(February 7, 2017) An OCRFA funded study, published on January 13, 2017 in Oncotarget, sheds light on EMSY, a gene that researchers at New York University Langone Medical Center now understand to have a role similar to those of BRCA1 and BRCA2. BRCA1 and BRCA2 are well known genes that, when working, help with DNA damage repair, which protects the body against cancers. When they are defective, or mutated, that repair process fails and allows cancers to grow. Overly active EMSY, like mutated BRCA1 or BRCA2, blocks the DNA damage repair process. This may explain why why some women with healthy, functional BRCA1 and BRCA2 genes are still developing cancer. One of the ways EMSY is different than the BRCA genes is that it can be affected by protein kinase A, an enzyme. When EMSY is over-active, protein kinase A reacts with EMSY to suppress DNA pair even more.
“Now that we know exactly how changes in EMSY spur cancer cell growth, we can start to design therapies to specifically target that activity and hopefully stop it,” says senior author and OCRFA Scientific Advisory Committee member Douglas Levine, MD.
“This work also suggests that treatments that work for patients with BRCA 1 or BRCA2 mutations might also be effective against EMSY-driven cancers because the disease mechanism is similar,” states first author and OCRFA grantee Petar Jelinic, PhD.
