DNA Damage/Repair Management in Cancers
Jehad F. Alhmoud, John F. Woolley, Ala‐Eddin Al Moustafa, Mohammed Imad Mallei
Abstract
DNA damage can alter nucleotide sequences and lead to expression of dysfunctional proteins that impact normal cellular physiology. Mutations or deletion of genes responsible for regulating cell division or tumor suppressors can also lead to genomic instability and cancer. DNA repair pathways are encoded by a class of proteins that detect DNA double stand breaks, chromosomal fragmentation, translocation and deletions, and can correct some alterations. The DNA damage response pathway responds to cellular damage by using signal sensors, transducers and effectors. Nucleotide excision repair is one of the major DNA repair pathways to protect the cells against DNA lesions that vary structurally and chemically. The direct repair mechanism depends on a single protein in eliminating the DNA damage and lesions. Base excision repair (BER) is an essential DNA repair pathway that corrects DNA damage from oxidative, alkylating and deamination events. The BER pathway repairs the damaged DNA throughout the cell cycle.