Greg Trottier

University of Toronto, Toronto, Ontario, Canada

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Publications (35)136.43 Total impact

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    ABSTRACT: To determine to what extent prostate cancer (PCa) risk prediction is improved by adding prostate-specific antigen (PSA) to a baseline model including genetic risk. Peripheral blood deoxyribonucleic acid was obtained from Caucasian men undergoing prostate biopsy at the University of Toronto (September 1, 2008 to January 31, 2010). Thirty-three PCa risk-associated single nucleotide polymorphisms were genotyped to generate the prostate cancer genetic score 33 (PGS-33). Primary outcome is PCa on study prostate biopsy. Logistic regression, area under the receiver-operating characteristic curves (AUC), and net reclassification improvement were used to compare models. Among 670 patients, 323 (48.2%) were diagnosed with PCa. The PGS-33 was highly associated with biopsy-detectable PCa (odds ratio, 1.66; P = 5.86E-05; AUC, 0.59) compared with PSA (odds ratio, 1.33; P = .01; AUC, 0.55). PSA did not improve risk prediction when added to a baseline model (age, family history, digital rectal examination, and PGS-33) for overall risk (AUC, 0.66 vs 0.66; P = .86) or Gleason score ≥7 PCa (AUC, 0.71 vs 0.73; P = .15). Net reclassification improvement analyses demonstrated no appropriate reclassifications with the addition of PSA to the baseline model for overall PCa but did show some benefit for reclassification of men thought to be at higher baseline risk in the high-grade PCa analysis. In a baseline model of PCa risk including the PGS-33, PSA does not add to risk prediction for overall PCa for men presenting for "for-cause" biopsy. These findings suggest that PSA screening may be minimized in men at low baseline risk. Copyright © 2015 Elsevier Inc. All rights reserved.
    Urology 01/2015; · 2.13 Impact Factor
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    ABSTRACT: Background:To examine whether diagnostic biopsy (B1), for patients on active surveillance (AS) for prostate cancer, performed at an outside referral centre (external) compared with our in-house tertiary center (internal), increased the risk of re-classification on the second (confirmatory) biopsy (B2).Methods:Patients on AS were identified from our tertiary center database (1997-2012) with PSA<10, Gleason sum (GS) ⩽6, clinical stage ⩽cT2, ⩽3 positive cores, <50% of single core involved, age ⩽75 years and having a B2. Patients who had <10 cores at B1 and delay in B2 >24 mo were excluded. Depending on center where B1 was performed, men were dichotomized to internal or external groups. All B2 were performed internally. Multivariate logistic regression examined if external B1 was a predictor of re-classification at B2.Results:A total of 375 patients were divided into external (n=71, 18.9%) and internal groups (n=304, 81.1%). At B2, more men in the external group re-classified (26.8%) compared with the internal group (13.8%)(P=0.008). On multivariate analysis, external B1 predicted grade-related re-classification (odds ratio (OR) 4.14, confidence interval (CI) 2.01-8.54, P<0.001) and volume-related re-classification (OR 3.43, CI 1.87-6.25, P<0.001). Other significant predictors for grade-related re-classification were age (OR 2.13 per decade, CI 1.32-3.57, P<0.001), PSA density (OR 2.56 per unit, CI 1.44-4.73, P<0.001), maximum % core involvement (OR 1.04 per percentage point, CI 1.01-1.09, P=0.02) and time between B1 and B2 (OR 1.43 per 6 months, CI 1.21-1.71, P<0.001).Conclusion:At our institution, patients on AS who had their initial B1 performed externally were more likely to have adverse pathological features and re-classify on internal B2.Prostate Cancer and Prostatic Disease advance online publication, 9 December 2014; doi:10.1038/pcan.2014.48.
    Prostate Cancer and Prostatic Diseases 12/2014; 18(1). · 2.83 Impact Factor
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    ABSTRACT: To evaluate the association between nonsteroidal anti-inflammatory drug (NSAID) use and the risk of prostate cancer (PC) detection in men undergoing biopsy. Men were identified using our academic institution's prospectively maintained prostate biopsy database. Patients were classified as aspirin (ASA) users, users of other NSAIDs, or nonusers. The primary outcome was any PC on biopsy, and the secondary outcome was clinically significant PC (CSPC; Gleason sum ≥7). Multivariate logistic regression analyses were performed to adjust for a priori defined clinical confounders. Of 839 patients, 408 (48.6%) were diagnosed with PC and 201 (24.0%) had CSPC. A higher proportion of ASA users (63.5%) and other NSAID users (61.2%) had PC compared with nonusers (41.9%; P <.001). CSPC was more common among ASA users (34.9%; P <.001) compared with other NSAID users (20.0%) and nonusers (20.9%). In multivariate regression analyses, ASA use (odds ratio [OR] = 2.04; 95% confidence interval [CI] = 1.32-3.13; P = .001) and other NSAID use (OR = 2.42; 95% CI = 1.36-431; P = .003) were associated with higher odds of PC detection, whereas ASA use was associated with higher odds of CSPC (OR = 1.62; 95% CI = 1.00-2.62; P = .048). In men undergoing biopsy, ASA and other NSAID use were associated with increased probability of detecting PC, whereas ASA use was associated with the risk of detecting CSPC. Although NSAID use might have a protective biological effect against PC, men who develop elevated prostate-specific antigen levels while on NSAIDs may nonetheless be less likely to have an inflammatory etiology and more likely to harbor PC. It may be warranted for clinicians to consider the influence of NSAIDs when evaluating patients being considered for biopsy. Copyright © 2014 Elsevier Inc. All rights reserved.
    Urology 10/2014; · 2.13 Impact Factor
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    ABSTRACT: We investigate the frequency of cancer and pathological progression found in transition zone (TZ) biopsies in men undergoing multiple re-biopsy while on AS. Our tertiary center AS prostate cancer database (1997-2012) has eligibility criteria: PSA ≤10, ≤cT2, no Gleason grade 4 or 5, ≤ 3 positive cores, no core >50% involved, age ≤ 75 years and having ≥1 biopsy after initial diagnostic biopsy. For analysis, men with total <10 cores at diagnostic biopsy (B1), and/or a confirmatory biopsy (B2) >24 months after B1, were excluded. Multiparametric magnetic resonance imaging was performed selectively to investigate incongruity between PSA and biopsy findings. Pathological progression was defined as grade and/or volume (>50% core involved). TZ progression was subdivided into exclusive-TZ (only TZ) and combination TZ (both TZ and PZ). A multivariate Cox proportional hazards model examined for predictors of TZ progression. 392 men were considered, with a median follow-up of 45.5 months. At each biopsy during AS (B2-B5+), the frequency of TZ disease was: TZ positive cores (18.6-26.7%), all TZ-progression (5.9-11.1%) and exclusive TZ-progression (2.7-6.7%). Volume-related progression occurred more frequently than grade-related (n=24 versus 9). Predictors of exclusive-TZ progression were maximum % single core (HR 1.99, C.I. 1.30-3.04, p=0.002), and MRI reporting cancer (HR 3.19, C.I. 1.23-8.27, p=0.02). Across multiple AS biopsies, 2.7-6.7% of men had TZ-exclusive progression. We recommend TZ biopsy be considered in all men at confirmatory biopsy. Subsequently, positive MRI findings or high % core involvement may be useful to identify patients at risk.
    The Journal of urology 04/2014; · 3.75 Impact Factor
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    ABSTRACT: To evaluate the associations between body mass index (BMI) and prostate volume (PV) and lower urinary tract symptoms in a multiethnic cohort. A cohort of men without prostate cancer seen at our institution was assembled, excluding those with previous transurethral resection of the prostate. Height and weight were measured to compute BMI, PV was measured by transrectal ultrasound, and the International Prostate Symptom Score (IPSS) questionnaire was administered. After stratified bivariate analyses, multiple linear regression and ordinal logistic regression models were used to assess the independent effect of BMI on PV and IPSS, respectively. The cohort included 1613 patients, and mean BMI was 27.1 kg/m(2). Patients with a BMI of <25.0, 25.0-29.9, and 30.0-34.9 had a median PV of 44.0 mL, 48.0 mL, and 52.0 mL, respectively. The African ethnicity subgroup generally had larger median PVs than European and Asian subgroups and had the largest differences in median PV between normal and obese men. There were no significant differences in IPSS or usage of benign prostatic hyperplasia medications between BMI categories. In multivariable analyses, higher BMI was associated with larger PV (P <.001) but not IPSS (P = .91). On the basis of our model, given a PV of 40 mL, 50 mL, and 60 mL, each 5 kg/m(2) increase in BMI was associated with a 2.19 mL, 2.74 mL, and 3.29 mL increase in PV, respectively. Body weight (P <.001) but not height (P = .13) was associated with PV. Higher BMI is associated with larger PV but not worse lower urinary tract symptoms (measured using IPSS). Usage rate of alpha blockers or 5 alpha reductase inhibitors was not significantly different between BMI categories.
    Urology 09/2013; · 2.13 Impact Factor
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    ABSTRACT: OBJECTIVE: To investigate if prostate biopsy templates with fewer cores can be used during active surveillance (AS) for prostate cancer. METHODS: At present, we use an AS protocol template (ASPT) consisting of 13-17 cores. We hypothesize in the setting of known cancer, sextant (6 cores) or standard extended (10-12 cores) templates, could be used with similar effect. We identified patients in our referral institution database (1997-2009) with entry prostate-specific antigen <10 ng/mL, stage ≤cT2, Gleason sum ≤6, ≤3 cores positive for cancer, <50% of single core involved, and age ≤75 years (N = 272). Patients fulfilling standard criteria for pathologic reclassification (N = 94) at any follow-up biopsy were selected for evaluation. By mapping tumor location on the pathologic reclassification determining biopsy, hypothetical scenarios of sextant or standard extended templates (SET) were compared with our ASPT and examined for frequency of cancer detection and pathologic reclassification. RESULTS: For the 94 patients analyzed, the median number of cores taken was 9.7 (6-22) at baseline and 15 (14-17) for the reclassification biopsy. The median time between baseline and the pathologic reclassification determining biopsy was 15.4 months. Analysis of subgroupings showed that sextant template would identify 84% of cancers and 47.9% of the reclassification events, whereas SET detected 99% of cancers and 81.9% of patients who pathologically reclassified. When only considering Gleason sum ≥7 related progression events, SET found 16.2% less (n = 57) compared with ASPT (n = 68). CONCLUSION: When monitoring patients on AS, a 13-17 core template detects more pathologic reclassification than standard sextant (18.1%) or extended (52.1%) biopsy templates.
    Urology 06/2013; · 2.13 Impact Factor
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    ABSTRACT: BACKGROUND: Many men (21-52%) are reported to have no cancer on the second, also known as the confirmatory, biopsy (B2) for prostate cancer active surveillance (AS). If these men had a reduced risk of pathologic progression, particularly grade related, the intensity of their follow-up could be decreased. OBJECTIVE: To investigate if men with no cancer on B2 are less likely to undergo subsequent pathologic progression. DESIGN, SETTING, AND PARTICIPANTS: Men were identified from our tertiary care center AS prostate cancer database (1995-2012). Eligibility criteria were prostate-specific antigen (PSA) ≤10, cT2 or lower, no Gleason grade 4 or 5, three or fewer positive cores, and no core >50% involved. Only patients with three or more biopsies were selected and then dichotomized on cancer status (yes or no) at B2. INTERVENTION: AS. OUTCOME MEASUREMENTS AND STATISTICAL ANALYSIS: Pathologic progression was defined as grade (advancement in Gleason score) and/or volume (more than three positive cores, >50% core involved). Progression-free survival was compared. Predictors of progression were investigated using a Cox proportional hazards model. RESULTS AND LIMITATIONS: Of the 286 patients remaining on AS after B2, 149 (52%) had no cancer and 137 (48%) had cancer. The median follow-up after B2 was 41 mo (interquartile range [IQR]: 26.5-61.9). Progression-free survival at 5 yr was 85.2% versus 67.3% for negative B2 versus cancer on B2, respectively (p = 0.002). Men with no cancer at B2 had a 53% reduction in risk of subsequent progression (hazard ratio [HR]: 0.47; 95% confidence interval [CI], 0.29-0.77; p = 0.003). Subanalysis showed prognostic indicators of volume-related progression were absence of cancer (HR: 0.36; 95% CI, 0.20-0.62; p = 0.0006) and PSA density (HR: 1.79; 95% CI, 1.12-2.89; p = 0.01). The only predictor of grade-related progression was age (HR: 1.05; 95% CI, 1.00-1.10; p = 0.04). Retrospective analysis was the major limitation of the study. CONCLUSIONS: Absence of cancer on B2 is associated with a significantly decreased risk of volume-related but not grade-related progression. This must be considered when counseling men on AS.
    European Urology 05/2013; · 10.48 Impact Factor
  • The Journal of Urology 04/2013; 189(4):e225-e226. · 3.75 Impact Factor
  • European Urology Supplements 03/2013; 12(1):e270-e271. · 3.37 Impact Factor
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    ABSTRACT: Prostatic adenocarcinoma is an epithelial malignancy characterized by marked histological heterogeneity. It most often has a multifocal distribution within the gland, and different Gleason grades may be present within different foci. Data from our group and others have shown that the genomic deletion of the phosphatase and tensin homolog deleted on chromosome 10 (PTEN) tumor suppressor gene and the disruption of the ETS gene family have a central role in prostate cancer and are likely to be associated with Gleason grade. In this study, prostate cancer samples were systematically analyzed to determine whether there was concordance between PTEN losses and TMPRSS2-ERG fusion rearrangements, within or between foci in multifocal disease, using well-annotated tissue microarrays (TMAs) consisting of 724 cores derived from 142 radical prostatectomy specimens. Three-color fluorescence in situ hybridization analysis of both the PTEN deletion and the TMPRSS2-ERG fusion was used to precisely map genetic heterogeneity, both within and between tumor foci represented on the TMA. PTEN deletion was observed in 56 of 134 (42%) patients (hemizygous=42 and homozygous=14). TMPRSS2-ERG fusion was observed in 63 of 139 (45%) patients. When analyzed by Gleason pattern for a given TMA core, PTEN deletions were significantly associated with Gleason grades 4 or 5 over grade 3 (P<0.001). Although TMPRSS2-ERG fusions showed a strong relationship with PTEN deletions (P=0.007), TMPRSS2-ERG fusions did not show correlation with Gleason grade. The pattern of genetic heterogeneity of PTEN deletion was more diverse than that observed for TMPRSS2-ERG fusions in multifocal disease. However, the marked interfocal discordance for both TMPRSS2-ERG fusions and PTEN deletions was consistent with the concept that multiple foci of prostate cancer arise independently within the same prostate, and that individual tumor foci can have distinct patterns of genetic rearrangements.Modern Pathology advance online publication, 28 September 2012; doi:10.1038/modpathol.2012.162.
    Modern Pathology 09/2012; · 6.36 Impact Factor
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    ABSTRACT: Active surveillance for low risk prostate cancer has become an acceptable management strategy. However, a percentage of these patients in active surveillance move on to active treatment. Our aim was to examine urinary incontinence (UI) rates in men who move on to treatment from active surveillance and compare it to quoted rates in the literature. We examined the question that a potential delay in the treatment of prostate cancer in those on active surveillance may result in an increase in incontinence rates. From July 1992 to June 2009, 443 men at our institution entered into active surveillance for newly diagnosed prostate cancer. We reviewed their medical records and data was abstracted from physician-reported medical records. The mean age of the entire group was 64.1 years old (range 40-80). Their mean prostate-specific antigen (PSA) was 7.65 (range 0.21-36) and their mean Gleason score was 6.2 (range 4-8). Of these patients on active surveillance, 150/443 (33.3%) went on to active treatment. Median time to active treatment was 31.5 months (range 3-180 months). Only 5 patients went onto active treatment less than 1 year after starting active surveillance. Of these patients who went onto active treatment, 85 had radiation alone, 48 had a radical prostatectomy (RP), 7 had a RP and radiation, 7 had HIFU alone, 2 had focal ablation and 1 had HIFU followed by salvage RP. Of those undergoing radiation (92 patients), 66 had external beam and 26 had brachytherapy. Prior to active treatment 25/443 (5.6%) patients had UI documented in their history. Of those 25 patients only 3 went on to a RP and all had persistent UI after surgery. Two of the 25 patients went on to radiation therapy and their UI resolved. In the active treatment groups, after RP alone, 14/48 (29.2%) patients had new onset UI that persisted at a mean of 47.2 months (range 11-149 months) postoperatively. Of these 14 patients, 7 patients (14.6%) had significant leakage (> 1 pad/day). After radiation therapy alone 2/85(2.4%) had new onset persistent UI at 34 and 49 months post radiation. Only 1/7 (14.3%) patients that had high intensity focused ultrasound (HIFU) alone had persistent UI at 38 months after HIFU. Of the 7 patients that had both a RP and radiation, 2 had persistent significant UI at 49 and 153 months after surgery. One patient that had HIFU and a RP had persistent UI at 23 months post surgery. The 2 patients that had focal ablation were dry. The UI rates in our cohort of active surveillance patients who move on to active treatment are similar to patients who undergo treatment immediately after prostate cancer is diagnosed as quoted in the literature. This suggests that active surveillance, as an initial mode of therapy, does not increase the risk of UI if active treatment occurs at a later date.
    The Canadian Journal of Urology 06/2012; 19(3):6287-92. · 0.91 Impact Factor
  • The Journal of Urology 04/2012; 187(4):e901-e902. · 3.75 Impact Factor
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    ABSTRACT: The effects of partial nephrectomy (PN) on postoperative blood pressure (BP) are not known, and PN has the potential to worsen BP. We therefore sought to determine whether PN alters postoperative BP. Patients who underwent PN for suspected malignancy at our institution from 2002 to 2008 were included. Data on BP and medication from before and after PN were retrieved from family physicians. BP and number of antihypertensive medications were compared after surgery with preoperative values by use of paired t tests and Chi-squared analyses, respectively. Of 74 patients undergoing PN and providing consent, 48 met the inclusion and exclusion criteria, with a median follow-up of 24 months. For the early postoperative period (1 month to 1 year after surgery), the mean BPs (132.3/77.0 mmHg) were unchanged compared with preoperative values (132.4/78.0 mmHg; p=0.59 systolic BP and p=0.30 diastolic BP). For the later postoperative period (beyond 1 year after surgery), the mean postoperative systolic BP was unchanged from the mean preoperative systolic BP (131.2 mmHg vs. 132.4 mmHg, respectively; p>0.30). However, the corresponding average diastolic BP was lower in the long term (78.0 mmHg versus 76.4 mmHg respectively; p=0.01). No significant difference in the mean number of BP medications prescribed preoperatively, at one year, and beyond one year was identified (p>0.37). PN does not result in initial or long-term postoperative deterioration in BP.
    Korean journal of urology 03/2012; 53(3):154-8.
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    ABSTRACT: Study Type - Prognosis (cohort) Level of Evidence 2b What's known on the subject? and What does the study add? ADIPOSE tissue secretes various endocrine and paracrine mediators. Some authors have begun to consider whether peri-prostatic fat (PPF) may interact with the prostate and play a role in carcinogenesis. It has recently been shown that the PPF quantity measured by CT is associated with more aggressive disease in patients undergoing radiation therapy. Our group studied a population not yet diagnosed with prostate cancer. By doing so we were able to identify PPF thickness on transrectal ultrasonography as a risk factor for prostate cancer detection upon biopsy, and as a risk factor for high-grade disease. Our study also raises interesting questions about the underlying mechanisms of the association between PPF quantity and prostate cancer. •  To determine if the amount of peri-prostatic fat (PPF) on transrectal ultrasonography (TRUS) is a risk factor for incident prostate cancer overall and high-grade prostate cancer (Gleason ≥4). •  A prospectively maintained database of patients undergoing prostate biopsy at Princess Margaret Hospital for cancer suspicion was used. •  All TRUS examinations were retrospectively reviewed upon 'blinding' to outcome. •  PPF thickness, measured as the distance between the prostate and the pubic bone, was used as an index of the quantity of PPF. •  PPF measurements, together with other prostate cancer risk factors, were evaluated against prostate cancer and high-grade prostate cancer detection upon biopsy with univariable and multivariable logistic regression and area under the receiver operating characteristic curve (AUC) analysis. •  Of the 931 patients, 434 (47%) were diagnosed with prostate cancer and 218 (23%) were diagnosed with high-grade prostate cancer. •  The mean (range) PPF thickness was 5.3 (0-15) mm. •  Increasing PPF thickness was associated with prostate cancer and high-grade prostate cancer diagnosis, with graded effect. When adjusting for other variables, the odds of detecting any prostate cancer and high-grade prostate cancer increased 12% (odds ratio [OR] 1.12, 95% confidence interval [CI] 1.02-1.23) and 20% (OR 1.20, 95% CI 1.07-1.34), respectively, for each millimetre increase in PPF thickness. •  The AUCs for the association of PPF with prostate cancer and high-grade prostate cancer were 0.58 (95% CI 0.54-0.62) and 0.59 (95% CI 0.55-0.64), respectively. •  The amount of PPF can be estimated with TRUS and is a predictor of prostate cancer and high-grade prostate cancer at biopsy. To our knowledge, this study is the first to investigate PPF quantity in patients without prior prostate cancer diagnosis.
    BJU International 02/2012; 110(7):980-6. · 3.13 Impact Factor
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    ABSTRACT: To study the effect of smoking on bladder cancer presentation and outcome in a large cystectomy population. A database including 546 patients from the University Health Network (Toronto, Canada) and Turku University Hospital (Turku, Finland) was studied. In addition to the association of smoking with clinicopathological parameters, the effect of smoking on survival was analyzed. Categorical data were analyzed by the chi-squared test and numerical data were analyzed by Student's t-test. The Kaplan-Meier method, log-rank test and a proportional hazards model were used to estimate the effect of smoking on survival. In total, 352 patients (64%) were smokers and 194 (36%) were non-smokers. Smokers had more frequently advanced tumours and nodal metastasis. The 10-year disease-specific survival (DSS) was 52% vs 66% for smokers and non-smokers, respectively (P = 0.039). Smokers also had significantly worse overall survival (10-year overall survival 37% vs 62%; P = 0.015). Smoking affected significant DSS among men (P = 0.012), although no effect was observed among women. In a univariate model smoking was associated with a hazard ratio (HR) of 1.4 (95% confidence interval, CI, 1.0-1.9) for bladder cancer specific mortality and 1.4 (95% CI, 1.1-1.8) for overall mortality. In a multivariate model, smoking did not impact on DSS (HR, 1.1; 95% CI, 0.8-1.6; P = 0.41). In addition to advanced stage and nodal metastasis, female sex was an independent risk factor for DSS (HR, 1.6; 95% CI, 1.1-2.3; P = 0.007). Smokers appear to have worse outcomes after radical cystectomy for bladder cancer; however, it does not appear to be an independent prognostic factor for survival. Smoking affected survival only among men. Women had poorer survival but smoking was not a contributing factor to this.
    BJU International 08/2011; 109(1):70-6. · 3.13 Impact Factor
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    ABSTRACT: •To compare the Prostate Cancer Prevention Trial Risk Calculator (PCPT-RC) and European Randomized Study of Screening for Prostate Cancer Risk Calculator (ERSPC-RC) in a single-institution Canadian cohort. •At Princess Margaret Hospital, 982 consecutive patients with PCPT-RC and ERSPC-RC covariables were prospectively catalogued before prostate biopsy for suspicion of prostate cancer (PCa). •Receiver-operating characteristic (ROC) curves were generated for each calculator and prostate-specific antigen (PSA). •Comparisons by area under the curve (AUC) and calibration plots were performed. •Predictors of PCa were identified by univariable and multivariable logistic regression. •PCa was detected in 46% and high-grade (HG) PCa (Gleason ≥4) in 23% of subjects with a median PSA level of 6.02 ng/mL. • Multivariable analysis identified transrectal ultrasonography nodule, prostate volume and PSA as the most important predictors of PCa and HG PCa. •ROC curve analysis showed that the ERSPC-RC (AUC = 0.71) outperformed the PCPT-RC (AUC = 0.63) and PSA (AUC = 0.55), for PCa prediction, P < 0.001. •The PCPT-RC was better calibrated in the higher prediction range (40-100%) than the ERSPC-RC, whereas the ERSPC-RC had better calibration and avoided more biopsies in the lower risk range (0-30%). •Discrimination of the ERSPC-RC continued to be superior to the PCPT-RC when the cohort was stratified by different clinical variables. •The ERSPC-RC had better discrimination for predicting PCa compared to the PCPT-RC in this Canadian cohort. •Calibration would need to be improved to allow routine use of the ERSPC-RC in Canadian practice.
    BJU International 04/2011; 108(8 Pt 2):E237-44. · 3.13 Impact Factor
  • The Journal of Urology 04/2011; 185(4). · 3.75 Impact Factor
  • The Journal of Urology 04/2011; 185(4). · 3.75 Impact Factor
  • European Urology Supplements 04/2011; 185(4). · 3.37 Impact Factor
  • The Journal of Urology 04/2011; 185(4). · 3.75 Impact Factor