Researchers identify genetic clues that could reveal aggressive prostate cancer
Peer-Reviewed Publication
Updates every hour. Last Updated: 25-Oct-2026 05:16 ET (25-Oct-2026 09:16 GMT/UTC)
An international team of researchers led by scientists from the University of Copenhagen and Rigshospitalet has mapped eight genetic ‘fingerprints’ that may explain why some men develop aggressive prostate cancer while others do not. The findings could eventually lead to more personalised treatment.
The work is based on reading the complete DNA of 959 tumours from men in seven countries — the largest set of prostate cancer genomes examined in this way. Eight faulty cellular processes together account for the DNA damage in 85% of prostate cancers. Most tumours are driven by several of the eight at once, and what differs between patients is which ones and in what balance. “The balance of these faulty processes is what determines how likely the cancer is to spread,” says Geoff Macintyre, head of the Computational Oncology Group at the CNIO, who co-led the study. The processes are almost all internal to the cell: hormone signalling, failures in DNA copying and repair, and ageing. The marks that tobacco and sunlight leave on other cancers are practically absent.These results offer clues that could help stratify patients and personalise treatment — but not yet.
Mutations are changes in the molecular “letters” that make up DNA, the genetic blueprint for cells. Mutations build up with age in every cell when DNA is damaged or when cells make mistakes in fixing or copying it. Most mutations are harmless, but when they disrupt genes, they can cause cancer and other diseases.
The Joint Research Unit in Advanced Therapies in Oncology, established by Universitat Jaume I in Castelló, the Príncipe Felipe Research Centre (CIPF) in Valencia and the General University Hospital of Castelló, will collaborate on the MORPHEUS project, funded through a 2025 European Research Council (ERC) Advanced Grant awarded to researcher María Jesús Vicent, Head of the Therapeutic Polymers Laboratory at CIPF and Distinguished Researcher at Universitat Jaume I (UJI). The unit will also participate in the MITONano project, funded by the Spanish Association Against Cancer (AECC). The European MORPHEUS project (Mechano-metabOlic Responsive nanoPlatform for HeterogEnous tumor Suppression) aims to develop a new generation of intelligent nanomedicines capable of "reading" the physical and metabolic characteristics of individual tumours and delivering treatment in a precise, sequential manner. The project focuses on solid tumours that are resistant to current therapies, beginning with cholangiocarcinoma, an aggressive and difficult-to-treat bile duct cancer. Its long-term goal is to establish a therapeutic strategy that can be applied to other cancers characterised by dense, rigid tumour environments, such as pancreatic cancer. MITONano proposes an innovative nanomedicine-based approach that specifically targets mitochondria, the energy-producing structures within tumour cells. By disrupting this energy supply, the treatment aims to inhibit tumour growth and survival while sparing healthy cells. These nanomedicines incorporate active compounds that act directly on mitochondria, making it possible to treat even the most chemotherapy-resistant forms of ovarian cancer. The project will also evaluate tools to identify which patients are most likely to benefit from this personalised therapy.
Researchers from the Heidelberg Faculty of Medicine at Heidelberg University and the Berlin Institute of Health at Charité have identified a subgroup of CAR T cells that may serve as a biomarker to gauge the success of low-dose therapies. The findings are published in “Nature Communications.”