A new study has found that aggressive prostate cancer is linked to a genetic mutation in untreated patients.

The research, carried out by scientists at the University of East Anglia (UEA) and the Institute of Cancer Research, London, explores why relapses could occur in some men following hormone therapy for prostate cancer.

The research could also help early identification of patients that will develop fatal prostate cancer, in order for them to receive life-extending therapy.

Patients diagnosed with early-stage prostate cancer are currently receiving treatments ranging from “watchful waiting” and hormone-withdrawal therapy to radiotherapy and surgery. Categorizing patients by carrying out additional tests can distinguish high-risk patients who need aggressive first line therapy from patients with a low risk of the disease spreading, to avoid unnecessary treatment.

Hormone-withdrawal therapy can cause a dramatic remission period, although the disease often relapses with a resistant form of cancer staying in the body. A third of these relapses are a result of the androgen receptor gene, an X-chromosome in men that prostate cancer thrives on and replicates.

Jeremy Clark, PhD, co-lead researcher at the University of East Anglia, said: “By the age of 60 [years], the majority of men will have signs of prostate cancer. However, only a small proportion of men will die of the disease. The question is — which of these cancers are dangerous and which are not? Deciding which cancers are going to progress and kill the patient is key to effective patient treatment.”

Clark explained that a third of prostate cancers boost androgen receptor genes even when not treated with hormone reduction therapy, and these cancers are likely to grow, ultimately killing the patient.

Clark added: “This discovery can be used to identify these killer cancers in patients much earlier than is currently possible. Patients could then be selected for more aggressive therapy before the cancer has developed full immunity.”

The study was published in the British Journal of Cancer.