Understanding why multiple prostate cancers appear together

Grant information

Institution – University of East Anglia
Supervisors – Professor Daniel Brewer and Professor Colin Cooper
PhD student - Claudia Buhigas
Grant award - £83,979
Duration of funding – 2016-2019
Status - Complete
Reference – TLD-S15-003

The project in a nutshell

• This project aims to understand why men often develop multiple different prostate cancers in their prostate at once.
• They will do this by studying the genetic code of both healthy and cancerous prostate tissue and explore any differences or changes they see.
• The project funds a PhD student to use their expertise in data analysis to explore this phenomenon.

Why did we fund this project?

• Over 80 per cent of men diagnosed with prostate cancer have more than one cancerous area in their prostate and understanding why this happens might provide important information to help prevent the disease.
• It may also help to establish if a man is suitable for treatments that target individual spots of cancer in the prostate, known as focal therapies.

What did the team do?

• The team noticed that apparently healthy prostate cells in men with prostate cancer contain mutations (changes in the DNA that drive cancer).
• Using different types of prostate tissue (including prostate cancer tissue, healthy prostate tissue from men with prostate cancer, and healthy prostate tissue from men who didn’t have prostate cancer) the team were able to compare the mutations present in the different tissue types.

What did the team achieve?

• The team have confirmed that in almost all men with prostate cancer there are many changes in the genetic code of normal prostate tissue. 
• The team showed that ‘normal’ prostate cells in men who had prostate cancer had more mutations than ‘normal’ prostate cells from men without prostate cancer.
• Based on the genetics of the samples analysed, the team can create maps to understand where the different mutations occurred. The team showed that in most men the mutations in normal cells are different to mutations in cancer cells.
• We now know that large regions of the prostate in men with prostate cancer harbour a number of mutations, making it an ideal place for new cancers to grow. The whole prostate is primed and ready to develop prostate cancer driven by an, as yet unknown, biological process.

How will this benefit men?

• This work has improved our knowledge of how prostate cancer first starts to develop and has transformed scientific understanding of how apparently healthy prostate cells become prostate cancer cells.
• This potentially has implications for treatments like surgery and focal therapy.
• This research might one day give us clues as to how to prevent prostate cancer and could contribute to better tests and treatments for men.