Prostate cancer is the second most common cancer and second leading cause of cancer death in men.
The research, published in Nature, is part of the International Cancer Genome Consortium - a global project committed to revealing genetic changes driving prostate cancer, using the most up-to-date gene-sequencing technology available.
The researchers also learned more about how the disease spreads through the body and forms new tumors. They discovered that the first group of cells that spread from the prostate continues to travel throughout the body, developing new tumors as it goes.
"We gained a much broader view of prostate cancer by studying both the original cancer and the cells that had spread to other parts of the body in these men," says study author Prof. Ros Eeles from the Institute of Cancer Reseach in London, UK. "And we found that all of the cells that had broken free shared a common ancestor cell in the prostate."
Prostate cancer is the second most common cancer in American men behind skin cancer and the second most common cause of cancer death behind lung cancer. Around 1 in 7 men will be diagnosed with prostate cancer during their lifetime.
According to American Cancer Society (ACS) estimates, in 2015, around 220,800 new cases of prostate cancer will be diagnosed, and 27,540 deaths will occur attributable to the disease.
The researchers have already discovered that cancer cells taken from different sites within a man's prostate can be very diverse genetically. Despite this, the new study found that cancer cells moving away from the prostate share genetic faults that are unique to the man whose cancer it is.
"The common faults we found in each man could potentially offer new targets for treatment," states Prof. Eeles. "But we found that, once cancer cells have spread, they continue to evolve genetically, so choosing the most effective treatments will remain a key challenge."
Shared mutations represent 'a potential Achilles heel' for prostate cancer
Prof. Steven Bova from the University of Tampere in Finland believes that in order to find these shared genetic faults, multiple biopsies may be needed. "We must also study more patients to learn how to apply these findings to develop more personalized treatments for people with the disease," he adds.
Learning how cancer cells change and evolve as they metastasize (spread to other parts of the body) and thus become resistant to certain forms of treatment is crucial to developing future treatments for all forms of cancer.
Senior author Dr. Ultan McDermott says that while the shared tumor-causing genetic faults mapped by their "family tree" represent a potential Achilles heel for prostate cancer, "many of these shared mutations are in tumor suppressor genes and our approach to therapeutically targeting these needs to be prioritized."
"We have to zoom in on this crucial junction and gather more data on the impact different therapies have on prostate cancer's evolution and spread," he adds.
The study authors conclude that these findings "elucidate in detail the complex patterns of metastatic spread and further our understanding of the development of resistance to androgen-deprivation therapy in prostate cancer."
Recently, Medical News Today reported on new research suggesting that taking vitamin D supplements could slow or reverse the progression of low-grade prostate tumors, reducing the need for surgery or radiation therapy.