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The timely and accurate repair of DNA damage is essential to maintenance of an intact genome and the prevention of tumorigenesis. Not surprisingly, an increase in DNA double strand break repair activity has been detected in pre-cancerous lesions. The non-homologous end-joining (NHEJ) pathway is essential to this process and involves more than 10 different proteins. We and others have demonstrated that mutation of one of these proteins, DNA-PKcs, predisposes certain strains of mice to thymic lymphoma development. We are therefore interested in identifying the underlying modifying gene(s) responsible for this strain-specific mechanism of tumor development.
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