For about a decade, scientists have recognized that many cases of hereditary breast cancer result from a mutation of a specific gene called BRCA1, which, in its normal state, helps keep tumor formation in check. About five to 10 percent of breast cancer cases arise from these genetic miscues, about half of which are linked to the abnormal functioning of BRCA1. But now scientists have discovered that a protein called cyclin D1, grossly overproduced in about half of all cases of breast cancer, can also disrupt BRCA1’s normal role as a cancer inhibitor. They found that because cyclin D1 binds to the same estrogen receptor as does BRCA1, when the cell is flooded with cyclin D1, BRCA1 is unable to activate a pathway that stops cancer development. The results reaffirm cyclin D1 as a candidate target for molecular therapeutic control of breast tumor development. “We’ve previously shown that if you have a gene therapy vector that blocks cyclin D1 in breast tumors, you can block the growth of those tumors,” said Richard Pestell, M.D., Ph.D., director of the Lombardi Comprehensive Cancer Center at Georgetown University Medical Center and senior author of the paper published in the August 1 issue of Cancer Research. Also part of the Georgetown University research team were Chenguang Wang, Ph.D., assistant professor at the Lombardi Comprehensive Cancer Center and the lead author of the article, and Georgetown Professor of Oncology Eliot M. Rosen, a co-investigator on the study, which was funded in part by a grant from the Department of Defense. Participating in the research from the Georgetown oncology department were Saijun Fan, Zhiping Li, Maofu Fu, Mahadev Rao, Yongxian Ma, and Chris Albanese.
