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Editorial
September 23/30, 1998

Proliferation Happens

Author Affiliations

From the University of Colorado School of Medicine (Drs Ahnen and Byers) and the Denver Department of Veterans Affairs Medical Center (Dr Ahnen), Denver, Colo.

JAMA. 1998;280(12):1095-1096. doi:10.1001/jama.280.12.1095

The use of surrogate end points in trials of colonic cancer chemoprevention has great appeal. Potential agents could be tested more quickly using far fewer patients than would be needed for trials using the development of colonic cancer or adenomas as end points. In this issue of THE JOURNAL, Holt and colleagues1 report that increased dietary intake of low-fat dairy foods can alter putative intermediate biomarkers of colonic cancer risk. This study raises 2 important questions about the use of surrogate end points for colonic cancer: (1) are there any surrogate end points, short of adenoma formation, that reliably reflect colonic cancer risk and (2) is there currently a defined role for surrogate end point studies in decision making about which agents to test in colonic cancer chemoprevention trials? The answer to both of these questions probably is no.

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