DNA Repair: a Double-Edged Sword

doi:10.1093/jnci/92.6.440

JNCI Journal of the National Cancer Institute 2000 92(6):440-441; doi:10.1093/jnci/92.6.440
© 2000 by Oxford University Press

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Journal of the National Cancer Institute, Vol. 92, No. 6, 440-441, March 15, 2000
© 2000 Oxford University Press

EDITORIALS

DNA Repair: a Double-Edged Sword

Qingyi Wei, Marsha L. Frazier, Bernard Levin

Affiliations of authors: Q. Wei, M. L. Frazier (Department of Epidemiology, Division of Cancer Prevention), B. Levin (Division of Cancer Prevention), The University of Texas M. D. Anderson Cancer Center, Houston.

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

It has been estimated that there is a 90% overlap between mutagenicityand carcinogenicity of environmental chemicals (1) and thatenvironmental exposure to carcinogens contributes to the developmentof more than 80% of human cancers (2). Cancer is also consideredto be a genetic disease because genetic alterations at eitherchromosomal or gene levels have been identified in most cancers.In multistep carcinogenesis (3), initial damage to DNA may leadto tumorigenesis and/or carcinogenesis due to functional imbalancebetween oncogenes (4), tumor suppressor genes (5), and DNA repairgenes (6), perhaps as a result . . . [Full Text of this Article]

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