# Real-world monitoring strategies and predictors guiding the transition from active surveillance to treatment in ISUP 1 prostate cancer

**Authors:** Giulia Giannini, Amer Mousa, Eberhard Steiner, Nastasiia Artamonova, Mona Kafka, Isabel Heidegger

PMC · DOI: 10.1007/s00432-026-06441-9 · 2026-03-04

## TL;DR

The study evaluates a structured monitoring protocol for low-risk prostate cancer patients to determine when to transition from monitoring to treatment.

## Contribution

A structured active surveillance protocol using PSA and MRI is proposed and validated for ISUP 1 prostate cancer.

## Key findings

- 37.1% of patients transitioned to treatment due to PSA progression or MRI changes.
- No prostate cancer-specific deaths occurred during the follow-up period.
- Structured protocols enabled timely detection of progression without overtreatment.

## Abstract

Active surveillance (AS) is the standard approach for managing ISUP 1 prostate cancer (PCa), ensuring oncological safety while minimizing overtreatment. However, AS protocols vary significantly. This study assessed a structured AS protocol incorporating PSA kinetics, multiparametric MRI (mpMRI), and targeted biopsies to identify predictors of treatment transition.

We retrospectively reviewed 89 patients with ISUP 1 PCa managed with AS between 2010 and 2024. Inclusion criteria were PSA < 10 ng/mL and ≤ 2 positive biopsy cores with ≤ 50% tumor involvement per core. Patients underwent regular PSA testing, mpMRI, and risk-adapted biopsies. Outcomes included treatment conversion, progression predictors, and the role of mpMRI.

Median follow-up was 52.8 months. PSA was monitored at a median interval of 4.8 months, and mpMRI every 15.7 months (median). At diagnosis, 68.5% underwent mpMRI, with PIRADS 4 as the most frequent. During AS, 66.3% underwent at least one re-biopsy, most commonly triggered by PSA progression (73%). Treatment was initiated in 37.1% after a median of 37.9 months due to PSA progression (54.5%), mpMRI changes (21.2%), combined PSA/mpMRI findings (6.1%), histological upgrading (9.1%), or patient preference (3%). Treatments included radical prostatectomy, EBRT or LDR brachytherapy. Among these patients, no PSA persistence was observed; biochemical recurrence occurred in 6.1%, metastases in 4.0%, and overall mortality in 4.5%, with no PCa-specific deaths.

A structured, risk-adapted AS protocol using PSA kinetics and mpMRI enabled personalized management and timely detection of progression. These findings support the standardization of AS protocols, which should be validated in larger cohorts.

## Linked entities

- **Diseases:** prostate cancer (MONDO:0005159)

## Full-text entities

- **Genes:** BCR (BCR activator of RhoGEF and GTPase) [NCBI Gene 613] {aka ALL, BCR1, CML, D22S11, D22S662, PHL}, FOLH1 (folate hydrolase 1) [NCBI Gene 2346] {aka FGCP, FOLH, GCP2, GCPII, NAALAD1, PSM}, PCA3 (prostate cancer associated 3) [NCBI Gene 50652] {aka DD3, NCRNA00019, PCAT3, PRUNE2-AS1}, NPEPPS (aminopeptidase puromycin sensitive) [NCBI Gene 9520] {aka AAP-S, MP100, PSA}
- **Diseases:** obstructive (MESH:D000402), depression (MESH:D003866), Malignant Tumors (MESH:D009369), anxiety (MESH:D001007), AS (OMIM:612348), ISUP 1 prostate cancer (MESH:D011471), metastases (MESH:D009362), deaths (MESH:D003643)
- **Chemicals:** Prolaris (-)
- **Species:** Homo sapiens (human, species) [taxon 9606]

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Source: https://tomesphere.com/paper/PMC12961084