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Department of Molecular Pharmacology and Biological Chemistry, and Robert H. Lurie Comprehensive Cancer Center, Northwestern University, Chicago, Illinois
Requests for reprints: Hiroaki Kiyokawa, Department of Molecular Pharmacology and Biological Chemistry, Northwestern University, 303 E. Superior Street, Lurie 3-113, Chicago, IL 60611. Phone: 312-503-0699; Fax: 312-503-0700; E-mail: kiyokawa{at}northwestern.edu.
Key Words: breast cancer cell cycle checkpoint knockout mice CHK1 RAS HER2/neu
CDC25A is a critical regulator of cell cycle progression and checkpoint response. Overexpression of this cyclin-dependent kinase phosphatase occurs often in human cancers. Our recent genetic studies in the mouse indicate that restricting CDC25A can limit tumorigenesis induced by the HER2/neu-RAS oncogenic pathway without compromising normal cell division or viability. These findings offer a sound foundation to justify development of CDC25A inhibitors for antitumor therapy. [Cancer Res 2008;68(5):1251–3]
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