of Androgen Deprivation Therapy for Node-Positive Prostate Cancer
Wong et al.
JCO 2009;27:100-105.
ABSTRACT | FULL TEXT  

Indications, Extent, and Benefits of Pelvic Lymph Node Dissection for Patients with Bladder and Prostate Cancer
Thurairaja et al.
The Oncologist 2009;14:40-51.
ABSTRACT | FULL TEXT  

National Academy of Clinical Biochemistry Laboratory Medicine Practice Guidelines for Use of Tumor Markers in Testicular, Prostate, Colorectal, Breast, and Ovarian Cancers
Sturgeon et al.
Clin. Chem. 2008;54:e11-e79.
ABSTRACT | FULL TEXT  

Tumor Growth Rates Derived from Data for Patients in a Clinical Trial Correlate Strongly with Patient Survival: A Novel Strategy for Evaluation of Clinical Trial Data
Stein et al.
The Oncologist 2008;13:1046-1054.
ABSTRACT | FULL TEXT  

Biological Mediators of Effect of Diet and Stress Reduction on Prostate Cancer
Saxe et al.
Integr Cancer Ther 2008;7:130-138.
ABSTRACT  

Results from a monocentric phase II trial of erlotinib in patients with metastatic prostate cancer
Gravis et al.
Ann Oncol 2008;19:1624-1628.
ABSTRACT | FULL TEXT  

Systems Pathology Approach for the Prediction of Prostate Cancer Progression After Radical Prostatectomy
Donovan et al.
JCO 2008;26:3923-3929.
ABSTRACT | FULL TEXT  

Genomic Alterations Indicate Tumor Origin and Varied Metastatic Potential of Disseminated Cells from Prostate Cancer Patients
Holcomb et al.
Cancer Res. 2008;68:5599-5608.
ABSTRACT | FULL TEXT  

Testing a Multigene Signature of Prostate Cancer Death in the Swedish Watchful Waiting Cohort
Mucci et al.
Cancer Epidemiol. Biomarkers Prev. 2008;17:1682-1688.
ABSTRACT | FULL TEXT  

Prostate Cancer-Specific Survival Following Salvage Radiotherapy vs Observation in Men With Biochemical Recurrence After Radical Prostatectomy
Trock et al.
JAMA 2008;299:2760-2769.
ABSTRACT | FULL TEXT  

Improved Prediction of Disease Relapse after Radical Prostatectomy through a Panel of Preoperative Blood-Based Biomarkers
Shariat et al.
Clin. Cancer Res. 2008;14:3785-3791.
ABSTRACT | FULL TEXT  

Preoperative Plasma Endoglin Levels Predict Biochemical Progression After Radical Prostatectomy
Svatek et al.
Clin. Cancer Res. 2008;14:3362-3366.
ABSTRACT | FULL TEXT  

Endorectal and Dynamic Contrast-Enhanced MRI for Detection of Local Recurrence After Radical Prostatectomy
Casciani et al.
Am. J. Roentgenol. 2008;190:1187-1192.
ABSTRACT | FULL TEXT  

External Validation of a Biomarker-Based Preoperative Nomogram Predicts Biochemical Recurrence After Radical Prostatectomy
Shariat et al.
JCO 2008;26:1526-1531.
ABSTRACT | FULL TEXT  

What to Do with an Abnormal PSA Test
Loeb and Catalona
The Oncologist 2008;13:299-305.
ABSTRACT | FULL TEXT  

Serum HER2 extracellular domain predicts an aggressive clinical outcome and biological PSA response in hormone-independent prostate cancer patients treated with docetaxel
Domingo-Domenech et al.
Ann Oncol 2008;19:269-275.
ABSTRACT | FULL TEXT  

Prediction of Prostate-Specific Antigen Recurrence in Men with Long-term Follow-up Postprostatectomy Using Quantitative Nuclear Morphometry
Veltri et al.
Cancer Epidemiol. Biomarkers Prev. 2008;17:102-110.
ABSTRACT | FULL TEXT  

Nine-Gene Molecular Signature Is Not Associated with Prostate Cancer Death in a Watchful Waiting Cohort
Mucci et al.
Cancer Epidemiol. Biomarkers Prev. 2008;17:249-251.
ABSTRACT | FULL TEXT  

Prognostic Significance of p53 and X-ray Repair Cross-complementing Group 1 Polymorphisms on Prostate-Specific Antigen Recurrence in Prostate Cancer Post Radical Prostatectomy
Huang et al.
Clin. Cancer Res. 2007;13:6632-6638.
ABSTRACT | FULL TEXT  

Prostate-specific antigen doubling time before onset of chemotherapy as a predictor of survival for hormone-refractory prostate cancer patients
Oudard et al.
Ann Oncol 2007;18:1828-1833.
ABSTRACT | FULL TEXT  

Decision Analyses in Consideration of Treatment Strategies for Patients with Biochemical Failure After Curative Therapy on Clinically Localized Prostate Cancer in the Prostate-Specific Antigen Era
Shimizu et al.
Jpn J Clin Oncol 2007;0:hym105v1-12.
ABSTRACT | FULL TEXT  

Imaging in Oncology from The University of Texas M. D. Anderson Cancer Center: Diagnosis, Staging, and Surveillance of Prostate Cancer
Kundra et al.
Am. J. Roentgenol. 2007;189:830-844.
ABSTRACT | FULL TEXT  

Identification of Patients With Prostate Cancer Who Benefit From Immediate Postoperative Radiotherapy: EORTC 22911
Van der Kwast et al.
JCO 2007;25:4178-4186.
ABSTRACT | FULL TEXT  

Prognostic Value of Preoperative Serum Cell-Free Circulating DNA in Men with Prostate Cancer Undergoing Radical Prostatectomy
Bastian et al.
Clin. Cancer Res. 2007;13:5361-5367.
ABSTRACT | FULL TEXT  

Preoperative Plasma HER2 and Epidermal Growth Factor Receptor for Staging and Prognostication in Patients with Clinically Localized Prostate Cancer
Shariat et al.
Clin. Cancer Res. 2007;13:5377-5384.
ABSTRACT | FULL TEXT  

Chromogranin A and biochemical progression-free survival in prostate adenocarcinomas submitted to radical prostatectomy
Alessandro et al.
Endocr Relat Cancer 2007;14:625-632.
ABSTRACT | FULL TEXT  

Targeting Human {gamma}{delta} T Cells with Zoledronate and Interleukin-2 for Immunotherapy of Hormone-Refractory Prostate Cancer
Dieli et al.
Cancer Res. 2007;67:7450-7457.
ABSTRACT | FULL TEXT  

Efficiency of Ultrasensitive Prostate-specific Antigen Assay in Diagnosing Biochemical Failure After Radical Prostatectomy
Shimizu et al.
Jpn J Clin Oncol 2007;37:446-451.
ABSTRACT | FULL TEXT  

Predicting the Outcome of Salvage Radiation Therapy for Recurrent Prostate Cancer After Radical Prostatectomy
Stephenson et al.
JCO 2007;25:2035-2041.
ABSTRACT | FULL TEXT  

Death in Patients With Recurrent Prostate Cancer After Radical Prostatectomy: Prostate-Specific Antigen Doubling Time Subgroups and Their Associated Contributions to All-Cause Mortality
Freedland et al.
JCO 2007;25:1765-1771.
ABSTRACT | FULL TEXT  

Initial Hormonal Management of Androgen-Sensitive Metastatic, Recurrent, or Progressive Prostate Cancer: 2007 Update of an American Society of Clinical Oncology Practice Guideline
Loblaw et al.
JCO 2007;25:1596-1605.
ABSTRACT | FULL TEXT  

Imaging Prostate Cancer: A Multidisciplinary Perspective
Hricak et al.
Radiology 2007;243:28-53.
ABSTRACT | FULL TEXT  

Stratification of Patient Risk Based on Prostate-Specific Antigen Doubling Time After Radical Retropubic Prostatectomy
Tollefson et al.
Mayo Clin Proc. 2007;82:422-427.
ABSTRACT | FULL TEXT  

A Prostate-Specific Antigen-Activated Channel-Forming Toxin as Therapy for Prostatic Disease
Williams et al.
JNCI J Natl Cancer Inst 2007;99:376-385.
ABSTRACT | FULL TEXT  

Treatment of prostate cancer with Ad5/3{Delta}24hCG allows non-invasive detection of the magnitude and persistence of virus replication in vivo
Rajecki et al.
Molecular Cancer Therapeutics 2007;6:742-751.
ABSTRACT | FULL TEXT  

Comparison of Free and Total Forms of Serum Human Kallikrein 2 and Prostate-Specific Antigen for Prediction of Locally Advanced and Recurrent Prostate Cancer
Steuber et al.
Clin. Chem. 2007;53:233-240.
ABSTRACT | FULL TEXT  

Prostate Cancer: A Practical Approach to Current Management of Recurrent Disease
Walczak and Carducci
Mayo Clin Proc. 2007;82:243-249.
ABSTRACT | FULL TEXT  

Functional MR Imaging of Prostate Cancer
Choi et al.
RadioGraphics 2007;27:63-75.
ABSTRACT | FULL TEXT  

Survival Associated With Treatment vs Observation of Localized Prostate Cancer in Elderly Men
Wong et al.
JAMA 2006;296:2683-2693.
ABSTRACT | FULL TEXT  

Docetaxel, Estramustine, and 15-Month Androgen Deprivation for Men With Prostate-Specific Antigen Progression After Definitive Local Therapy for Prostate Cancer
Taplin et al.
JCO 2006;24:5408-5413.
ABSTRACT | FULL TEXT  

Potential Attenuation of Disease Progression in Recurrent Prostate Cancer With Plant-Based Diet and Stress Reduction
Saxe et al.
Integr Cancer Ther 2006;5:206-213.
ABSTRACT  

Adoption of a Plant-Based Diet by Patients with Recurrent Prostate Cancer
Nguyen et al.
Integr Cancer Ther 2006;5:214-223.
ABSTRACT  

Expression of Variant TMPRSS2/ERG Fusion Messenger RNAs Is Associated with Aggressive Prostate Cancer.
Wang et al.
Cancer Res. 2006;66:8347-8351.
ABSTRACT | FULL TEXT  

Best practice in primary care pathology: review 4
Smellie et al.
J. Clin. Pathol. 2006;59:893-902.
ABSTRACT | FULL TEXT  

Defining Biochemical Recurrence of Prostate Cancer After Radical Prostatectomy: A Proposal for a Standardized Definition
Stephenson et al.
JCO 2006;24:3973-3978.
ABSTRACT | FULL TEXT  

The cost of prostate cancer chemoprevention: a decision analysis model.
Svatek et al.
Cancer Epidemiol. Biomarkers Prev. 2006;15:1485-1489.
ABSTRACT | FULL TEXT  

Chronic Administration of Valproic Acid Inhibits Prostate Cancer Cell Growth In vitro and In vivo.
Xia et al.
Cancer Res. 2006;66:7237-7244.
ABSTRACT | FULL TEXT  

Molecular Load of Pathologically Occult Metastases in Pelvic Lymph Nodes Is an Independent Prognostic Marker of Biochemical Failure After Localized Prostate Cancer Treatment
Ferrari et al.
JCO 2006;24:3081-3088.
ABSTRACT | FULL TEXT  

Phase II Study of Pomegranate Juice for Men with Rising Prostate-Specific Antigen following Surgery or Radiation for Prostate Cancer.
Pantuck et al.
Clin. Cancer Res. 2006;12:4018-4026.
ABSTRACT | FULL TEXT  

Cyclooxygenase-2 Selective Inhibitors and Prostate Cancer: What Is the Clinical Benefit?
DuBois
JCO 2006;24:2691-2693.
FULL TEXT  

Celecoxib Versus Placebo for Men With Prostate Cancer and a Rising Serum Prostate-Specific Antigen After Radical Prostatectomy and/or Radiation Therapy
Smith et al.
JCO 2006;24:2723-2728.
ABSTRACT | FULL TEXT  

How Early Is Early: Androgen Deprivation for Prostate-Specific Antigen Relapse in Prostate Cancer
Duchesne et al.
JCO 2006;24:2964-2964.
FULL TEXT  

The emerging roles of DNA methylation in the clinical management of prostate cancer.
Perry et al.
Endocr Relat Cancer 2006;13:357-377.
ABSTRACT | FULL TEXT  

Preoperative nomogram predicting the 10-year probability of prostate cancer recurrence after radical prostatectomy.
Stephenson et al.
JNCI J Natl Cancer Inst 2006;98:715-717.
ABSTRACT | FULL TEXT  

Therapeutic vaccines for prostate cancer.
Tarassoff et al.
The Oncologist 2006;11:451-462.
ABSTRACT | FULL TEXT  

A prospective study of calcium intake and incident and fatal prostate cancer.
Giovannucci et al.
Cancer Epidemiol. Biomarkers Prev. 2006;15:203-210.
ABSTRACT | FULL TEXT  

Retained Seminal Vesicles After Radical Prostatectomy: Frequency, MRI Characteristics, and Clinical Relevance
Sella et al.
Am. J. Roentgenol. 2006;186:539-546.
ABSTRACT | FULL TEXT  

Time to Detectable Metastatic Disease in Patients with Rising Prostate-Specific Antigen Values following Surgery or Radiation Therapy
Slovin et al.
Clin. Cancer Res. 2005;11:8669-8673.
ABSTRACT | FULL TEXT  

Promoter Hypermethylation as an Independent Prognostic Factor for Relapse in Patients with Prostate Cancer Following Radical Prostatectomy
Rosenbaum et al.
Clin. Cancer Res. 2005;11:8321-8325.
ABSTRACT | FULL TEXT  

Active Surveillance for Prostate Cancer: For Whom?
Klotz
JCO 2005;23:8165-8169.
ABSTRACT | FULL TEXT  

Utility of Prostate-Specific Antigen Kinetics in Addition to Clinical Factors in the Selection of Patients for Salvage Local Therapy
Lee and D'Amico
JCO 2005;23:8192-8197.
ABSTRACT | FULL TEXT  

Parameters for Treatment Decisions for Salvage Radiation Therapy
Hayes and Pollack
JCO 2005;23:8204-8211.
ABSTRACT | FULL TEXT  

Early Versus Delayed Androgen Deprivation for Prostate Cancer: New Fuel for an Old Debate
Ryan and Small
JCO 2005;23:8225-8231.
ABSTRACT | FULL TEXT  

Geographic and Socioeconomic Variation in the Treatment of Prostate Cancer
Krupski et al.
JCO 2005;23:7881-7888.
ABSTRACT | FULL TEXT  

Racial Differences in Prognostic Value of Adult Height for Biochemical Progression Following Radical Prostatectomy
Freedland et al.
Clin. Cancer Res. 2005;11:7735-7742.
ABSTRACT | FULL TEXT  

When Prostate Brachytherapy Fails: A Case Report and Discussion
Kadoch et al.
The Oncologist 2005;10:799-805.
ABSTRACT | FULL TEXT  

Prostate Size and Risk of High-Grade, Advanced Prostate Cancer and Biochemical Progression After Radical Prostatectomy: A Search Database Study
Freedland et al.
JCO 2005;23:7546-7554.
ABSTRACT | FULL TEXT  

Assessing Benefit and Risk in the Prevention of Prostate Cancer: The Prostate Cancer Prevention Trial Revisited
Klein et al.
JCO 2005;23:7460-7466.
ABSTRACT | FULL TEXT  

Predictors of Prostate Cancer-Specific Mortality After Radical Prostatectomy or Radiation Therapy
Zhou et al.
JCO 2005;23:6992-6998.
ABSTRACT | FULL TEXT  

Postoperative Nomogram Predicting the 10-Year Probability of Prostate Cancer Recurrence After Radical Prostatectomy
Stephenson et al.
JCO 2005;23:7005-7012.
ABSTRACT | FULL TEXT  

Targeted Elimination of Prostate Cancer by Genetically Directed Human T Lymphocytes
Gade et al.
Cancer Res. 2005;65:9080-9088.
ABSTRACT | FULL TEXT  

Prostate-Specific Antigen Nadir and Cancer-Specific Mortality Following Hormonal Therapy for Prostate-Specific Antigen Failure
Stewart et al.
JCO 2005;23:6556-6560.
ABSTRACT | FULL TEXT  

Is Prostate-Specific Antigen a Valid Surrogate End Point for Survival in Hormonally Treated Patients With Metastatic Prostate Cancer? Joint Research of the European Organisation for Research and Treatment of Cancer, the Limburgs Universitair Centrum, and AstraZeneca Pharmaceuticals
Collette et al.
JCO 2005;23:6139-6148.
ABSTRACT | FULL TEXT  

Preoperative PSA Velocity Is an Independent Prognostic Factor for Relapse After Radical Prostatectomy
Patel et al.
JCO 2005;23:6157-6162.
ABSTRACT | FULL TEXT  

Identifying Patients at Risk for Significant Versus Clinically Insignificant Postoperative Prostate-Specific Antigen Failure
D'Amico et al.
JCO 2005;23:4975-4979.
ABSTRACT | FULL TEXT  

Risk of Prostate Cancer-Specific Mortality Following Biochemical Recurrence After Radical Prostatectomy
Freedland et al.
JAMA 2005;294:433-439.
ABSTRACT | FULL TEXT  

PSA Kinetics and Risk of Death From Prostate Cancer: In Search of the Holy Grail of Surrogate End Points
Anscher
JAMA 2005;294:493-494.
FULL TEXT  

Prostate Cancer Clinical Trial End Points: "RECIST"ing a Step Backwards
Scher et al.
Clin. Cancer Res. 2005;11:5223-5232.
ABSTRACT | FULL TEXT  

Androgen Deprivation Therapy for Prostate Cancer
Sharifi et al.
JAMA 2005;294:238-244.
ABSTRACT | FULL TEXT  

Evaluation and Management of Prostate-specific Antigen Recurrence After Radical Prostatectomy for Localized Prostate Cancer
Naito
Jpn J Clin Oncol 2005;35:365-374.
ABSTRACT | FULL TEXT  

The presence of benign prostatic glandular tissue at surgical margins does not predict PSA recurrence
Kernek et al.
J. Clin. Pathol. 2005;58:725-728.
ABSTRACT | FULL TEXT