by Elayna Shanker
Approximately 1 in 40 individuals of Ashkenazi Jewish decent are carriers of the BRCA mutation—a mutation in a tumor suppressor gene that puts individuals at a much higher risk of developing both breast and ovarian cancer. For too long, individuals who carry a faulty BRCA gene have had limited options: either they manage the risk of developing a fatal condition, or they undergo life-changing surgeries where breast tissue and/or ovaries are surgically removed. There are no known preventative methods that reduce the risk of cancer for patients with mutated copies of this gene.
Fortunately, researchers at the Walter and Eliza Hall Institute have identified a drug that may inhibit the development of breast cancer caused specifically by mutations in BRCA1. This drug, denosumab, has historically been used to treat patients with osteoporosis and forms of bone cancer as it is known to inhibit the cellular signaling pathway important for osteoclast (bone cell) differentiation1. This same pathway, however, was recognized in cancer precursor cells taken from BRCA1 mutant breast tissue2. In a laboratory trial, inhibition of the pathway via denosumab resulted in decreased cell growth and proliferation—making it a realistic treatment for cancer delay or prevention2. Clinical trials are already underway to test the effectiveness of denosumab outside of the lab.
These findings are monumental for both cancer research and genetic screening. At the Center, we are hopeful that denosumab will, one day, be an effective and noninvasive option for carriers of the BRCA mutation!
Read the full article here: https://www.sciencedaily.com/releases/2016/06/160620120247.htm
(1) Bruhn, C. "[Denosumab. The first inhibitor of RANK-ligand for treatment of osteoporosis]." Medizinische Monatsschrift fur Pharmazeuten 33, no. 10 (2010): 370-375.
(2) Walter and Eliza Hall Institute. "'Holy grail' of breast cancer prevention in high-risk women may be in sight: Existing medicine may prevent cancer in women with breast cancer risk gene." ScienceDaily. www.sciencedaily.com/releases/2016/06/160620120247.htm (accessed June 24, 2016).