DNA Repair Gene Polymorphisms and Their Relation With DNA Damage, DNA Repair, and Total Antioxidant Capacity in Childhood Acute Lymphoblastic Leukemia Survivors. Issue 5 (July 2015)

• Record Type: Journal Article
• Authors: Dincer, Yildiz; Yüksel, Selin; Batar, Bahadir; Güven, Mehmet; Onaran, Ilhan; Celkan, Tiraje
• Is Part Of: Journal of pediatric hematology/oncology. Volume 37:Issue 5(2015)
• Publication Date: 2015-07
• Subjects: Pediatric hematology -- Periodicals; Tumors in children -- Periodicals; 618.9215
• DOI: 10.1097/MPH.0000000000000133
• Languages: English
• ISSNs: 1077-4114

Abstract

<abstract> <title> <x xml:space="preserve">Abstract</x> </title> <sec> <p>Oxidative stress and defective DNA repair are major contributory factors in the initiation and progression of carcinogenesis. Chemotherapy and radiotherapy cause oxidative DNA damage, consume antioxidant capacity, and impair DNA repair activity. These effects of chemotherapy and radiotherapy may be contributory factors in the development of secondary malignancy in cancer survivors. Basal, H<sub>2</sub>O<sub>2</sub>-induced, and postrepair DNA damage; urinary 8-hydroxydeoxyguanosine level as a marker of oxidatively damaged DNA; and serum total antioxidant capacity were measured; <italic>XPD</italic> Lys751Gln, <italic>XRCC1</italic> Arg399Gln, and <italic>XRCC1</italic> Arg194Trp polymorphisms were analyzed in childhood acute lymphoblastic leukemia (ALL) survivors. Basal and H<sub>2</sub>O<sub>2</sub>-induced DNA damage were found to be higher in the ALL survivor group versus the control group, however, there was no significant difference between the other parameters. No association was found between the examined parameters and polymorphisms of <italic>XPD</italic> 751 and <italic>XRCC1</italic> 399 and both the groups. <italic>XRCC1</italic> 194Trp allele was found to be associated with a low level of postrepair DNA damage in the ALL survivors. In conclusion, basal DNA damage and susceptibility to oxidation are high in childhood ALL survivors. This situation which may easily lead to occurrence of a secondary cancer does not seem to be a result of deficient DNA repair.</p> </sec> </abstract>