Prostate cancer, the most common cancer in men, often occurs as many smaller tumours in the same prostate, all with different genetic fingerprints – something called ‘multi-focal’ disease.
Quite how often is still a matter of debate – some studies suggest six out of ten men with prostate cancer have multifocal disease. Others suggest it’s more like nine out of ten.
And just as the degree of this variation is still unknown, scientists are also trying to work out how it arises. Cracking this puzzle could open up new opportunities to work out how much of a man’s prostate is affected by the disease, giving doctors a better idea of how to treat it.
The leading theory is that the entire prostate is affected by a process, or processes, that cause it to slowly develop more and more cancer-like characteristics, and that different areas eventually tip over the edge into cancer.
And new research published in the journal Nature Genetics goes a long way to confirm this idea.
The collaborative research team included scientists from The Institute of Cancer Research (ICR) in London, the Wellcome Trust Sanger Institute, and the University of Cambridge, who were working as part of a global project called the International Cancer Genome Consortium. This project is tasked with mapping the vast number of genetic changes found in lots of different types of cancer, and Cancer Research UK is supporting two teams – one looking at oesophageal cancer, another looking at prostate cancer.
And the prostate cancer team have found that what appears to be ‘normal’ prostate tissue might not be that normal after all.
Read full original article: Hide and seek: tracing prostate cancer’s origins