Researchers from the University of East Anglia have made an important discovery about how prostate cancer can start to grow.

A new study published today reveals that the prostate as a whole, including cells that look normal, looks different in men with prostate cancer.

This suggests that tissue cells throughout the prostate are primed and ready to develop prostate cancer.

This means that it may be better to treat the whole prostate rather than just the areas of the prostate that have cancer.

The team hopes their work can help scientists better understand the causes of prostate cancer, and even prevent it altogether.

Prostate cancer is the most common cancer in men and kills a man every 45 minutes in the UK.

Often when men are diagnosed with prostate cancer, clusters of cancerous cells can be found in several places in the prostate.

We wanted to know if this was due to changes in “normal” prostate cells throughout the prostate. »

Prof Daniel Brewer, Principal Investigator, UEA Norwich Medical School

Cancer is caused by changes in DNA, the genetic code for life, that appear in every cell. The team studied the DNA code in 121 tissue samples from 37 men with and without prostate cancer.

Professor Brewer said: “The samples we studied included tissue from the cancer and tissue from elsewhere in the prostate, which appear normal under the microscope.

“This produces a massive amount of data and by applying a large amount of computing power we can determine the differences that have occurred in the DNA, giving us insight into how cancer develops.

“We found that ‘normal’ prostate cells from men with prostate cancer had more mutations (changes in DNA) than ‘normal’ prostate cells from men without prostate cancer.

“Based on the genetics of the analyzed samples, we created maps to understand where the different mutations occurred. And we showed that in most men, mutations in normal cells are different from mutations in normal cells. cancerous.

“‘Normal’ prostate cells in men with prostate cancer appear to provide a beneficial environment for the development and growth of prostate cancer cells.

“In other words, the entire prostate is primed and ready to develop prostate cancer caused by a yet unknown biological process.

“This work has improved our knowledge of how prostate cancer begins to develop and may one day give us clues on how to prevent or treat it.

“And this shows that it may be better to treat the whole prostate rather than just the areas of the prostate that have cancer,” he added. Dr Hayley Luxton, Senior Head of Research Impact at Prostate Cancer UK, said: “This new research shows for the first time how normal prostate cells can facilitate the growth and spread of prostate cancer. .

“Researchers found that normal prostate cells in men with prostate cancer had specific genetic changes that caused them to act like rich compost, providing the perfect environment for cancer cells to grow and develop. of the prostate. These findings give us important new insights into early development. prostate cancer, which could one day give us clues on how to prevent it. »

This research was conducted by UEA, in collaboration with University of Cambridge, Institute of Cancer Research, London, Wellcome Sanger Institute, Universities of Oxford, St Andrews, York, Manchester, Tampere (Finland) and University College London – as well as Cambridge University Hospitals NHS Foundation Trust, Royal Marsden NHS Foundation Trust, HCA Healthcare UK Laboratories and Earlham Institute.

It was funded by Cancer Research UK, the Dallaglio Foundation and a Prostate Cancer UK Movember Training, Leadership & Development Award.

The project has also received support from Prostate Cancer Research, Big C Cancer Charity, Bob Champion Cancer Trust, The Masonic Charitable Foundation successor to The Grand Charity, The Alan Boswell Group, The King Family and The Hargrave Foundation.

“The architecture of clonal expansions in morphologically normal tissues of cancerous and non-cancerous prostates” is published in the journal Molecular Oncology on September 22, 2022.