CDK2 and cyclin E knockout mice: lessons from breast cancer

The recent discovery that murine embryos can develop normally in spite of ablation of either CDK2 or cyclin E challenges the previously held dogma that cyclin E-CDK2 activity is strictly required for the cell-division cycle. However, genetic, cellular, biochemical and clinical evidence correlate aberrant cyclin E expression with tumorigenesis and poor patient prognosis, particularly in breast cancer. Thus cyclin E is a crucial regulator of estrogen-mediated growth signaling in breast tissue and, in spite of the apparent dispensability of cyclin E-CDK2 in development, the relationship between cyclin E and the development of breast cancer is convincing.