Researchers from the Broad Institute of Harvard of MIT and Harvard and the Dana-Farber Cancer Institute in Boston sequenced the genomes of prostate tumour tissue along with unaffected tissue taken from seven men to see how DNA had been damaged or mutated in the cancer tissue.
They found that large segments of DNA had been cut out and re-inserted into new locations. This genome shuffling, not described before in prostate cancer, could shed light on how genes mutate and cause cancer development.
'Whole genome sequencing gives us fascinating new insights into a category of alterations that may be especially important in prostate cancer', said study author Dr Levi Garraway of The Broad Institute.
Because all of the tumours sequenced so far have been from patients with high risk tumours, the team is not yet able to differentiate between aggressive and benign tumours. But by sequencing more cancer patients over the next several years, the researchers hope to be able to better classify prostate cancer cases by looking at specific gene changes, allowing for earlier identification of aggressive tumours and individually tailored treatment.
The study also found a large number of novel single gene mutations in the cancer tissue, some of which could be responsible for cancer development. The researchers also hope to now isolate the numbers of potentially cancer-related genetic changes enabling them to select a few target genes and cell processes to investigate as avenues for treatment.
Prostate cancer is second only to lung cancer in terms of loss of life. It is the most prevalent cancer among British men, affecting a third of men over the age of 50 and accounting for about 10,000 deaths every year in England and Wales.
The findings were published in the journal Nature.