DNA repair: a double-edged sword.

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Abstract
It has been estimated that there is a 90% overlap between mutagenicity and carcinogenicity of environmental chemicals (1) and that environmental exposure to carcinogens contributes to the development of more than 80% of human cancers (2). Cancer is also considered to be a genetic disease because genetic alterations at either chromosomal or gene levels have been identified in most cancers. In multistep carcinogenesis (3), initial damage to DNA may lead to tumorigenesis and/or carcinogenesis due to functional imbalance between oncogenes (4), tumor suppressor genes (5), and DNA repair genes (6), perhaps as a result of mutation fixation of the damage. During carcinogenesis, both endogenous and exogenous exposures to carcinogens or genotoxic agents cause cell cycle delays (7) that allow cells to repair DNA damage, suggesting that efficient DNA repair is central to maintaining normal cell cycle and growth.