ArticleEuropean radiology2026
Variation in prostate cancer growth rates in an MRI-based active surveillance cohort.
Article in European radiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
- Commented on by
- Commented on by
Authors and funding
8 authors.
Funding
Abstract
backgroundUnderstanding tumour growth rates helps optimise screening and active surveillance (AS) schedules. We estimated prostate cancer growth rate accounting for individual variation in a longitudinal AS cohort. MATERIALS AND
methodsWe modelled tumour growth in 145 biopsy-confirmed prostate cancer patients undergoing MRI-based AS. Primary lesion volumes were measured longitudinally using planimetry. We compared three mixed-effects models (exponential, Gompertz, and logistic) and investigated relationships between growth rate and clinical characteristics. We estimated the natural trajectory of prostate cancer lesions starting at a single cell to clinical detectability (diameter ≈ 1 cm), with diameters estimated based on spherical volume.
resultsAll three models fit observed data well; however, only the Gompertz model provided reasonable estimates from a single cell to an MRI-detectable size (diameter ≈ 3 mm). The Gompertz growth parameter (mean = 0.07, range = 0.02-0.15), describing exponential growth deceleration, was positively correlated with: patient age; lesion volume at AS onset; prostate-specific antigen (PSA) level; and PSA density. Lesions with Gleason 3 + 4 had faster volume doubling times than Gleason 3 + 3 lesions (mean = 3.5 and 5.2 years, respectively). On average, it would take 17 years (95% CI [15, 19]) for a lesion to grow from a single cell to an MRI-detectable size and an additional 12 years to reach a clinically detectable size (95% CI [10, 13]). At age 50, 75% of lesions would remain undetectable by MRI.
conclusionsProstate cancer shows slow growth with large variation between patients, posing a challenge for early detection. KEY POINTS: Question What is the population distribution of growth rates and the natural history of prostate cancer? Findings Prostate cancer typically grows slowly, with considerable variation between individuals. On average, lesions take 17 years to grow from initiation to an MRI-detectable size. Clinical relevance Small lesions undetectable on MRI may take many years to reach a clinically significant size, posing a challenge for early detection, as it increases the risk of detecting indolent lesions that may never cause harm.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.