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March 9, 1994

Statement on Use of DNA Testing for Presymptomatic Identification of Cancer Risk

Author Affiliations

National Institutes of Health, Bethesda, Md (chair); Monteflore Medical Hospital Center, Bronx, NY; Stanford (Calif) University; Washington University, St Louis, Mo; California Institute of Technology, Pasadena; University of California, San Francisco; Johns Hopkins University, Baltimore, Md (ad hoc); Massachusetts Institute of Technology, Cambridge; Johns Hopkins University, Baltimore, Md; Dorothy Nelkin; New York (NY) University; Columbia University, New York, NY; Bull Information Systems, Billerica, Mass; University of Wisconsin, Madison; University of California, Irvine; Princeton (NJ) University.
From the National Center for Human Genome Research, National Institutes of Health, Bethesda, Md. A complete list of the authors appears at the end of this article.

JAMA. 1994;271(10):785. doi:10.1001/jama.1994.03510340075038

RECENT advances in the genetics of cancer have raised the possibility of widespread DNA testing for the detection of predisposition to cancer. This may allow individuals at high risk to avail themselves of preventive measures and potentially avoid early death. At least one company has already announced plans to begin offering testing for genetic cancer risk. While much alleviation of human suffering may eventually result from these advances in cancer genetics, a number of important questions must be addressed before widespread testing of this sort can be recommended.

Two relatively common heritable cancer risk genes have recently been located. Among people with colon cancer, it appears that as many as 10% carry an altered germline copy of a gene called MSH2.1-3 Individuals with an altered MSH2 gene face an approximately 80% risk of colon cancer; women also have an elevated risk of endometrial and ovarian cancer. Intense medical surveillance

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