Briefing
An international research consortium involving the Centro Nacional de Investigaciones Oncológicas (CNIO) in Madrid presented on 9 September 2026 in Nature the complete genomic analysis of 959 prostate tumours . The authors describe eight recurring, sometimes combined cellular processes that together explain around 85 per cent of the observed damage to deoxyribonucleic acid (deoxyribonucleic acid, abbreviated as deoxyribonucleic acid). The study is based on whole-genome sequences from several countries and uses mutational signatures, characteristic patterns of genetic changes, to infer underlying mechanisms.
The key finding is that many tumours are not driven by a single mechanism, but by combinations of different processes whose relative contributions vary from case to case. This may explain why diseases that appear clinically similar can take very different courses: some patterns correlate with more aggressive behaviour and a higher risk of metastasis, while others are associated with more indolent disease.
The main clinical relevance is improved classification of the large group of patients at intermediate risk, for whom existing tests have limited ability to distinguish between observed outcomes. The identified mutational signatures could provide a basis for biomarkers that enable more precise risk stratification and help guide treatment decisions — for example, when weighing active surveillance against early systemic treatment. The researchers stress, however, that prospective, standardised validation studies are needed before such markers can be included in guidelines or routine tests.
The CNIO’s contribution is significant for Spain because it lays the groundwork for promptly launching national validation programmes. Prostate cancer is one of the most common tumours in men in Spain; around 35,000 new cases and approximately 6,000 deaths are reported for 2025. The authors consider their dataset a robust basis for future clinical trials and for developing personalised treatment strategies.
Editor: Andreas M. Brucker (Article created with AI assistance).