Prostate cancer mutation found to triple risk of death

by | 7th May 2019 | News

The research also identified clues for how some patients with prostate cancer could be treated more effectively using immunotherapy and a breast cancer treatment.

The largest ever study of advanced prostate cancer genomics has revealed that men with mutations in the retinoblastoma gene in their tumours were more than three times as likely to die and nearly seven times as likely to relapse on standard treatments as those without the gene.

Scientists identified the gene mutation in the tumours of men, which could help to pick out patients for more intensive treatment in the future.

The gene in question – the retinoblastoma gene – is known as RB1 because mutations in it cause a rare children’s eye cancer of the same name and is known to play a central role in stopping healthy cells from dividing uncontrollably.

Professor Johann de Bono, Regius Professor of cancer research at The Institute of Cancer Research, London, and consultant medical oncologist at The Royal Marsden NHS Foundation trust, said that the study “really got under the bonnet of prostate cancer to understand the ‘engine’ driving tumour growth and explore how a wide range of genes affect the disease and its response to treatment.

“We identified one particular genetic mutation that seems to indicate that tumours are going to be very aggressive, and that the affected men need the most intensive treatment we have available.

“Our research could also open up various new approaches to prostate cancer treatment, and offers the intriguing suggestion that some patients could benefit from immunotherapy alongside an existing breast cancer drug. That’s a great example of how genetic research can find the common links between cancers, and ensure research into one cancer type can also benefit patients with other tumours.”

The research also identified clues for how some patients with prostate cancer could be treated more effectively using immunotherapy and a breast cancer treatment.

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