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Dietary Modulation of Carcinoma Development in a Mouse Model for Human Familial Adenomatous Polyposis¹

Strang Cancer Prevention Center and The New York Hospital-Cornell Medical Center, New York, New York 10021 [K. Y., K. F., H. N., M. L.]; Department of Molecular Genetics, Albert Einstein College of Medicine, Bronx, New York 10461 [W. E., K. L., R. K.]; and Memorial Sloan-Kettering Cancer Center, New York, New York 10021 [D. L.]

Familial adenomatous polyposis (FAP) is caused by a dominant mutation in the adenomatous polyposis coli (APC) gene. Individuals with FAP progressively develop adenomas and carcinomas of the colon and rectum. We developed a mouse model for this disorder by genetically modifying the Apc gene. The resulting mice Apc1638 progressively develop neoplasms in the colon and remainder of the gastrointestinal tract. In this study when Apc1638 mice were fed a Western-style diet, they developed an increased incidence of the end point of carcinomas and number of invasive tumors. The findings therefore demonstrated dietary modulation of carcinoma incidence in mice with a targeted mutation providing a model for the study of gene-environment interactions in cancer.

¹ The work is supported by NIH Grants CA67944 and PO1 CA-29502-15, ACS Grant RPG-95-022-03-CN, and Cancer Center Grant CA13330 (to Albert Einstein College of Medicine).

² To whom requests for reprints should be addressed, at Strang Cancer Research Laboratory at The Rockefeller University, Theobald Smith Hall, Suite 136, 1230 York Avenue, New York, NY 10021.

Received 6/16/98. Accepted 10/14/98.

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