DNA Repair, Cancer and Cancer Therapy

Abstract

The success of an organism to survive from one generation to the next is largely dependent upon the fidelity of replication of its genetic material, deoxyribonucleic acid (DNA). Unfortunately, DNA in living cell is labile and subject to many chemical alterations, and these alterations, if not corrected, can to lead to diseases such as cancer (Fig. 1) (Pallis & Karamouzis, 2010). All eukaryotic cells have evolved a multifaceted response to counteract the potentially deleterious effects of DNA damage (Fig. 2). Upon sensing DNA damage, cell cycle checkpoints are activated to arrest cell cycle progression to allow time for repair before the damage is passed on to the next generation of cells. Depending on the type of damage, other cellular mechanisms such as transcriptional program activation, DNA repair pathways, and apoptosis can also be induced. All of these processes are coordinated so the genetic material is faithfully maintained, duplicated, and segregated within the cell. Important goals of cancer research are to determine the molecular mechanisms that are involved in the formation of genetic changes in human genes as a consequence of DNA mutations and to explain how cancer cells withstand and counteract DNA damage by the use of different defense mechanisms ranging from free radical scavengers to sophisticated DNA repair mechanisms.