Definitive Therapy For Prostate Cancer Research Articles

Implications of Definitive Prostate Cancer Therapy on Soft Tissue Margins and Survival in Patients Undergoing Radical Cystectomy for Bladder Urothelial Cancer

We evaluated the possibility of an existing link between definitive prostate cancer treatment and its effect on positive soft tissue surgical margins at radical cystectomy. A secondary objective was to determine whether definitive prostate cancer treatment was associated with bladder cancer survival end points. There were 749 patients who underwent radical cystectomy between 2000 and 2013. After excluding females and patients with nonurothelial histologies 561 men were identified, of whom 69 (12.3%) received single or multimodal definitive prostate cancer treatment. Univariate and multivariable logistic regression was used to determine an association between clinical and pathological features such as definitive prostate cancer treatment and positive soft tissue surgical margins. Cox regression models and competing risk regression were used to investigate the impact of definitive prostate cancer treatment and positive surgical margins on survival. The median age of the male population was 70.0 years. There were 57cases of positive soft tissue surgical margins in our cohort of 561 men (10.2%). Of men who underwent previous definitive prostate cancer treatment 20 of 69(29.0%) had positive surgical margins compared to 37 of 492 (7.5%) who never received definitive prostate cancer treatment (p <0.0001). Brachytherapy, radiotherapy, hormonal therapy and radical prostatectomy significantly increased the rate of positive margins. Brachytherapy (OR 5.8), radiotherapy (OR 2.7) and hormonal therapy (OR 5.1) remained independent predictors of positive margins on multivariate analysis. Positive margins were associated with negative effects on recurrence-free (HR 3.1), cancer specific (HR 4.1) and overall survival (HR 2.8). Patients with a history of definitive prostate cancer treatment are at increased risk for positive soft tissue surgical margins. Positive margins significantly impact bladder cancer recurrence-free, cancer specific and overall survival following radical cystectomy. Careful patient counseling and surgical planning are crucial when treating patients undergoing radical cystectomy who have ahistory of definitive prostate cancer treatment.

Income inequality and treatment of African American men with high-risk prostate cancer

PurposeDefinitive treatment of high-risk prostate cancer with radical prostatectomy or radiation improves survival. We assessed whether racial disparities in the receipt of definitive therapy for prostate cancer vary by regional income. Patients and methodsA cohort of 102,486 men (17,594 African American [AA] and 84,892 non-Hispanic white) with localized high-risk prostate cancer (prostate-specific antigen >20ng/ml or Gleason≥8 or stage≥cT2c) diagnosed from 2004 to 2010 was identified in the Surveillance, Epidemiology, and End Results database. Income was measured at the census-tract-level. We used multivariable logistic regression to assess patient and cancer characteristics associated with the receipt of definitive therapy for prostate cancer. Multivariable Fine and Gray competing risks analysis was used to evaluate factors associated with prostate cancer death. ResultsOverall, AA men were less likely to receive definitive therapy than white men (adjusted odds ratio [AOR] = 0.51; 95% CI: 0.49–0.54; P<0.001), and there was a significant race/income interaction (Pinteraction = 0.016) such that there was a larger racial treatment disparity in the bottom income quintile (AOR = 0.49; 95% CI: 0.45–0.55; P<0.001) than in the top income quintile (AOR = 0.60; 95% CI: 0.51–0.71; P<0.001). After a median follow-up of 35 months, AA men in the bottom income quintile suffered the greatest prostate cancer mortality (adjusted hazard ratio = 1.47; 95% CI: 1.17–1.84; P = 0.001), compared with white men in the top income quintile. ConclusionsRacial disparities in the receipt of definitive therapy for high-risk prostate cancer are greatest in low-income communities, suggesting that interventions to reduce racial disparities should target low-income populations first.

Time to failure after definitive therapy for prostate cancer: implications for importance of aggressive local treatment

PurposeTo explore patterns of time to failure in men receiving high doses of permanent seed brachytherapy with or without external beam radiation therapy as a function of risk status.Material and methodsTwo thousand two hundred and thirty four patients were treated with prostate brachytherapy with median follow up of 8.0 years. The population was 35% low risk, 49% intermediate risk, and 16% high risk (NCCN). Median day 0 implant D90 was 119% and V100 was 98%. Treatment failure was defined as PSA > 0.40 ng/mL after nadir. Rates of biochemical failure, distant metastases, and prostate cancer death were determined with non-prostate death as a competing risk.ResultsFor all patients, the 10-year biochemical failure, distant metastases, and cause-specific mortality were 4.4%, 1.4%, and 1.3%, respectively. The biochemical failure rates were 1.3%, 4.8%, and 10.0% for men with low, intermediate, and high risk disease, respectively. Median time to failure was 2.8 years. In men who died from prostate cancer, the median time from treatment failure to death was 4.2 years. Overall, 83% of biochemical failures and 97% of metastases occurred within the first 4 years after treatment.ConclusionsWith the dose escalation achieved by high quality brachytherapy dosimetry, even high-risk prostate cancer patients have excellent long term biochemical outcomes. Treatment failures occur early, and one third become metastatic and progress rapidly to prostate cancer death. The low frequency and pattern of failures suggest the presence of micrometastatic disease prior to treatment is rare, even in high risk patients.

Detection of metastatic disease as a leading cause of screening failure in a phase III trial of zibotentan versus placebo in patients with nonmetastatic castration-resistant prostate cancer (CRPC).

4655 Background: Many patients with biochemical relapse after definitive therapy for prostate cancer receive androgen deprivation therapy. PSA levels eventually will rise despite castrate levels of testosterone. Many of these patients have nonmetastatic disease and do not develop metastases for a median of 30 mos (Smith MR JCO, 2005). However, there is no standard therapy for patients with nonmetastatic CRPC. ENTHUSE M0 (Study 15) is a global phase III study, now closed to enrollment, comparing zibotentan 10 mg vs placebo in nonmetastatic CRPC patients. Coprimary endpoints are overall survival and radiographic progression or death. Patients are screened for metastases by bone and CT/MRI scans. An unexpectedly high number of patients failed screening, prompting this analysis. Methods: All screened patients were included. For each investigator, the number of patients who enrolled and who failed screening were recorded. Screen fail reasons were recorded. Screen failure rates were computed by clinical specialty (oncology or urology) and geographic region by dividing the number of screen failures by the number of enrolled patients in each category. Results: As of January 14, 2011, 2583 patients completed screening, and 1169 (45%) failed screening. Screen failure rates were not different by clinical specialty or by geographic region. The leading causes of screen failures by clinical specialty are listed in the table. Conclusions: These data suggest that detectable asymptomatic metastatic disease may exist in about 30% of presumed nonmetastatic CRPC. These findings stress the value of periodic staging studies in men with CRPC, as those with detectable metastatic CRPC may benefit from emerging therapies. Screen failure criteria, n (%) Oncology (631 patients enrolled) Urology (1,885 patients enrolled) Detection of metastatic disease 184 (29) 566 (30) Creatinine clearance of <50 mL/min 45 (7) 156 (8) Long QTc interval 24 (4) 82 (4) Absence of biochemical progression 27 (4) 76 (4) Testosterone level >70 ng/dL (noncastrate) 15 (2) 71 (4) Total screen failures, n 283* 873* * Some patients had >1 reason for screening failure.

Role of detection of metastatic disease as a leading cause of screening failure in an ongoing phase III trial of zibotentan versus placebo in patients with nonmetastatic castration-resistant prostate cancer (CRPC).

135 Background: Many patients with biochemical relapse after definitive therapy for prostate cancer receive androgen deprivation therapy. Although most patients experience a decline in PSA, PSA eventually rises despite a castrate level of testosterone. Many of these patients have non-metastatic disease and do not develop metastases for a median of 30 mos (Smith MR. JCO, 2005). However, there is no standard therapy for asymptomatic patients with non-metastatic CRPC. ENTHUSE M0 (Study 15) is an ongoing global phase III study comparing zibotentan 10 mg (an oral specific endothelin A receptor antagonist) vs placebo in non-metastatic CRPC patients. Co-primary endpoints are overall survival and progression-free survival; secondary endpoints are safety, PSA, quality of life, and time to symptomatic progression. Eligible patients are screened for metastases by bone and CT/MRI scan and other parameters. An unexpectedly high number of patients failed screening, prompting this analysis. Methods: All patients who were screened were included in the analysis. Reasons for exclusion were recorded. Results: As of June 3, 2010, 1,756 patients completed screening. Of these patients, 960 (55%) were randomized and 796 (45%) failed screening. The leading causes of screen failures are listed in the table. Exclusion rates by investigator specialty and country will be reported. Conclusions: As 30% of patients had metastatic disease on screening and were excluded, these data suggest that the frequency of asymptomatic metastases is high in men thought to have non-metastatic CRPC. These findings stress the value of periodic staging studies in men progressing from hormone sensitive to non-metastatic CRPC as metastatic CRPC patients may benefit from standard treatments or research treatments on other protocols. [Table: see text] [Table: see text]

The effect of Gleason score on the predictive value of prostate‐specific antigen doubling time

To evaluate the influence of the pathological Gleason score on the predictive value of the prostate-specific antigen (PSA) doubling time (DT), as this variable predicts a patient's risk of disease progression both before and after definitive therapy for prostate cancer, and there is an inverse correlation between the Gleason score and PSA production. We evaluated all men treated with radical prostatectomy (RP) between 1990 and 1999 who did not receive neoadjuvant or adjuvant therapy. We identified 2296 patients who had multiple PSA values available before RP, and 1323 who had biochemical recurrence after RP and had at least two PSA values available before starting secondary therapy. Systemic progression and cancer-specific survival (CSS) rates were estimated using the Kaplan-Meier method and Cox proportional hazard regression models. A PSA DT of <18 vs >18 months predicted a lower 10-year systemic progression-free survival for patients with tumours having a pathological Gleason score of <7 (98% vs 99%, P = 0.005), 7 (82% vs 91%, P = 0.003) and 8-10 (57% vs 73%, P = 0.042). A PSA DT after RP of <12 months was significantly associated with a lower 10-year systemic progression-free survival for patients with tumours having a Gleason score of <7 (77% vs 94%, P < 0.001) and 7 (61% vs 86%, P < 0.001), but not 8-10 (61% vs 75%, P = 0.11). The ability of PSA DT before and after RP to predict systemic progression and CSS decreased with increasing Gleason score. The PSA DT remains associated with outcome both before and after RP across increasing pathological Gleason scores, although the predictive ability of PSA DT is diminished in Gleason 8-10 cancers.

1215 DO UROLOGIC PROCEDURES SUCH AS PROSTATE NEEDLE BIOPSY AND VASECTOMY CAUSE ERECTILE DYSFUNCTION?

You have accessJournal of UrologySexual Function/Dysfunction/Andrology: Evaluation1 Apr 20101215 DO UROLOGIC PROCEDURES SUCH AS PROSTATE NEEDLE BIOPSY AND VASECTOMY CAUSE ERECTILE DYSFUNCTION? Dan Lewinshtein, Jason Kim, Stephen Lukasewycz, and Christopher Porter Dan LewinshteinDan Lewinshtein More articles by this author , Jason KimJason Kim More articles by this author , Stephen LukasewyczStephen Lukasewycz More articles by this author , and Christopher PorterChristopher Porter More articles by this author View All Author Informationhttps://doi.org/10.1016/j.juro.2010.02.717AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookTwitterLinked InEmail INTRODUCTION AND OBJECTIVES Prior studies suggest that prostate needle biopsy (PNB) and vasectomy may cause erectile dysfunction (ED). We explored the relationship between a prior PNB or vasectomy and rates of ED. METHODS We reviewed a prospectively organized database of 890 patients who underwent transrectal ultrasound (TRUS)-guided PNB. ED was modeled as a categorical variable as either any, moderate-severe, or severe based on International Index of Erectile Function (IIEF) scores. Binary logistic regression was used to evaluate the predictive ability of PNB and vasectomy. They were adjusted for age in multivariate analysis.IIEF scores were obtained prior to each biopsy procedure. RESULTS Median age and IIEF score were 63 years and 19 points, respectively. According to IIEF scores, 22%, 11%, 15%, 34% had severe, moderate, mild-moderate, and mild ED, respectively. 18% had no ED. Vasectomy status was available in 391 patients, of whom 41% had prior vasectomy. On univariate analysis, age (OR=1.1, p<0.001), prior PNB (OR=1.83, p<0.002) and prior vasectomy (OR=0.41, p<0.001) were all associated with moderate-severe ED. Only age (OR=1.1, p<0.001) and vasectomy (OR=0.39, p<0.002) were predictive for severe ED. On multivariate analysis, age was predictive for moderate-severe (OR=1.08, p<0.001) and severe (OR=1.09, p<0.001) ED, while vasectomy was protective against moderate-severe (OR=0.41, P<0.001) and severe (OR=0.41, p<0.003) ED. PNB status was no longer significant (p>0.05) after adjustment for other covariates. CONCLUSIONS Age is a strong predictor of ED. Prior vasectomy is associated with a reduced risk of ED. Prior PNB, after adjustment for other variables, does not increase the risk of ED. Furthermore, ED was common in this cohort, and thus patients undergoing definitive therapy for prostate cancer should be counselled appropriately prior to treatment. Seattle, WA© 2010 by American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetails Volume 183Issue 4SApril 2010Page: e470 Advertisement Copyright & Permissions© 2010 by American Urological Association Education and Research, Inc.MetricsAuthor Information Dan Lewinshtein More articles by this author Jason Kim More articles by this author Stephen Lukasewycz More articles by this author Christopher Porter More articles by this author Expand All Advertisement Advertisement PDF downloadLoading ...

Predicting life expectancy in prostate cancer patients

Due to its long natural history, prostate cancer illustrates best the need for tools that adequately predict life expectancy. We reviewed the actual tools available for clinicians involved in therapeutic decisions in newly diagnosed prostate cancer and examined their accuracy to provide individual life expectancy. Life tables, comorbidity indices, and multivariate prognostic models can assist clinicians for life expectancy predictions. However, the accuracy of life tables (60.9%) and comorbidity indices (accuracy unknown) may be as weak as clinician-derived life expectancy predictions (69%). Actually, statistical models provide the highest accuracy (69-84.3%). To date, Walz et al. developed the most accurate model (84.3%), predicting the risk of death of nonprostate cancer-related causes within 10 years of definitive therapy. Clinicians need the most accurate estimates of life expectancy in situations in which there is uncertainty regarding the need for aggressive local therapy. As the accuracy of clinician-derived life expectancy prediction is relatively modest, clinicians may benefit from assisted life expectancy prediction by life tables and statistical tools in their daily clinical practice. This would enhance the accuracy of the life expectancy predictions of individual candidates to definitive therapy for prostate cancer. Actually, nomograms provide the most accurate health-adjusted life expectancy prognostication.

Commentary on A double-blind randomized crossover study of oral thalidomide versus placebo for androgen dependent prostate cancer treated with intermittent androgen ablation: Figg WD, Hussain MH, Gulley JL, Arlen PM, Aragon-Ching JB, Petrylak DP, Higano CS, Steinberg SM, Chatta GS, Parnes H, Wright JJ, Sartor O, Dahut WL, Medical Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes

We determined whether thalidomide can prolong progression-free survival in men with biochemically recurrent prostate cancer treated with limited androgen deprivation therapy. A total of 159 patients were enrolled in a double-blind randomized trial to determine if thalidomide can improve the efficacy of a gonadotropin-releasing hormone agonist in hormone responsive patients with an increasing prostate specific antigen after primary definitive therapy for prostate cancer. Patients were randomized to 6 months of gonadotropin-releasing hormone agonist followed by 200 mg per day oral thalidomide or placebo (oral phase A). At the time of prostate specific antigen progression gonadotropin-releasing hormone agonist was restarted for 6 additional months. Patients were then crossed over to the opposite drug and were treated until prostate specific antigen progression (oral phase B). Testosterone and dihydroxytestosterone were likewise monitored throughout the study. During oral phase A, the median time to prostate specific antigen progression was 15 months for the thalidomide group compared with 9.6 months on placebo (P = 0.21). The median time to prostate specific antigen progression during oral phase B for the thalidomide group was 17.1 vs. 6.6 months on placebo (P = 0.0002). No differences in time to serum testosterone normalization between the thalidomide and placebo arms were documented during oral phase A and oral phase B. Thalidomide was tolerable although dose reductions occurred in 47% (58 of 124) of patients. Despite thalidomide having no effect on testosterone normalization, there was a clear effect on prostate specific antigen progression during oral phase B. This is the first study, to our knowledge, to demonstrate the effects of thalidomide using intermittent hormonal therapy.

A Double-Blind Randomized Crossover Study of Oral Thalidomide Versus Placebo for Androgen Dependent Prostate Cancer Treated With Intermittent Androgen Ablation

We determined whether thalidomide can prolong progression-free survival in men with biochemically recurrent prostate cancer treated with limited androgen deprivation therapy. A total of 159 patients were enrolled in a double-blind randomized trial to determine if thalidomide can improve the efficacy of a gonadotropin-releasing hormone agonist in hormone responsive patients with an increasing prostate specific antigen after primary definitive therapy for prostate cancer. Patients were randomized to 6 months of gonadotropin-releasing hormone agonist followed by 200 mg per day oral thalidomide or placebo (oral phase A). At the time of prostate specific antigen progression gonadotropin-releasing hormone agonist was restarted for 6 additional months. Patients were then crossed over to the opposite drug and were treated until prostate specific antigen progression (oral phase B). Testosterone and dihydroxytestosterone were likewise monitored throughout the study. During oral phase A the median time to prostate specific antigen progression was 15 months for the thalidomide group compared to 9.6 months on placebo (p = 0.21). The median time to prostate specific antigen progression during oral phase B for the thalidomide group was 17.1 vs 6.6 months on placebo (p = 0.0002). No differences in time to serum testosterone normalization between the thalidomide and placebo arms were documented during oral phase A and oral phase B. Thalidomide was tolerable although dose reductions occurred in 47% (58 of 124) of patients. Despite thalidomide having no effect on testosterone normalization, there was a clear effect on prostate specific antigen progression during oral phase B. This is the first study to our knowledge to demonstrate the effects of thalidomide using intermittent hormonal therapy.

PSA Recurrence in Men Following Definitive Therapy for Prostate Cancer with Gleason Score 9/10, 8, and 7 with Tertiary Grade 5 Disease

PSA Recurrence in Men Following Definitive Therapy for Prostate Cancer with Gleason Score 9/10, 8, and 7 with Tertiary Grade 5 Disease

Positive Surgical Margins in Soft Tissue Following Radical Cystectomy for Bladder Cancer and Cancer Specific Survival

We evaluated risk factors for positive soft tissue surgical margins and the impact of soft tissue surgical margins on metastatic progression and disease specific survival in patients treated with radical cystectomy for bladder cancer. A total of 1,589 patients who underwent radical cystectomy for primary urothelial cancer at our institution were included in the study. Several variables were analyzed including gender, age, use of perioperative chemotherapy, tumor stage, tumor grade, presence of carcinoma in situ, pathological vascular invasion, bladder pathology, status of soft tissue surgical margins, lymph node status, number of lymph nodes removed and number of positive lymph nodes. End points were freedom from progression to metastases and disease specific survival. Positive soft tissue surgical margins were detected in 67 patients (4.2%). Risk factors for positive soft tissue surgical margins were female gender (p = 0.04), pathological stage, vascular invasion in the radical cystectomy specimen, lymph node metastases (all p < or = 0.001) and median number of positive lymph nodes (p = 0.002). In addition, nonpure transitional cell carcinoma histology (p = 0.001) was associated with positive soft tissue surgical margins. In the 5 years after cystectomy, rates of disease specific survival for the negative and positive soft tissue surgical margin groups were 72% (95% CI 69-75) and 32% (95% CI 19-54), respectively. On multivariate analysis disease specific death was associated with tumor stage, positive soft tissue surgical margins, vascular invasion, presence of positive lymph nodes, number of nodes removed and number of positive nodes. Risk factors for positive soft tissue surgical margins are female gender, locally advanced cancer, presence of vascular invasion and mixed histology. Patients with positive soft tissue surgical margins have poor prognosis, and positive soft tissue surgical margins were found to be independently associated with disease specific death.

Biochemical recurrence after definitive prostate cancer therapy. Part I: Defining and localizing biochemical recurrence of prostate cancer*

The introduction of prostate-specific antigen into clinical practice heralded a dramatic shift in the epidemiology of prostate cancer. The diagnosis and treatment of lower stage disease in younger men with fewer competing co-morbidities has resulted in a longer period of post-treatment cancer surveillance and the potential for disease recurrence. Life-long periodic prostate-specific antigen testing for biochemical recurrence is standard of care; however, there is no single definition of biochemical recurrence that reliably predicts clinical recurrence. This review explores the complexities of biochemical recurrence, a thorough understanding of which is crucial to making appropriate treatment decisions after primary treatment. It also evaluates the array of diagnostic tests frequently employed when biochemical recurrence has occurred. There is a disconnection between biochemical recurrence and progression to clinical disease. The definition of biochemical recurrence varies both by the prostate-specific antigen cut-point used and by the primary therapy employed. Furthermore, biochemical recurrence by itself appears not to be as reliable a predictor of eventual clinical recurrence as prostate-specific antigen doubling time. Current imaging modalities are rarely useful in localizing disease when biochemical recurrence is first detected. The correct interpretation of biochemical recurrence is crucial to treatment decision-making. New data show that prostate-specific antigen doubling time during prostate-specific antigen recurrence may be a valid surrogate for death from the disease. The potential therefore exists for prostate-specific antigen doubling time to be accepted as a trial endpoint, which might accelerate drug approval by the United States Food and Drug Administration.

Biochemical recurrence after definitive prostate cancer therapy. Part II: Treatment strategies for biochemical recurrence of prostate cancer*

Through the prostate-specific antigen era, the proportion of men less than 55 years old with newly diagnosed prostate cancer more than doubled to almost 15%. As increasing numbers of men are living longer with prostate cancer, larger proportions will eventually present to our collective practices with rising prostate-specific antigen levels. Such prostate-specific antigen relapses, conservatively estimated to affect approximately 50 000 men each year, have become the most common form of advanced prostate cancer in the current period. Increasing evidence suggests that early hormonal therapy improves progression-free survival and may alter the cancer-specific survival. However, there is a cost to pay in side-effects when androgen deprivation is administered over prolonged periods. The non-steroidal anti-androgen bicalutamide may offer an equivalent progression-free survival to castration without the complications of androgen deprivation. Observational data seem to indicate that high-risk individuals (i.e. those with high-grade, high-stage disease or a prostate-specific antigen doubling time less than 12 months) may also receive benefit from early therapy. The definition of advanced prostate cancer has changed. Multimodal therapy improves cancer-specific outcomes especially in men with high-risk disease. The potential opportunities for novel therapeutic agents with low associated morbidity are great.

Impact of biochemical failure on long-term clinical outcome after radical prostatectomy for prostate cancer in Japan.

Detailed information is needed to understand the impact of biochemical failure (bF) on long-term outcome after definitive therapy for prostate cancer. In all, 223 consecutive men treated with radical retropubic prostatectomy were followed and long-term clinical outcome was investigated. Pathological examination revealed more locally advanced tumors in this study compared with the typical cohorts seen in the Western series. The Cox proportional hazards model indicates pretreatment prostate-specific antigen levels and risk group stratification to be a significant predictors for bF (P<0.05), but not for overall survival. Seminal vesicle involvement was a significant predictor of systemic progression, cancer death and overall survival (P<0.05). Positive surgical margin and bF were also found to be independent predictors of overall survival (P<0.05). In contrast to reports from Western countries, this study found a significant correlation between bF after radical prostatectomy and overall survival. This may reflect years-later detection of prostate cancer in Japan compared with Western series. Biochemical failure may ultimately be translated into decreased overall survival after sufficient follow-up.

US consumers seek Canadian imports, generics to save on drugs

US consumers seek Canadian imports, generics to save on drugs

RACIAL/ETHNIC DISPARITIES IN THE TREATMENT OF LOCALIZED/REGIONAL PROSTATE CANCER

Racial/ethnic disparities in the utilization of definitive therapy for prostate cancer are well recognized in the United States. The effect of race on the use of contemporary definitive therapies, including brachytherapy, and the assessment of Hispanic men with regard to racial/ethnic disparity has not been fully characterized. We evaluated treatment patterns using Surveillance, Epidemiology and End Results registry data on 142340 localized/regional stage cases between 1992 and 1999 in white, black and Hispanic American men. Definitive therapy was defined as radical prostatectomy, external beam radiation, brachytherapy or combinations thereof. Logistic regression models were constructed to determine the odds of receiving definitive treatment, adjusting for age, marital status, tumor grade, and Surveillance, Epidemiology and End Results site. Black and Hispanic men were less likely to receive definitive therapy than white men (p <0.001). Higher tumor grade was associated with decreasing odds of definitive therapy for black and Hispanic men (p <0.001) compared to white men. The racial/ethnic disparities in the use of definitive therapy decreased between 1992 and 1999 with the greatest decrease in Hispanic men. Hispanic and black men were less likely than white men to receive definitive therapy. The disparity in the use of definitive therapy between 1992 and 1999 decreased significantly in Hispanic men, although a significant disparity in the use of definitive therapy persisted in black men. Our observation of an association between tumor grade and the racial/ethnic disparity in definitive therapy ties together relevant biological and social factors that may contribute to the observed racial/ethnic disparity in mortality.

Family history of prostate cancer and relapse after definitive external beam radiation therapy

Purpose The influence of family history on outcome after definitive therapy for prostate cancer has been disputed. One series reported increased relapse rates in men with a positive family history of prostate cancer treated with radical prostatectomy or radiation therapy, whereas others have reported no difference in outcome. We examined our series of patients treated with definitive external beam radiation therapy to determine if a positive family history for prostate cancer is associated with better or worse outcome. Methods and materials Family history information was available for 538 patients treated with radiation therapy for prostate cancer between 1983 and 2001. Prostate cancer in one or more first-degree relatives (father, brother, or son) was considered a positive family history. The endpoint of interest was time to prostate-specific antigen failure or initiation of hormonal therapy after radiation therapy. Results Ninety-seven of 538 patients (18%) had a positive family history. There were no significant differences between the positive and negative family history groups. Family history had no effect on relapse-free survival rates in the entire cohort ( p = 0.94) or in any subgroup. African American patients with a positive family history had significantly worse 5-year relapse-free survival rates, although there were few patients in this subgroup. Neither family history nor race was a statistically significant predictor of relapse in multivariate analysis; however, combined African American race and positive family history was associated with worse relapse-free survival rates. Conclusions In this large study of patients receiving definitive radiation therapy for localized prostate cancer, no relationship was found between positive first-degree family history of prostate cancer and relapse. The influence of family history on clinical outcome may be more understandable once the gene or genes responsible for hereditary prostate cancer are identified.

Elucidating the Etiology of Erectile Dysfunction After Definitive Therapy for Prostatic Cancer

Purpose: To determine the etiology of treatment-induced erectile dysfunction among patients who underwent surgery or radiotherapy for prostatic cancer. Methods and Materials: Ninety-eight patients were evaluated for erectile dysfunction after definitive therapy for prostate cancer with Duplex ultrasonography before and after intracorporal prostaglandin injection. Patients were classified as having arteriogenic, cavernosal, mixed (arteriogenic/cavernosal), or neurogenic impotence based upon the results of the Duplex studies. Results: Among patients who underwent radical prostatectomy (RP), 31 (52%) had cavernosal dysfunction, 19 (32%) had arteriogenic dysfunction, 3 (5%) were classified as mixed, and 7 (12%) as neurogenic dysfunction. Among patients treated with radiotherapy (RT), 24 (63%) had arteriogenic dysfunction, 12 (32%) had cavernosal dysfunction, 1 (2.5%) were classified as mixed, and 1 (2.5%) as neurogenic dysfunction. A multivariate analysis identified prior RT as the only predictor of an arteriogenic etiology ( p < 0.001) and prior RP as the only predictor of a cavernosal etiology ( p < 0.04) for erectile dysfunction among these patients. In the RP and RT groups, the median erectile responses were 70 and 65%, respectively. Arterial peak flows <25 cc/min predicted for a suboptimal erectile response with intracavernosal prostaglandin injections. Among 47 patients with arterial peak flows <25 cc/min, 21 (55%) had erectile responses of <70%, while for 51 patients with arterial peak flows ≥25 cc/min, 31 (39%) had erectile responses of <70% ( p < 0.039). Conclusions: While the etiology of erectile dysfunction after definitive therapy for prostatic cancer is likely a multifactorial phenomenon, these data suggest that the predominant etiology among patients who undergo RT is arteriogenic and among patients who undergo RP is veno-occlussive/cavernosal pathology. This information may have implications for the design of more effective therapies to address erectile dysfunction in this patient population.

Yield of imaging and scintigraphy assessing biochemical failure in prostate cancer patients

A retrospective study was undertaken to determine the diagnostic yield of computed tomography (CT) and bone scan in patients with biochemical failure after definitive therapy for prostate cancer. The records of the Radiation Oncology Division were screened for patients presenting with prostate cancer between January 1, 1993, and December 31, 1996. Of 198 patients, 44 developed biochemical failure postoperatively (n = 24) or postradiotherapy (n = 20), and were not treated with hormones prior to restaging. Review was made of restaging studies performed at the time of biochemical failure. Postoperatively, 5% (1 of 20) of bone scans and 11% (2 of 18) of CT scans were positive. Postradiotherapy, 30% (6 of 20) of bone scans and 30% (3 of 10) of CT scans were positive. Our study showed that imaging studies are of low utility in the evaluation of patients with biochemical failure after definitive therapy of prostate cancer given that most patients begin hormonal therapy irrespective of the results of restaging studies. If salvage therapy is considered, imaging results may have a role in the decision-making process.