Genomic instability plays an important role in cancer susceptibility, though the mechanics of its development remain unclear. An often-stated hypothesis is that error-prone phenotypes in DNA replication or aberrations in translesion DNA synthesis lead to genomic instability and cancer. Mutations in core DNA replication proteins have been identified in human cancer, although DNA replication is essential for cell proliferation and most mutations eliminating this function are deleterious. With recent developments in this field we review and discuss the possible involvement of DNA replication proteins in carcinogenesis.
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