The finding, published in the journal Nature, is based on the complete DNA analysis of 959 tumors from men in seven countries, representing the largest set of prostate cancer genomes studied with this depth to date.
Researchers discovered that most tumors exhibit a combination of these eight processes, and it is the balance between them that determines the likelihood of cancer spreading. These defective cellular processes are related to hormonal signaling, failures in cell replication and repair systems, and aging.
Prostate cancer is the second most common tumor in men worldwide and the fifth leading cause of cancer death in this demographic. Current difficulty lies in distinguishing between patients who will live with the disease for decades and those for whom it will be fatal, a distinction these results may help improve in the future.
Unlike other tumors, such as lung or skin cancer, prostate cancer's 'mutational signatures' show hardly any traces of environmental toxins like tobacco or sunlight. "What surprised us most was the magnitude of damage originating from inside the cell," states Barbara Hernando, a researcher at the CNIO and lead co-author of the study.
While these findings open the door to future biomarkers for patient stratification and personalized treatments, experts caution that clinical implications are still distant. "Before this reaches a hospital, these findings must be confirmed in other patient groups," notes Geoff Macintyre, head of the Computational Oncology group at the CNIO and study co-leader.
The study was conducted within the framework of the Pan Prostate Cancer Group, an international consortium that has gathered the world's largest collection of prostate cancer genomes. The research analyzed 959 tumors from 1,001 men across seven countries, with clinical follow-up for up to seven years.
