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Hijacking the Chromatin Remodeling Machinery: Impact of SWI/SNF Perturbations in Cancer

¹ Department of Pathology and Laboratory and Lineberger Cancer Center, University of North Carolina, Chapel Hill, North Carolina and ² Department of Cancer Biology, Department of Urology, and Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, Pennsylvania

Requests for reprints: Karen E. Knudsen, Thomas Jefferson University/Kimmel Cancer Center, 233 South 10th Street, Bluemle Building- Room 1008, Philadelphia, PA 19107. Phone: 215-503-8574; Fax: 215-923-4498; E-mail: karen.knudsen{at}kimmelcancercenter.org.

There is increasing evidence that alterations in chromatin remodeling play a significant role in human disease. The SWI/SNF chromatin remodeling complex family mobilizes nucleosomes and functions as a master regulator of gene expression and chromatin dynamics whose functional specificity is driven by combinatorial assembly of a central ATPase and association with 10 to 12 unique subunits. Although the biochemical consequence of SWI/SNF in model systems has been extensively reviewed, the present article focuses on the evidence linking SWI/SNF perturbations to cancer initiation and tumor progression in human disease. [Cancer Res 2009;69(21):8223–30]