11 - 13 Recent studies indicate that SNPs in DNA repair genes may modulate the DNA repair phenotype, particularly when these SNPs are located within coding or regulating regions, leading to alterations in protein expression and in functional properties of repair enzymes. Hundreds of SNPs in repair genes have been identified, and several epidemiologic studies have suggested wide population variability in DNA repair capacity phenotype as having a possible association with cancer risk. DNA repair is genetically regulated, 10 and 1 mechanism that may lead to the observed interindividual variations in repair capacity is the presence of single-nucleotide polymorphisms (SNPs) in DNA repair genes. 9 DNA repair proteins function as members of multiprotein complexes, making it likely that amino acid residues at protein-protein interfaces involved in the active sites will be important for protein function. In the general population, interindividual variability in DNA repair capacity has been reported, and an association between reduced DNA repair and susceptibility to a variety of cancers, including breast, colon, and lung cancers 2 - 6 and HD, 7 has been documented.Ĭonsiderable progress has been made in identifying gene products that play a role in DNA repair pathways in mammalian cells, 8 and it has been shown that defects in proteins involved in these pathways can have severe biologic effects.
DNA damage and subsequent repair are critical for maintaining genomic integrity and stability. 1 Although the etiology of HD remains mostly unknown, it is likely that as with most cancers, both environmental and genetic factors are involved. The American Cancer Society estimated that 8220 new cases of Hodgkin disease (HD) would be diagnosed in the US in 2008, and that 1350 people would die of the disease.