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Tumor Biology |
Department of Oncology [W. Y., A. V., J. M., C. N., G. C., M. H., L. H. A.], Department of Cell Biology [W. E., L. H. A.], and Department of Molecular Genetics [R. K.], Albert Einstein Cancer Center, Bronx, New York 10467, and Department of Medicine, St. Luke’s-Roosevelt Hospital Center and Columbia University, New York, New York 10025 [P. R. H.]
Sulindac, a nonsteroidal anti-inflammatory drug, inhibits intestinal tumorigenesis in humans and rodents. Sulindac induced complex alterations in gene expression, but only 0.1% of 8063 sequences assayed were altered similarly by the drug in rectal biopsies of patients treated for 1 month and during response of colonic cells in culture. Among these changes was induction of the cyclin-dependent kinase inhibitor, p21WAF1/cip1. In Apc1638+/- mice, targeted inactivation of p21 increased intestinal tumor formation in a gene-dose-dependent manner, but inactivation of p21 completely eliminated the ability of sulindac to both inhibit mitotic activity in the duodenal mucosa and to inhibit Apc-initiated tumor formation. Thus, p21 is essential for tumor inhibition by this drug. The array data can be accessed on the Internet at http://sequence.aecom.yu.edu/genome/.
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