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Revving the Throttle on an Oncogene: CDK8 Takes the Driver Seat

¹ Department of Medical Oncology, Dana-Farber Cancer Institute; ² Departments of Pathology and ³ Medicine, Brigham and Women's Hospital, Boston, Massachusetts; and ⁴ Broad Institute of Harvard and MIT, Cambridge, Massachusetts

Requests for reprints: William C. Hahn, Dana-Farber Cancer Institute 44 Binney Street Dana 1538 Boston MA 02115. Phone: 617-632-2641; Fax: 617-632-4005; E-mail: william_hahn{at}dfci.harvard.edu.

The Wnt/β-catenin pathway plays an important role in initiation in most, if not all, colon cancers. Prior work has provided important insights into the regulation of β-catenin stability in the cytoplasm; however, relatively little is known about the mechanism by which β-catenin activates gene transcription in the nucleus. Using genetic approaches, studies in human colon cancers and Drosophila have identified CDK8 as a colon cancer oncogene that regulates β-catenin transcriptional activity. These convergent observations provide new insights into the regulation of nuclear β-catenin activity and identify a novel therapeutic target for β-catenin-driven malignancies. [Cancer Res 2009;69(20):OF7899–901]

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