"Since BRCC36 directly affects BRCA1 and BRCA1 is activated after exposure to radiation, we wanted to see if BRCC36 might be important in this response," said Xiaowei Chen, Ph.D., a Fox Chase postdoctoral researcher in the laboratory of geneticist Andrew K. Godwin, Ph.D., and the study's lead author.
Working with breast-cancer cell line MCF-7, the Fox Chase scientists reduced BRCC36 expression by 80 percent. They then exposed the cells to radiation, similar to that used in breast cancer treatment. They found that the number of breast cancer cells killed by the radiation increased by about 10 percent compared to cells that did not have their BRCC36 levels reduced.
"These findings hold promise for future breast cancer treatments," Chen said. "BRCC36 may be a target to manage radiation-resistant breast cancer cells. Our next step is to find out why the cells with reduced BRCC36 are more sensitive to radiation."
Along with Chen, study authors are Godwin and surgical fellow Cletus Arciero, M.D. The research is supported in part by the AACR Anna D. Barker Fellowship, the Eileen Stein-Jacoby Fund and a grant from the Department of Defense.
Fox Chase Cancer Center was founded in 1904 in Philadelphia as the nation's first cancer hospital. In 1974, Fox Chase became one of the first institutions designated as a National Cancer Institute Comprehensive Cancer Center. Fox Chase conducts basic, clinical, population and translational research; programs of prevention, detection and treatment of cancer; and community outreach. For more information about Fox Chase activities, visit the Center's web site at www.fccc.edu or call 1-888-FOX CHASE.