Researchers from The University of East Anglia (UEA) have contributed to the world’s largest study into genes that drive prostate cancer.

They have identified 80 molecular weaknesses that could be targeted by drugs to treat the disease. Approximately 25 percent of the gene mutations identified involve the targets of existing drugs that are either licensed or in clinical trials.

This critical research opened up 60 new potential lines of attack against prostate cancer for further investigation, as well as identifying new genes associated with the disease’s development.

Genetic information was obtained from the tumours of 112 men with prostate cancer, pooled with data from other studies, together analysing samples from 930 cancer patients.

Professor Paul Workman, Chief Executive of The Institute of Cancer Research, London, said: “This study has uncovered a remarkably large number of new genes that drive the development of prostate cancer, and given us vital information about how to exploit the biology of the disease to find potential new treatments.”

Using canSAR, a comprehensive database for cancer drug discovery, researchers discovered that 80 of the proteins in the network were possible drug targets.

Just 11 of these were targeted by existing licensed drugs and 7 by drugs in clinical trials, while 62 were identified as potential targets to explore.

During the investigation, the team established a timeline of genetic changes in prostate cancer.

This allowed a way to be paved to improve spotting the disease as current methods of diagnosis, such as PSA testing, have been found to be unreliable.

The timeline could also help predict how the disease evolves in individual patients, allowing treatment to be adapted to combat drug resistance.

Professor Collin Cooper, Chair of Genetics at Norwich Medical School said: “The study provides an important step towards personalising treatment for men with prostate cancer. We have identified many pathways by which this cancer develops, for which new drugs can be used to disrupt those pathways and potentially improve treatment.”