The genetic mutation WNT9B, which plays a normal role in the development of the prostate during embryonic stages, has been linked to a heightened risk of prostate cancer in adults, as revealed by recent research.
Recent research among men with a family history of prostate cancer has identified a genetic form of the disease.
A study conducted by Vanderbilt University Medical Center and published in JCO Precision Oncology found that the inherited mutated gene WNT9B increases the likelihood of developing adult prostate cancer.
This finding was confirmed across five different study groups, totaling around half a million patients from both the U.S. and Europe, with estimates indicating that the risk of prostate cancer could increase by two to twelve times, according to the lead researcher, Dr. Jeffrey Smith, an associate professor of Medicine in the Division of Genetic Medicine.
“In contrast to breast cancer, only a handful of significant prostate cancer genes have been identified so far,” noted Smith.
“The inherited risk for prostate cancer is about double that of breast cancer; however, its genetic makeup is much more complex, presenting significant challenges for global research efforts,” he explained.
A pathogenic gene mutation refers to a change in the DNA sequence that may lead to a person developing or being at risk for specific genetic disorders or diseases, including various forms of cancer. These harmful variants can either be inherited or arise during an individual’s lifetime.
Some well-known high-risk genes associated with prostate cancer are WNT9B, HOXB13 (which also plays a role in embryonic prostate development), the 8q24 locus, and BRCA2.
“The risk of prostate cancer from a pathogenic WNT9B mutation is comparable to the risk of breast cancer linked to mutations that are frequently tested for in breast cancer management,” stated Smith. “Understanding these inherited mutations can help in selecting effective treatments and can also have broader implications for family members.”
Smith mentioned that future studies will explore whether either inherited or acquired mutations can affect clinical outcomes, paving the way for personalized precision care.
Other contributors from Vanderbilt include William Dupont, PhD, and Angela Jones, MS.
This research was supported by grants from the Veterans Health Administration, the V Foundation for Cancer Research, and a National Institutes of Health grant (P30CA068485). The study utilized data from the Million Veteran Program, Office of Research and Development, Veterans Health Administration, which was backed by MVP000 and MVP046.
