title: CDK2 and cyclin E knockout mice: lessons from breast cancer.
abstract: 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.
authors.affiliation: Department of Pharmacological and Physiological Science, Saint Louis University School of Medicine, Saint Louis, MO 63104, USA. lentsnh@slu.edu
authors.forename: Nathan H
authors.initials: NH
authors.lastname: Lents
authors.forename: Joseph J
authors.initials: JJ
authors.lastname: Baldassare
mesh_terms: D000818:Animals; D001943:Breast Neoplasms / Q000378:metabolism*; D042846:CDC2-CDC28 Kinases / Q000235:genetics / Q000378:metabolism*; D018797:Cell Cycle Proteins; D019927:Cyclin E / Q000235:genetics / Q000378:metabolism*; D051357:Cyclin-Dependent Kinase 2; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D051379:Mice; D018345:Mice, Knockout
chemical_list: D018797:Cell Cycle Proteins; D019927:Cyclin E; D042846:CDC2-CDC28 Kinases; C495893:Cdk2 protein, mouse; D051357:Cyclin-Dependent Kinase 2