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Background

The prognostic relevance of multifocal and multicentric breast cancer remains unclear and current staging systems do not consider focality. The aim of this study was to explore whether women with multifocal breast cancer have less favourable tumour characteristics and worse survival compared with women with unifocal breast cancer.

Methods 

Patient and tumour characteristics were obtained from Breast Cancer Database Sweden 3.0, which includes data for all Swedish women diagnosed with invasive breast cancer between 2008 and 2019 and who underwent surgery. Overall and breast cancer-specific survival rates were calculated using the Kaplan-Meier method and multivariable analysis was used to identify independent predictors of survival using the Cox proportional hazard model.

Results

A total of 71 419 women were included in the study: 59 445 (83.2%) had unifocal breast cancer, 7286 (10.2%) had multifocal breast cancer with two invasive foci, and 4688 (6.6%) had multifocal breast cancer with three or more invasive foci. Multifocal breast cancer was associated with higher clinical T and N categories compared with unifocal breast cancer. The median follow-up time was 5.96 (interquartile range 3.078.80) years. The breast cancer-specific 10-year survival rates were 86.1% for women with multifocal breast cancer with three or more foci, 86.5% for women with multifocal breast cancer with two foci, and 88.4% for women with unifocal breast cancer. In a multivariable analysis adjusted for patient and tumour characteristics, the HR for breast cancer-specific death was 1.17 (95% c.i. 1.03 to 1.32) for women with multifocal breast cancer with three or more foci compared with women with unifocal breast cancer. There was no statistically significant difference in overall survival between the three groups.

Conclusion

The present study suggests that focality provides prognostic information that is additional to that provided by traditional tumour characteristics.

Objectives: This study aimed to compare the effectiveness of software-based fusion-targeted biopsies (STBx) versus cognitive fusion-targeted biopsies (CogTBx) in detecting prostate cancer (PCa) and clinically significant PCa.

Materials and methods: Men aged 30-85 were included in a target trial emulation if they had undergone a STBx or CogTBx of Prostate Imaging Reporting and Data System (PI-RADS) 3-5 lesions in 2020-2024. Using log-link binary regression models with inverse probability of treatment weighting to adjust for confounding, we estimated the associations between biopsy technique and detection of PCa and clinically significant PCa (Gleason ≥3 + 4 and Gleason ≥4 + 3) by use of adjusted relative risks (aRR) with 95% confidence intervals (CIs) obtained via bootstrapping.

Results: A total of 2092 men who underwent STBx and 7933 men who underwent CogTBx in 2020-2024 were identified in PCBase Xtend. The overall proportion diagnosed with PCa was 64%. STBx detected PCa with a slightly higher frequency (aRR, 1.05; 95% CI, 1.02-1.09), corresponding to an absolute increase of 3.3 percentage points (95% CI 1.2-5.3). The relative risk for detection of Gleason ≥4 + 3 was somewhat larger (aRR, 1.13; 95% CI, 1.03-1.23). The largest relative difference for detection of PCa was observed in PI-RADS 3 lesions (aRR, 1.12; 95% CI, 1.01-1.24), and this pattern became even more apparent when the outcome was restricted to clinically significant PCa.

Conclusions: Software-based fusion-targeted biopsies detected slightly more PCa and clinically significant PCa compared to cognitive fusion-targeted biopsies, particularly in men with PI-RADS 3 lesions. Prioritizing PI-RADS 3 lesions for software-based targeted fusion biopsy could optimize diagnostic effectiveness.

Introduction and objectives: Definitions of prostate specific antigen progression for men with prostate cancer on androgen deprivation therapy (ADT) are mainly derived from randomised trials, and their applicability to the clinical practice remains uncertain. This study aimed to assess how different PSA-based definitions of progressions while on ADT affect estimates of progression, treatment initiation, and outcomes in men with prostate cancer.

Methods: Using data from the Prostate Cancer database of Sweden with extended treatments and endpoints data (PCBase Xtend), we identified 3718 men who initiated ADT between 2009 and 2022 and who had longitudinal PSA and treatment data. PSA progression was defined according to four modified guideline-based definitions ranging from the European Association of Urology (EAU) that has the most stringent criteria for progression to our previously used and less stringent definition (PCBase). We analysed cumulative incidence of PSA progression, treatment for castration resistant prostate cancer before and after PSA progression, and prostate cancer-specific mortality, accounting for competing risks.

Results: ADT was prescribed as the primary treatment in 52% of included men. The number of men with PSA progression ranged by definition from 1047 men (28%, EAU) to 2378 men (64%, PCBase) at 10 years after initiation of ADT. Earlier progression was observed with less stringent criteria, with a difference in median time to progression of 3 months (PCBase vs EAU). Despite variation in incidence proportion of PSA progression, the proportion of men treated within 5 years after progression was similar (45-52%), as was prostate cancer-specific mortality (26-27%) across definitions.

Conclusion: While definitions of PSA progression significantly impacted estimated incidence proportion of disease progression, they had limited influence on treatment initiation and long-term mortality. These findings suggest that in the clinical practice, decisions are guided by factors other than formal progression criteria. PSA-based definitions can be useful in observational studies if supported by sensitivity analyses.

Background and objective

There are several methods for estimating prostate-specific antigen (PSA) doubling time (DT), and many men exhibit long periods of undetectable PSA below 0.1 ng/ml after radical prostatectomy (RP). We quantified between-method differences in estimated PSA-DT at PSA relapse after RP and evaluated how these differences affect discrimination of prostate cancer (PCa) death.

Methods

Men who underwent RP in 2007–2024 and subsequently developed a PSA relapse, defined as two consecutive values above 0.2 ng/ml, were included. We estimated PSA-DT from the date of the first undetectable PSA after RP until PSA relapse using four methods: (1) all detectable PSAs only, (2) two most recent detectable PSAs, (3) three most recent PSAs (with the third forced to 0.1 ng/ml if ≤0.1 ng/ml), and (4) all PSAs using a missing data approach. Discrimination of 10-yr PCa death was assessed using concordance index (C-index).

Key findings and limitations

A total of 3826 men were included. Median PSA-DT ranged from 4.4 to 8.6 mo, with a wide range in PSA-DT across different estimation methods. All four methods discriminated PCa death to a similar level, with C-index ranging from 0.70 to 0.74, which was slightly lower than the C-index (0.77) for the absolute PSA level at relapse. This study was restricted to men with PSA relapse after RP and may not be generalizable to other patient categories.

Conclusions and clinical implications

PSA-DT after RP was sensitive to the choice of estimation method, and all methods had comparable prognostic value to the last measured PSA level.

Objective

To estimate risk of prostate-specific antigen (PSA) relapse after radical radiotherapy (RT) for prostate cancer (PCa), and risk of PCa death after relapse according to Gleason score and time to relapse.

Patients and Methods

Men in the National Prostate Cancer Register of Sweden who underwent primary radical RT in 2007–2024 were followed until 31 December 2024. Relapse was defined as a PSA level increase of ≥2 ng/mL above nadir (Phoenix criteria). Competing risk cumulative incidence analyses were used to estimate risk of PSA relapse and risk of PCa death after relapse according to Gleason score and time to relapse.

Results

The 10-year risk of relapse in 26 634 men treated with RT was 25% (95% confidence interval [CI] 24–25%). The 10-year risk of PCa death after relapse was 35% (95% CI 33–37%). In men with relapse after >3 years the risk was 18% for Gleason score 6 and 19% for Gleason score 3 + 4, while in men with a relapse within 18 months the risk was 52% for Gleason score 4 + 3 and 75% for Gleason score 9–10. In men with a relapse at 1 year after RT there was a four-fold higher risk of PCa death for men with Gleason score 9–10 compared to men with Gleason score 6 (86% vs 22%). In contrast, in men with a relapse at 10 years after RT there were little differences in risk of PCa death according to Gleason (14% vs 23%).

Conclusion

In this population-based study of RT for PCa, there was a wide range in the estimates of risk of PCa death after relapse in highly granular groups according to Gleason score and time to relapse. Notably, some estimates did not align with the European Association of Urology relapse risk group classification.

Evidence on long-term outcomes after a negative biopsy, particularly prostate cancer mortality, remains limited, and optimal follow-up strategies are unclear. This nationwide population-based study assessed whether prostate-specific antigen (PSA) decline or stability during 5-a reductase inhibitor (5-ARI) therapy after a negative biopsy identifies men at very low risk of prostate cancer and prostate cancer death. Using Prostate Cancer data Base Sweden (PCBaSe Xtend), we identified men with longitudinal PSA and biopsy data who had at least one negative prostate biopsy between 2007 and 2018 and who initiated 5-ARI therapy with defined exposure and adherence criteria. PSA change during the first 2 yr of treatment was evaluated using PSA velocity and classified as stable or increasing. Follow-up started 2 yr after treatment initiation. Among 1248 men, 901 had stable PSA and 347 had increasing PSA. After 10 yr, the cumulative incidence proportion of prostate cancer was 8.3% (95% confidence interval [CI] = 6.0-12%) in men with stable PSA and 18% (95% CI = 13-24%) in men with increasing PSA; most cancers in men with stable PSA were low grade. Prostate cancer mortality was very low among men with stable PSA (standardized mortality ratio [SMR] = 0.19; 95% CI = 0.04-0.56) and higher in men with increasing PSA (SMR = 1.20; 95% CI = 0.52-2.37. Stable PSA during 5-ARI therapy after a negative biopsy was associated with very low prostate cancer mortality; whether this should influence PSA surveillance intensity requires further study.

(c) 2026 The Author(s).

Published by Elsevier B.V. on behalf of European Association of Urology. This is an open access article under the CC BY-NC-ND license (http://creative

Background and aim: Magnetic resonance imaging (MRI) is crucial for prostate cancer (Pca) diagnosis, risk stratification, and treatment planning. However, large-scale observational studies require structured MRI data, which are often only obtainable from free-text reports. We aimed to extract information from narrative prostate MRI reports and to describe subsequent biopsy outcomes in a nationwide population-based cohort.

Methods: We identified 108,361 prostate MRI examinations in Prostate Cancer database Sweden with extended treatments and endpoints data (PCBase Xtend) performed in 2015-2023. A rule-based text recognition algorithm was created and used to extract Prostate Imaging Reporting and Data System (PI-RADS) score and prostate volume from free-text MRI reports. Extracted data were validated against manually extracted information in the National Prostate Cancer Register (NPCR). We examined biopsy rates and Gleason score according to PI-RADS, Prostate Specific Antigen (PSA) density, and calendar year.

Results: The proportion of reports with identifiable PI-RADS scores increased from 38% in 2015-2016 to 83% in 2022-2023, with excellent agreement with NPCR data (correlation coefficient r = 0.94). Extracted prostate volumes correlated well with those in NPCR (r = 0.88). Biopsy rates decreased for PI-RADS 3 lesions over time, particularly in men with PSA density < 0.15 ng/ml/ml, while the proportion of men with PI-RADS 5 lesions who underwent biopsy increased. Almost all prostate cancers in men with PI-RADS 3 lesions were Gleason 6 or 7 (3+4). Gleason 9-10 was almost exclusively found in PI-RADS 5 lesions.

Conclusions: Automated extraction of information from unstructured MRI reports is feasible and accurate. The observed temporal trends reflecting increasing quality and standardization of prostate MRI support its use in large-scale epidemiological research.

A family history of prostate cancer in first-degree relatives is an established risk factor for prostate cancer, but the specific associations between prostate cancer characteristics in fathers and the risk of high-risk prostate cancer in their sons remain unclear. We identified men in Prostate Cancer data Base Sweden whose fathers had been diagnosed with prostate cancer in 1998-2005. We compared the observed number of prostate cancer diagnoses in these men with the expected number in the Swedish male population, estimating standardized incidence ratios (SIR). The median age of the 25,287 included sons of men with prostate cancer was 52 years (interquartile range 47-57 years) at end of follow-up. Their overall risk of a prostate cancer diagnosis was higher if the father had been diagnosed at less than 65 years old (SIR, 4.3, 95% confidence interval [CI], 3.8-5.0), compared with having a father diagnosed when 70 years old or older (SIR, 2.3; 95% CI 1.9-2.8). Sons of fathers diagnosed at less than 65 had a higher risk of Gleason score >= 8 cancers (SIR, 2.3; 95% CI 1.1-4.1) than sons of fathers diagnosed at 70 years old or older (SIR, 1.2; 95% CI 0.4-2.6). Having a father with a Gleason >= 8 cancer was associated with an increased risk for a Gleason >= 8 cancer (SIR, 2.6; 95% CI 1.1-5.1). These population-based results suggest that the father's prostate cancer characteristics should be considered when counseling men on prostate-specific antigen testing and diagnostic strategies.

Background and purpose

HYPO-RT-PC was the first phase 3 trial showing the long-term efficacy and safety of extremely hypofractionated radiotherapy schedules (ultra-hypofractionation or stereotactic body radiotherapy) compared with standard radiotherapy in localised prostate cancer. We aimed to verify their safety in the context of a clinical trial, by comparing events of potentially radiotherapy-related morbidity according to routinely collected health data between the arms and with men unexposed to prostate radiotherapy.

Materials and methods

We included Swedish residents in the per-protocol population and unexposed men matched with the ultra-hypofractionation group. Primary outcomes were genitourinary and gastrointestinal events defined by linking the Common Terminology Criteria for Adverse Events version 5.0 to diagnosis and intervention codes in broad (any related condition) and narrow code sets (strongly related conditions) tested separately. Inpatient care, interventions, and causes of death, identified in Swedish national healthcare registers, were events. Outcomes were analysed as time-to-event, adjusted for Charlson Comorbidity Index and socioeconomic status.

Results

Five hundred and forty-one participants (92%) from each trial arm and 2705 unexposed men were included. We found no statistically significant differences between the radiotherapy groups (broad code sets: genitourinary events, adjusted hazard ratio 0.95, 95% confidence interval 0.71–1.25; gastrointestinal events, 1.24, 0.91–1.69). Compared with the unexposed men, 10-year excess cumulative incidence was 8% and 5% for genitourinary and 5% and 4% for gastrointestinal events when applying the broad and narrow code sets, respectively, without excess mortality events.

Conclusion

The results support the HYPO-RT-PC findings by showing similar morbidity between ultra-hypofractionated and standard radiotherapy. Excess events were estimated to 4–8%, without increased associated mortality.