title: hOGG1 Ser326Cys polymorphism and risk of childhood acute lymphoblastic leukemia in a Chinese population.
abstract: Oxidative DNA damage caused by reactive oxygen species can produce 8-oxoguanine (8-oxoG) in DNA, which is misread and leads to G:C→T:A transversions. This can be carcinogenic. Repair of 8-oxoG by the base excision repair pathway involves the activity of human 8-oxoG DNA glycosylase 1 (hOGG1). Accumulating evidence suggests that the hOGG1 Ser326Cys polymorphism affects the activity of hOGG1 and might serve as a genetic marker for susceptibility to several cancers. To determine whether this polymorphism is associated with risk of childhood acute lymphoblastic leukemia (ALL) in Chinese children, we genotyped the hOGG1 Ser326Cys polymorphism (rs1052133) in a case-control study including 415 cases and 511 controls. We found that there was a significant difference in the genotype distributions of the hOGG1 Ser326Cys polymorphism between cases and controls (P = 0.046), and the combined genotypes Ser/Ser and Ser/Cys were associated with a statistically significantly decreased risk of ALL (adjusted odds ratio [OR] = 0.66, 95% confidence interval [CI] = 0.49-0.88, P = 0.005). Furthermore, we found a decreased risk for high risk ALL (adjusted OR = 0.60, 95% CI = 0.40-0.88, P = 0.005), low risk ALL (adjusted OR = 0.68, 95% CI = 0.47-0.99, P = 0.042), and B-phenotype ALL (adjusted OR = 0.63, 95% CI = 0.46-0.86, P = 0.003) among children with the Ser/Ser and Ser/Cys genotypes. Our results suggest that the hOGG1 Ser326Cys polymorphism is associated with susceptibility to childhood ALL in a Chinese population.
authors.affiliation: Department of Hematology and Oncology, The Affiliated Nanjing Children's Hospital of Nanjing Medical University, Nanjing Department of Hematology and Oncology, The Affiliated Children's Hospital of Soochow University, Suzhou Department of Molecular and Genetic Toxicology, Cancer Center of Nanjing Medical University, Nanjing, China.
authors.forename: Qian
authors.initials: Q
authors.lastname: Li
authors.forename: Lizhen
authors.initials: L
authors.lastname: Huang
authors.forename: Liucheng
authors.initials: L
authors.lastname: Rong
authors.forename: Yao
authors.initials: Y
authors.lastname: Xue
authors.forename: Qin
authors.initials: Q
authors.lastname: Lu
authors.forename: Yaoyao
authors.initials: Y
authors.lastname: Rui
authors.forename: Jie
authors.initials: J
authors.lastname: Li
authors.forename: Na
authors.initials: N
authors.lastname: Tong
authors.forename: Meilin
authors.initials: M
authors.lastname: Wang
authors.forename: Zhengdong
authors.initials: Z
authors.lastname: Zhang
authors.forename: Yongjun
authors.initials: Y
authors.lastname: Fang
mesh_terms: D000293:Adolescent; D016022:Case-Control Studies; D002648:Child; D002675:Child, Preschool; D002681:China; D004249:DNA Damage; D045647:DNA Glycosylases / Q000235:genetics*; D005260:Female; D005787:Gene Frequency; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006147:Guanine / Q000031:analogs & derivatives* / Q000096:biosynthesis / Q000378:metabolism; D006801:Humans; D007223:Infant; D008297:Male; D016133:Polymerase Chain Reaction; D020641:Polymorphism, Single Nucleotide; D054198:Precursor Cell Lymphoblastic Leukemia-Lymphoma / Q000235:genetics* / Q000378:metabolism; D017382:Reactive Oxygen Species
chemical_list: D017382:Reactive Oxygen Species; C024829:8-hydroxyguanine; D006147:Guanine; D045647:DNA Glycosylases; C479058:oxoguanine glycosylase 1, human