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.

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.

Triple-negative breast cancer (TNBC) is an aggressive breast cancer subtype characterized by limited targeted treatment options, a high propensity for distant metastasis and variable responses to immune checkpoint blockade. Increasing evidence indicates that the tumor microbiome can influence cancer progression and therapeutic responses, yet the mechanisms through which intratumoral bacteria reshape the TNBC microenvironment remain poorly understood. Fusobacterium nucleatum, a Gram-negative anaerobic bacterium associated with several cancers, has been detected in breast tumors and linked to metastatic progression, but its contribution to metabolic and immune regulation in TNBC has remained unclear.