Search

Objectives: The PIRADS Steering Committee has called for "higher quality data before making evidence-based recommendations on MRI without contrast enhancement as an initial diagnostic work up," however, recognizing biparametric (bp) MRI as a reasonable option in a low-risk setting such as screening. With bpMRI, more men can undergo MRI at a lower cost and they can be spared the invasiveness of intravenous access. The aim of this study was to assess cancer detection in bpMRI vs mpMRI in sequential screening for prostate cancer (PCa). Methods: Within the ongoing Göteborg PCa screening 2 trial, we assessed cancer detection in 551 consecutive participants undergoing prostate MRI. In the same session, readers first assessed bpMRI and then mpMRI. Four targeted biopsies were performed for lesions scored PIRADS 3–5 with bpMRI and/or mpMRI. Results: Cancer was detected in 84/551 cases (15.2%; 95% CI: 12.4–18.4) with mpMRI and in 83/551 cases (15.1%; 95% CI: 12.3–18.2%) with bpMRI. The relative risk (RR) for cancer detection with bpMRI compared to mpMRI was 0.99 (95% one-sided CI: > 94.8); bpMRI was non-inferior to mpMRI (10% non-inferiority margin). bpMRI resulted in fewer false positives, 45/128 (35.2%), compared to mpMRI, 52/136 (38.2%), RR = 0.92; 95% CI: 0.84–0.98. Of 8 lesions scored positive only with mpMRI, 7 were false positives. The PPV for MRI and targeted biopsy was 83/128 (64.8%) for bpMRI and 84/136 (61.8%) for mpMRI, RR = 1.05, 95% CI: 1.01–1.10. Conclusions: In a PSA-screened population, bpMRI was non-inferior to mpMRI for cancer detection and resulted in fewer false positives. Key Points: • In screening for prostate cancer with PSA followed by MRI, biparametric MRI allows radiologists to detect an almost similar number of prostate cancers and score fewer false positive lesions compared to multiparametric MRI. • In a screening program, high sensitivity should be weighed against cost and risks for healthy men; a large number of men can be saved the exposure of gadolinium contrast medium by adopting biparametric MRI and at the same time allowing for a higher turnover in the MRI room. [ABSTRACT FROM AUTHOR]

To describe the study design of the GÖTEBORG prostate cancer screening (PC) 2 (Göteborg-2), a prospective, randomised, population-based trial of PC screening. This trial evaluates whether prostate-specific antigen (PSA) testing followed by 3 Tesla prostate magnetic resonance imaging (MRI) and targeted biopsy can reduce overdiagnosis, while maintaining the detection of clinically significant cancer, compared to PSA-screening and systematic biopsy. A random sample of men 50–60 years in the Göteborg area, Sweden, identified from the Total Population Register, were randomised to either a screening or control group (CG). Participants in the screening group (SG) were further randomised into one of three arms: (1) PSA-test; if PSA ≥ 3 ng/mL, then MRI and systematic biopsy, plus targeted biopsy to suspicious lesions as per Prostate Imaging – Reporting and Data System, version 2 (PI-RADSv2) 3–5; (2) PSA-test; if PSA ≥ 3 ng/mL, then MRI, and targeted biopsy only if PI-RADSv2 3–5; (3) identical to Arm 2, except lower PSA-cut-off ≥1.8 ng/mL. The primary outcome is the detection rate of clinically insignificant PC (defined as Gleason Score 3 + 3 [Grade Group 1]) comparing all men with PSA ≥ 3 ng/mL in Arm 1 vs. Arm 2 + 3. Randomisation and enrolment started in September 2015. Accrual has hitherto resulted in 38,770 men randomised to the SG. The participation rate is 50%. Invitation to the first screening round was completed in June 2020. The Göteborg-2 trial will provide new knowledge about the performance of prostate MRI in a screening setting. [ABSTRACT FROM AUTHOR]

Background The incidence of prostate cancer has increased substantially since it became common practice to screen asymptomatic men for the disease. The European Randomized Study of Screening for Prostate Cancer (ERSPC) was initiated in 1993 to determine how prostate-specific antigen (PSA) screening affects prostate cancer mortality. Variations in the screening algorithm, such as the interval between screening rounds, likely influence the morbidity, mortality, and quality of life of the screened population. Methods We compared the number and characteristics of interval cancers, defined as those diagnosed during the screening interval but not detected by screening, in men in the screening arm of the ERSPC who were aged 55-65 years at the time of the first screening and were participating through two centers of the ERSPC: Gothenburg (2-year screening interval, n = 4202) and Rotterdam (4-year screening interval, n = 13301). All participants who were diagnosed with prostate cancer through December 31, 2005, but at most 10 years after the initial screening were ascertained by linkage with the national cancer registries. A potentially life-threatening (aggressive) interval cancer was defined as one with at least one of the following characteristics at diagnosis: stage M1 or N1, plasma PSA concentration greater than 20.0 ng/mL, or Gleason score greater than 7. We used Mantel Cox regression to assess differences between rates of interval cancers and aggressive interval cancers at the two centers. All statistical tests were two-sided. Results The 10-year cumulative incidence of all prostate cancers in Rotterdam versus Gothenburg was 1118 (8.41%) versus 552 (13.14%) (P<.001), the cumulative incidence of interval cancer was 57 (0.43%) versus 31 (0.74%) (P = .51), and the cumulative incidence of aggressive interval cancer was 15 (0.11%) versus 5 (0.12%) (P= .72). Conclusion The rate of interval cancer, especially aggressive interval cancer, was low in this study. The 2-year screening interval had higher detection rates than the 4-year interval but did not lead to lower rates of interval and aggressive interval prostate cancers. [ABSTRACT FROM AUTHOR]

Higher age increased the risk of prostate cancer and the risk of higher Gleason score. These findings should be considered when counseling men for early diagnosis and treatment for prostate cancer. Studies have suggested associations between greater age, increased risk of prostate cancer (PC), and higher Gleason score. The present study aimed at investigating these associations within the Göteborg-1 randomized, population-based PC screening trial. The screening arm of the Göteborg-1 screening trial comprises 10 000 randomly selected men (aged 50–64 yr at randomization) from the Göteborg region of Sweden. Between 1995 and 2014, they were biennially invited to prostate-specific antigen (PSA) testing to an upper age limit of 70 yr (range 67–71 yr). PSA ≥3 ng/ml triggered a prostate biopsy (sextant biopsy 1995–2009, thereafter a ten-core biopsy). The impact of age on Gleason score, given a screen-detected PC, was investigated with multinomial logistic regression analyses adjusted for year of testing and screening round. Overall, 7625 men had at least one PSA test and 1022 men were diagnosed with PC. For men with screen-detected PC, age was associated with the risk of clinically significant PC above and beyond screening round and year of testing (p < 0.001). For each 1-yr increase in age, the risk of being diagnosed with a Gleason score ≥3 + 4 cancer (vs <7) increased by 11% (95% confidence interval [CI] 4.7–17), whereas the risk of being diagnosed with a Gleason score ≥4 + 3 cancer (vs <7) increased by 8.5% (95% CI –1.6 to 20). The increased risk of a higher Gleason score in older men should be considered when counseling men regarding early diagnosis and treatment for PC. We found that older age increased both the risk of prostate cancer and the risk of more aggressive prostate cancer. [ABSTRACT FROM AUTHOR]