Abstract
The contribution of polymorphisms in carcinogen metabolizing genes to overall cancer rates may vary widely between groups with differing allele frequencies and with varying levels of carcinogenic exposure. Their effects are modified by interactions with each other and with other genes, particularly those involved in DNA repair. Studies on the combined effects of particular polymorphisms on colorectal and other cancers, and also on intermediate markers such as DNA adduct formation, are discussed. Such susceptibility genes are of considerable scientific interest, but do not confer high enough risks to be clinically relevant.

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