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JNCI Journal of the National Cancer Institute 2001 93(2):84-85; doi:10.1093/jnci/93.2.84
© 2001 by Oxford University Press
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Journal of the National Cancer Institute, Vol. 93, No. 2, 84-85, January 17, 2001
© 2001 Oxford University Press

EDITORIAL

Public Health Burden of Cancer in Ataxia-Telangiectasia Heterozygotes

Michael Swift

Correspondence to: Michael Swift, M.D., The Institute for the Genetic Analysis of Common Diseases, New York Medical College, 4 Skyline Dr., Hawthorne, NY 10532 (e-mail: michael_swift@nymc.edu).

Knowing that mutations of a specific gene predispose to certain cancers is an important step toward more effective preventive or therapeutic measures for those cancers. The history of ataxia-telangiectasia (A-T) research illustrates how advances in genetic and molecular genetic technology are clarifying and quantifying the role of mutations at this genetic locus in common diseases and mortality in the general population.

An exceptionally high incidence of cancer was observed in patients with the rare autosomal recessive syndrome A-T (1) shortly after Boder and Sedgewick (2) published their remarkably complete initial characterization of this disorder in 1958. I hypothesized (3) that mutations at the A-T locus (sometimes referred to as the ATM, for "ataxia-telangiectasia mutated," locus) might contribute substantially to the public health burden of cancer, despite the rarity . . . [Full Text of this Article]

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