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For the development of cancer, it is generally accepted that certain key events are frequently involved. Two of them are the expression of DNA damage and inadequate repair of the damage. Expression of different types of DNA damage, particularly after exposure to environmental mutagens and carcinogens, have been well-characterized. Examples of the different types of DNA damages are shown in Figure 1 and each type of damage requires repair from specific and genetically-controlled DNA repair pathways. DNA singleand double-strand breaks from exposure to X-rays, for example, require the non-homologous end-joining and/or homologous recombination repair pathways. Repair of pyrimidine dimers from exposure to UV-light requires the excision repair pathway. Among the different types of repair activities, the repair of DNA double-strand breaks is most troublesome to cells because there is not a homologous DNA strand to provide complementary sequences for the repair therefore mistakes are frequently made as a consequence of the repair of DNA double-strand breaks. The often observed consequence from induction of DNA damage and inadequate repair of the damage is expression of chromosome abnormalities, gene mutations and genomic instability in most cancer cells. Therefore, better characterization of DNA damage and its repair activities can provide more precise determination of cancer and of prognosis.

Can laboratory assays for measurement of cellular DNA damage and its repair be useful for prediction of cancer and prognosis?