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% of breast cancer cases arise from these genetic miscues, about half of which are linked to the abnormal functioning of BRCA1.
But now scientists Georgetown University Medical Center 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.