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JNCI Journal of the National Cancer Institute 2003 95(10):697-699; doi:10.1093/jnci/95.10.697
© 2003 by Oxford University Press
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Journal of the National Cancer Institute, Vol. 95, No. 10, 697-699, May 21, 2003
© 2003 Oxford University Press

EDITORIAL

Potential Pitfalls in the Use of Surrogate Endpoints in Colorectal Adenoma Chemoprevention

Bernard Levin

Correspondence to: Bernard Levin, M.D., Division of Cancer Prevention, University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Blvd., Box 203, Houston, TX 77030 (e-mail: blevin@mdanderson.org).

The first 10% of the full text of this article appears below.

Colorectal cancer is the second most common cause of cancer death for both men and women in the United States (1). Understanding the relationship between adenomatous polyps and colorectal carcinoma is important in evaluating the effectiveness of chemoprevention. The relationship is complex, with the adenoma-to-carcinoma pathway characterized by a series of genetic alterations involving a number of genes, including APC, K-RAS, DCC, and p53 (2). In colorectal cancers, frequent loss of heterozygosity at multiple chromosomal loci, including 5q, 17p, and 18q, is observed. Such lesions are classified as microsatellite stable. Recent attention has also focused on an alternative pathway involved in the pathogenesis of colorectal cancer that accounts for 15%–20% of colorectal cancers, including hereditary non–polyposis colorectal cancer. This alternative pathway involves microsatellite instability and is also associated with . . . [Full Text of this Article]


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