Rising Serum Prostate-specific Antigen Level Research Articles

Diagnosis of early biochemical recurrence after radical prostatectomy or radiation therapy in patients with prostate cancer: State of the art

Biochemical recurrence after primary treatment in prostate cancer is not uncommon. A rising serum prostate-specific antigen level represents a first sign of disease relapse. At this time of low disease burden, imaging and particularly magnetic resonance imaging and positron emission tomography/computed tomography (PET/CT) are essential to determine the localization of the recurrence, which may be local, in lymph nodes, and/or metastatic. Imaging results allow best determine modalities of salvage treatment, which can be local by using radiotherapy or other focal treatments or systemic using hormonotherapy. Current evidence suggests that multiparametric magnetic resonance imaging, PET/CT with prostate specific membrane antigen and lympho-magnetic resonance imaging are effective and complementary to detect local recurrences and distant metastases.

Clinical Impact of 68Ga-PSMA PET/CT in a Patient With Biochemical Recurrence of Prostate Cancer

A 64-year-old man with history of prostate adenocarcinoma underwent radical prostatectomy in 2003. He remained with undetectable prostate-specific antigen (PSA) levels until 2014, when he then presented rising serum PSA levels and performed a Tc-MDP bone scan that was negative for metastases. In August 2015, his PSA was 4.89 ng/dL, and restaging images with pelvic MR and F-FDG PET/CT were both negative. Therefore, the patient underwent a Ga-PSMA PET/CT that showed marked tracer uptake in a single mediastinal lymph node. Histopathology demonstrated metastatic adenocarcinoma secondary to prostate cancer, altering patient management to hormone therapy instead of pelvic radiotherapy.

Aggressive variants of castration-resistant prostate cancer.

A subset of patients with advanced castration-resistant prostate cancer may eventually evolve into an androgen receptor (AR)-independent phenotype, with a clinical picture associated with the development of rapidly progressive disease involving visceral sites and hormone refractoriness, often in the setting of a low or modestly rising serum prostate-specific antigen level. Biopsies performed in such patients may vary, ranging from poorly differentiated carcinomas to mixed adenocarcinoma-small cell carcinomas to pure small cell carcinomas. These aggressive tumors often demonstrate low or absent AR protein expression and, in some cases, express markers of neuroendocrine differentiation. Because tumor morphology is not always predicted by clinical behavior, the terms "anaplastic prostate cancer" or "neuroendocrine prostate cancer" have been used descriptively to describe these rapidly growing clinical features. Patients meeting clinical criteria of anaplastic prostate cancer have been shown to predict for poor prognosis, and these patients may be considered for platinum-based chemotherapy treatment regimens. Therefore, understanding variants within the spectrum of advanced prostate cancer has important diagnostic and treatment implications.

Is there an anti-androgen withdrawal syndrome for enzalutamide?

The anti-androgen withdrawal syndrome (AAWS) can be seen in one-third of patients after discontinuation of first-generation non-steroidal anti-androgen therapy. With the introduction of new agents for anti-androgen therapy as well as alternate mechanisms of action, new therapeutic options before and after docetaxel chemotherapy have arisen (Ohlmann et al. in World J Urol 30(4):495-503, 2012). The question regarding the occurrence of an enzalutamide withdrawal syndrome (EWS) has not been evaluated yet. In this study, we assess prostate-specific antigen (PSA) response after discontinuation of enzalutamide. In total 31 patients with metastatic castration-resistant prostate cancer (mCRPC) underwent an enzalutamide withdrawal and were evaluated. Data were gathered from 6 centres in Germany. Patients with continuous oral administration of enzalutamide with rising serum PSA levels were evaluated, starting from enzalutamide withdrawal until subsequent therapy was initiated, follow-up ended or death of the patient occurred. Statistical evaluation was performed applying one-sided binomial testing using R-statistical software, version 3.0.1. Mean withdrawal follow-up was 6.5 weeks (range 1-26.1 weeks). None of the 31 patients showed a PSA decline. Mean relative PSA rise over all patients was 73.9 % (range 0.5-440.7 %) with a median of 44.9 %. If existent, an AAWS is at least very rare for enzalutamide in patients with mCRPC after taxane-based chemotherapy and does not play a clinical role in this setting. This may be attributed to the different pharmacodynamics of enzalutamide. Longer duration of therapy or a longer withdrawal interval may reveal a rare EWS in the future.

Dietary habits and prostate cancer detection: a case–control study

Many studies have suggested that nutritional factors may affect prostate cancer development. The aim of our study was to evaluate the relationship between dietary habits and prostate cancer detection. We studied 917 patients who planned to have transrectal ultrasonography-guided prostatic biopsy based on an elevated serum prostate-specific antigen (PSA) level, a rising serum PSA level or an abnormal digital rectal examination. Before receiving the results of their biopsy, all patients answered a self-administered food frequency questionnaire. In combination with pathology data we performed univariable and multivariable logistic regression analyses for the predictors of cancer and its aggressiveness. Prostate cancer was found in 42% (386/917) of patients. The mean patient age was 64.5 (standard deviation [SD] 8.3) years and the mean serum PSA level for prostate cancer and benign cases, respectively, was 13.4 (SD 28.2) mug/L and 7.3 (SD 4.9) mug/L. Multivariable analysis revealed that a meat diet (e.g., red meat, ham, sausages) was associated with an increased risk of prostate cancer (odds ratio [OR] 2.91, 95% confidence interval [CI] 1.55-4.87, p = 0.027) and a fish diet was associated with less prostate cancer (OR 0.54, 95% CI 0.32-0.89, p = 0.017). Aggressive tumours were defined by Gleason score (>/= 7), serum PSA level (>/= 10 mug/L) and the number of positive cancer cores (>/= 3). None of the tested dietary components were found to be associated with prostate cancer aggressivity. Fish diets appear to be associated with less risk of prostate cancer detection, and meat diets appear to be associated with a 3-fold increased risk of prostate cancer. These observations add to the growing body of evidence suggesting a relationship between diet and prostate cancer risk.

Weighing the data on diet and prostate cancer

In 2001, my colleagues and I asked whether the link between nutrition and prostate cancer was evidence-based or merely a suspicion.1 The descriptive epidemiology of prostate cancer suggests that it is indeed a preventable disease. The evidence and scientific data of a variety of prevention strategies include, among many others, dietary fat reduction.2 Omega-3 and omega-6 polyunsaturated fatty acids are essential fatty acids. The Western diet contains a disproportionally high amount of omega-6 and a low amount of omega-3 polyunsaturated fatty acids, and the resulting high omega-6/omega-3 ratio is thought to contribute to cardiovascular disease, inflammation and cancer. Studies in human populations have linked high consumption of fish or fish oil to a reduced risk of colon, prostate and breast cancer, although other studies have failed to find a significant association. Nonetheless, the available epidemiological evidence, combined with the demonstrated effects of omega-3 polyunsaturated fatty acids on cancer in animal and cell culture models, has motivated the development of clinical interventions using omega-3 polyunsaturated fatty acids in the prevention of cancer.3 In this issue of CUAJ, Amin and colleagues4 have addressed an interesting issue, namely, the impact of nutritional factors on prostate cancer development. They looked at a database of 917 patients planned to have transrectal ultrasonography–guided biopsies based on an elevated serum prostate-specific antigen (PSA) level, a rising serum PSA level or an abnormal digital rectal examination. They also performed univariable and multivariable logistic regression analysis for prediction of cancer and its aggressiveness using a self-administered food frequency questionnaire given before the biopsies. The authors found that on multivariable analyses, a meat diet including red meat, ham and sausages was associated with an increased risk of prostate cancer, and a fish diet was associated with less prostate cancer. None of the tested dietary components were associated with prostate cancer aggressiveness. The authors have nicely pointed out the strengths and weaknesses of their study, including its limitations. By definition, case–control studies are prone to certain types of unavoidable biases. However, the strength of the paper lies in its multivariable analysis and the detailed questionnaire that patients completed before undergoing the prostate biopsy. Noteworthy, red meat, ham and sausages as well as fish clearly had unfavourable and favourable impacts, respectively. Potatoes, interestingly enough, had a protective odds ratio close to statistical significance although it is not clear whether this has something to do with potatoes themselves or whether patients who eat a lot of potatoes actually have other types of dietary habits that protect them. With respect to the incidence of aggressive prostate cancer and its relation to diet, it is not clear whether the absence of an association was due to the low number of cancers found in that group or whether increasing the number of these patients would have potentially brought positive results. For instance, with respect to pulses, such as beans and peas, the odds ratio for a Gleason score above 7 and number of cancer cores above 3 was, respectively, 1.86 and 2.89. Most odds ratios close to 3 would probably be significant on a large patient population. Recently, the association between prostate cancer risk and fresh and preserved fish consumption among participants of a population-based case–control study (1534 cases, 1607 controls) was investigated in Canada.5 Fish intake was measured using a dietary questionnaire that collected frequency of consumption of a given portion size of both fresh and preserved fish. Logistic regression analysis demonstrated an inverse association between preserved fish and prostate cancer risk for all levels of consumption, but reductions only reached statistical significance for the category of 1 to 3 servings of preserved fish per month (odds ratio 0.78, confidence interval 0.64–0.95). Consumption of any fat or energy from preserved fish was also associated with reduced risk. There was no suggestion of reduced prostate cancer risk with consumption of fresh and canned fish. These results suggest that consumption of preserved fish may reduce the risk of developing prostate cancer. It is not crystal clear why the difference between preserved and fresh fish is so important, but it warrants further study. These sometimes contradictory results highlight our limitations in the understanding and effectiveness of prostate cancer preventive means and the numerous grey areas that need additional investigations.

Quality of Life, Morbidity, and Mortality Results of a Prospective Phase II Study of Intermittent Androgen Suppression for Men with Evidence of Prostate-Specific Antigen Relapse After Radiation Therapy for Locally Advanced Prostate Cancer

Background Observations of quality of life (QOL), morbidity, and mortality were obtained from the results of a prospective phase II study of intermittent androgen suppression for recurrent prostate cancer after radiation therapy. Patients and Methods Patients with histologically confirmed adenocarcinoma of the prostate and a rising serum prostate-specific antigen level after external-beam radiation of the prostate were treated intermittently with a 36-week course of cyproterone and leuprolide. At predetermined intervals, QOL was assessed using the Southwest Oncology Group 9346 QOL and the American Urological Association symptom score questionnaires. Progression-free and overall survival rates were estimated using the Kaplan-Meier method. Parameters related to progression were explored with univariate and multivariate analyses. Results The incidence of adverse events was higher when patients were on treatment. Fatigue, dyspnea, and hematuria were the most common symptoms and signs recorded (50.5%, 24.8%, and 17.4%, respectively). Less frequent were myocardial infarction (7.3%), cerebrovascular accident (6.4%), and deep vein thrombosis (5.5%). Quality of life improved when off treatment, as indicated by a shift toward baseline levels in the scales depicting physical and work functions, hot flashes, impotence, sexual performance, urgency, and nocturia. Biochemical recurrence-free survival at 5 years was 70%, with a median > 6 years. The overall 5-year survival was 80%, similar to that of an age-matched population of normal men. Conclusion Intermittent androgen suppression is a potentially useful treatment for locally recurrent prostate cancer after radiation therapy with QOL benefits in the off-treatment interval and no apparent deleterious effects on short- to medium-term survival.

Case 18-2007

A 54-year-old man came to the Multidisciplinary Genitourinary Clinic of the Cancer Center for advice on management of prostate cancer. A slowly rising serum prostate-specific antigen level led to a needle biopsy of the prostate 2 weeks after the consultation. Examination of the biopsy specimens revealed adenocarcinoma, with a Gleason score of 7, involving the left lobe. A treatment recommendation was made.

Unexpected response of hormone-refractory prostate cancer to treatment with an antileukemic chemotherapy regimen

Our patient was a 61-year-old man with hormone-refractory prostate cancer and a rapidly rising serum prostate-specific antigen level. During the course of therapy for prostate cancer, abnormal blood counts and subsequent bone marrow biopsy led to a diagnosis of acute lymphoblastic leukemia. He was treated with a chemotherapeutic regimen in standard use for lymphoblastic leukemia, which resulted in an unusual response of his prostate cancer, with declining serum prostate-specific antigen levels that had reached undetectable levels at the time of the patient's death from acute sepsis and leukemic relapse. Autopsy showed minimal evidence of prostate cancer, localized to the prostate.

Cancer Treatment-Induced Bone Loss (CTIBL) in Prostate Cancer: Pathophysiology, Preclinical Findings, and Treatment with Zoledronic Acid

Objective: Androgen deprivation therapy (ADT) is the treatment of choice for men with advanced prostate cancer, and the most common indication for the initiation of ADT is a rising serum prostate-specific antigen level after failed local therapy. Consequently, potentially long periods of androgen suppression exist in these patients, resulting in clinically significant bone loss. This review will discuss the pathophysiology of cancer treatment-induced bone loss (CTIBL) and the treatment and prevention of CTIBL with zoledronic acid. Methods: Relevant information was identified through searches of published studies, abstracts from scientific meetings, and review articles. Results: The treatment of prostate cancer patients with surgical or pharmacologic ADT results in the activation of osteoclast-mediated bone resorption, leading to reductions in bone mineral density (BMD) and increased fracture risk. Preclinical evidence from a murine prostate cancer model also suggests that ADT may potentially increase the risk of bone metastasis. Bone loss caused by long-term ADT and bone metastases can result in significant skeletal morbidity in patients with prostate cancer. Zoledronic acid has been shown to increase BMD in prostate cancer patients receiving ADT, and is the only bisphosphonate effective in reducing the risk of skeletal complications in prostate cancer patients with bone metastases in the setting of hormone-refractory disease. In addition, preclinical evidence suggests that zoledronic acid may prevent tumor metastasis to bone. Conclusions: Zoledronic acid can provide clinical benefit for patients with advanced prostate cancer throughout the course of their disease. In these patients BMD should be monitored routinely, and zoledronic acid treatment should be considered to prevent bone loss.

Detecting Metastatic Pelvic Lymph Nodes by 18F-2-Deoxyglucose Positron Emission Tomography in Patients with Prostate-Specific Antigen Relapse after Treatment for Localized Prostate Cancer

Aim: To evaluate whether positron emission tomography (PET) with ¹⁸F-2-deoxyglucose (FDG) can detect pelvic lymph node metastases in prostate cancer patients who had elevated serum prostate-specific antigen (PSA) levels after treatment. Methods: Twenty-four patients with a rising serum PSA level after treatment for localized prostate cancer were examined with FDG-PET before pelvic lymph node dissection. All patients had negative findings on whole body bone scan and equivocal pelvic computed tomography (CT) results. The results of FDG-PET were then compared to the histology of the pelvic lymph nodes obtained at surgery. Results: Lymph node metastases were detected by histopathological examination in 16/24 (66.7%) patients. At the sites with histopathologically proven metastases, increased FDG uptake was found in 12/16 (75.0%) patients. In addition, there were 4 patients with false-negative results, but no patient with a false-positive result on FDG-PET images. The sensitivity, specificity, accuracy, positive predictive value, and negative predictive value of FDG-PET in detecting metastatic pelvic lymph nodes were 75.0, 100.0, 83.3, 100.0, and 67.7%, respectively. Conclusions: These results suggest that FDG-PET may be a valuable diagnostic tool in the staging of pelvic lymph nodes in patients with PSA relapse after treatment of localized prostate cancer when the whole body bone scan is negative and pelvic CT findings are equivocal.

Increased expression of PSA mRNA during brachytherapy in peripheral blood of patients with prostate cancer

Objectives. To determine the extent of iatrogenic tumor cell dissemination during brachytherapy by assessing prostate-specific antigen (PSA) mRNA expression in circulating prostate tumor cells using reverse transcriptase-polymerase chain reaction (RT-PCR) analysis. The instrumentation used in the radioisotope seed placement of the prostate causes trauma to blood vessels and provides a vascular access for tumor cells that can lead to potential iatrogenic dissemination and systemic failure. Methods. Twenty-five patients treated for brachytherapy were recruited in the study. Controls included 4 normal men and 1 woman; case controls included 4 patients who underwent prostate biopsy for prostate cancer diagnosis. Peripheral blood (10 mL) was collected before, during, and after the brachytherapy procedure. Total RNA was isolated from mononuclear cells and phosphorus-32 RT-PCR was performed to analyze the mRNA expression of PSA and G6PDH genes. Results. Of 25 patients, 23 were negative for PSA mRNA expression and 2 were positive for PSA mRNA expression before brachytherapy. Of the 23 patients who were negative for PSA mRNA expression before treatment, 15 patients (65%) turned positive during or after brachytherapy and the remaining 8 patients remained negative throughout the treatment. Eight of the 25 patients developed rising serum PSA levels. Of these 8 patients, 1 (12.5%) did not have PSA mRNA expression in the peripheral blood before, during, or after brachytherapy; the remaining 7 patients who developed rising serum PSA levels had PSA mRNA expression after brachytherapy ( P = 0.03). Conclusions. These findings strongly suggest that iatrogenic shedding of prostate cells occurs as a result of brachytherapy and raises the concern that these cells liberated at the time of brachytherapy increase the risk of metastatic deposits and results in systemic failure, as measured by serum PSA levels.

Molecular prediction of progression in patients with conservatively managed prostate cancer

Objectives. To report our results with the use of reverse transcriptase-polymerase chain reaction (RT-PCR) as a potential predictor of prostate cancer (CaP) progression in patients managed with watchful waiting. There has been much recent debate about the safety of treating older patients with localized CaP with watchful waiting. The RT-PCR is an assay that can detect small numbers of prostate cells in circulating blood. Methods. Blood samples were taken from male and female control patients and from patients with advanced, hormone-treated and untreated localized (watchful-waiting) CaP. Sensitive nested RT-PCR assays were carried out on these samples using primers for both prostate-specific antigen (PSA) and prostate-specific membrane antigen mRNA. Results. Fifty-one blood samples were taken from patients managed with watchful waiting. Fourteen of these had positive RT-PCR results. These patients had a significantly higher PSA velocity than did the patients with negative RT-PCR results. Circulating prostate cells were detected in 18 of 24 patients with advanced CaP, 2 of 34 patients with stable, hormone-treated CaP, and in none of the negative controls. The assay was able to detect 20 LNCaP cells reliably when added to a 5-mL volunteer blood sample. Conclusions. A significant minority (27%) of patients with untreated localized CaP had detectable circulating prostate cells, and these patients tended to have a progressively rising serum PSA level. Despite low-grade disease and sometimes low serum PSA values, these patients may be at risk of early metastatic progression. RT-PCR, in conjunction with existing prognostic tests, may be of use in predicting which “watchful-waiting” patients are at risk of early progression.

Postoperative nomogram for disease recurrence after radical prostatectomy for prostate cancer.

Although models exist that place patients into discrete groups at various risks for disease recurrence after surgery for prostate cancer, we know of no published work that combines pathologic factors to predict an individual's probability of disease recurrence. Because clinical stage and biopsy Gleason grade only approximate pathologic stage and Gleason grade in the prostatectomy specimen, prediction of prognosis should be more accurate when postoperative information is added to preoperative variables. Therefore, we developed a postoperative nomogram that allows more accurate prediction of probability for disease recurrence for patients who have received radical prostatectomy as treatment for prostate cancer, compared with the preoperative nomogram we previously published. By Cox proportional hazards regression analysis, we modeled the clinical and pathologic data and disease follow-up for 996 men with clinical stage T1a-T3c NXM0 prostate cancer who were treated with radical prostatectomy by a single surgeon at our institution. Prognostic variables included pretreatment serum prostate-specific antigen level, specimen Gleason sum, prostatic capsular invasion, surgical margin status, seminal vesicle invasion, and lymph node status. Treatment failure was recorded when there was either clinical evidence of disease recurrence, a rising serum prostate-specific antigen level (two measurements of 0.4 ng/mL or greater and rising), or initiation of adjuvant therapy. Validation was performed on this set of men and a separate sample of 322 men from five other surgeons' practices from our institution. Cancer recurrence was noted in 189 of the 996 men, and the recurrence-free group had a median follow-up period of 37 months (range, 1 to 168 months). The 7-year recurrence-free probability for the cohort was 73% (95% confidence interval, 68% to 76%). The predictions from the nomogram appeared to be accurate and discriminating, with a validation sample area under the receiver operating characteristic curve (ie, a comparison of the predicted probability with the actual outcome) of 0.89. A postoperative nomogram has been developed that can be used to predict the 7-year probability of disease recurrence among men treated with radical prostatectomy.

A Preoperative Nomogram for Disease Recurrence Following Radical Prostatectomy for Prostate Cancer

Background: Few published studies have combined clinical prognostic factors into risk profiles that can be used to predict the likelihood of recurrence or metastatic progression in patients following treatment of prostate cancer. We developed a nomogram that allows prediction of disease recurrence through use of preoperative clinical factors for patients with clinically localized prostate cancer who are candidates for treatment with a radical prostatectomy. Methods: By use of Cox proportional hazards regression analysis, we modeled the clinical data and disease follow-up for 983 men with clinically localized prostate cancer whom we intended to treat with a radical prostatectomy. Clinical data included pretreatment serum prostate-specific antigen levels, biopsy Gleason scores, and clinical stage. Treatment failure was recorded when there was clinical evidence of disease recurrence, a rising serum prostate-specific antigen level (two measurements of 0.4 ng/mL or greater and rising), or initiation of adjuvant therapy. Validation was performed on a separate sample of 168 men, also from our institution. Results: Treatment failure (i.e., cancer recurrence) was noted in 196 of the 983 men, and the patients without failure had a median follow-up of 30 months (range, 1-146 months). The 5-year probability of freedom from failure for the cohort was 73% (95% confidence interval = 69%-76%). The predictions from the nomogram appeared accurate and discriminating, with a validation sample area under the receiver operating characteristic curve (i.e., comparison of the predicted probability with the actual outcome) of 0.79. Conclusions: A nomogram has been developed that can be used to predict the 5-year probability of treatment failure among men with clinically localized prostate cancer treated with radical prostatectomy.

TREATMENT OF EARLY RECURRENT PROSTATE CANCER WITH 1,25-DIHYDROXYVITAMIN D3 (CALCITRIOL)

Purpose Substantial experimental and epidemiological data indicate that 1,25-dihydroxy-vitamin D3 (calcitriol) has potent antiproliferative effects on human prostate cancer cells. We performed an open label, nonrandomized pilot trial to determine whether calcitriol therapy is safe and efficacious for early recurrent prostate cancer. Our hypothesis was that calcitriol therapy slows the rate of rise of prostate specific antigen (PSA) compared with the pretreatment rate. Materials and Methods After primary treatment with radiation or surgery recurrence was indicated by rising serum PSA levels documented on at least 3 occasions. Seven subjects completed 6 to 15 months of calcitriol therapy, starting with 0.5 micro g. calcitriol daily and slowly increasing to a maximum dose of 2.5 micro g. daily depending on individual calciuric and calcemic responses. Each subject served as his own control, comparing the rate of PSA rise before and after calcitriol treatment. Results As determined by multiple regression analysis, the rate of PSA rise during versus before calcitriol therapy significantly decreased in 6 of 7 patients, while in the remaining man a deceleration in the rate of PSA rise did not reach statistical significance. Overall the decreased rate of PSA rise was statistically significant (p = 0.02 Wilcoxon signed rank test). Dose dependent hypercalciuria limited the maximal calcitriol therapy given (range 1.5 to 2.5 micro g. daily). Conclusions This pilot study provides preliminary evidence that calcitriol effectively slows the rate of PSA rise in select cases, although dose dependent calciuric side effects limit its clinical usefulness. The development of calcitriol analogues with decreased calcemic side effects is promising, since such analogues may be even more effective for treating prostate cancer.

A preoperative nomogram for disease recurrence following radical prostatectomy for prostate cancer.

Few published studies have combined clinical prognostic factors into risk profiles that can be used to predict the likelihood of recurrence or metastatic progression in patients following treatment of prostate cancer. We developed a nomogram that allows prediction of disease recurrence through use of preoperative clinical factors for patients with clinically localized prostate cancer who are candidates for treatment with a radical prostatectomy. By use of Cox proportional hazards regression analysis, we modeled the clinical data and disease follow-up for 983 men with clinically localized prostate cancer whom we intended to treat with a radical prostatectomy. Clinical data included pretreatment serum prostate-specific antigen levels, biopsy Gleason scores, and clinical stage. Treatment failure was recorded when there was clinical evidence of disease recurrence, a rising serum prostate-specific antigen level (two measurements of 0.4 ng/mL or greater and rising), or initiation of adjuvant therapy. Validation was performed on a separate sample of 168 men, also from our institution. Treatment failure (i.e., cancer recurrence) was noted in 196 of the 983 men, and the patients without failure had a median follow-up of 30 months (range, 1-146 months). The 5-year probability of freedom from failure for the cohort was 73% (95% confidence interval = 69%-76%). The predictions from the nomogram appeared accurate and discriminating, with a validation sample area under the receiver operating characteristic curve (i.e., comparison of the predicted probability with the actual outcome) of 0.79. A nomogram has been developed that can be used to predict the 5-year probability of treatment failure among men with clinically localized prostate cancer treated with radical prostatectomy.