The number of DNA repair genes so far identified in humans is 130, and it is anticipated that additional repair genes will be discovered. Enzymes encoded by these genes constantly monitor the genome and repair damaged nucleotides resulting from exposure to environmental and endogenous DNA damaging agents.1 If a DNA repair pathway is compromised or inactivated, cells can become hypermutable and more susceptible to cancer.2 Thus, DNA repair capacity can be considered a biomarker of cancer susceptibility and may potentially be a biomarker of susceptibility to other human diseases as well. However, DNA repair capacity is difficult to assess using an epidemi-ological approach because of redundancy in DNA repair pathways (i.e., DNA repair enzymes perform overlapping functions).

This chapter presents an update to our 2000 review of markers of DNA repair and susceptibility to cancer in humans3 focusing on studies published after 1998 and through the first half of 2001. This compilation is not meant to be exhaustive. Mismatch repair genes, potentially important biomarkers for hereditary nonpolyposis colorectal cancer and other human cancers, have been excluded. Not all the results are shown in the tables, since several studies considered multiple genes. More information is given in the text.

There has been an understandable shift from phenotypic assays of DNA repair capacity to genotyping for alterations in DNA repair genes. This review documents that change. Sixteen studies focus on phenotypic assays419 and 28 studies focus on genotypic assays;17,20-45 only one study published after 1998 combined phenotype and genotype in relationship to human can-cer.17 Study design and results are discussed, and epidemiologic factors that affect the integrity and the generalizability of these studies are considered.

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