Abstract
Maintenance of genomic integrity is critical for the control of cell proliferation and survival. The genome is susceptible to DNA damage, which generates DNA lesions blocking the progression of DNA replication. Cells have multiple mechanisms to respond to DNA damage during replication; stabilization of the stalled replication fork, bypass the damage using specific DNA polymerases or recombination, or converting the damage into a second lesion. Responses by cells to DNA damage by these mechanisms can either activate DNA-repair pathway or programmed cell death (1). Failure or abnormal responses to DNA damage results in accumulation of mutations and promotes transformation of normal cells into cancer cells.
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