title: NAD(P)H:quinone oxidoreductase 1 null genotype is not associated with pediatric de novo acute leukemia.
abstract: BACKGROUND
  NAD(P)H:quinone oxidoreductase1 (NQO1) is a two-electron reductase that detoxifies quinones derived from the oxidation of phenolic metabolites of benzene. Exposure to benzene metabolites increases the risk of hematotoxicity and leukemia. NQO1 enzyme activity protects the cells against metabolites of benzene. C to T base substitution at nucleotide 609 of NQO1 cDNA (C609T) results in loss of enzyme activity. Low NQO1 activity may play a role in etiology of acute leukemia.
  
  
  METHODS
  We analyzed NQO1 C609T gene polymorphism using the PCR-RFLP method in 273 patients with de novo acute leukemia (189 acute lymphoblastic leukemia (ALL), and 84 acute myeloid leukemia (AML) and 286 healthy volunteers to investigate the role of NQO1 polymorphism in the etiology of acute leukemia.
  
  
  CONCLUSIONS
  The frequency of homozygosity for NOQ1 C609T polymorphism was 3.5% in the healthy control population and 2.5% in pediatric acute leukemia. The NQO1 C609T allele frequency was not statistically different in the children with acute leukemia in comparison to the controls (odds ratio (OR), 0.76; 95% confidence interval (CI), 0.58-1.01; P = 0.06). The distribution of NQO1 genotypes among children with acute leukemia was not statistically different from the control group (P = 0.13). These findings do not support the role of NQO1 C609T polymorphism in the etiology of de novo pediatric acute leukemia.
authors.affiliation: Department of Genetics, Institute for Experimental Medical Research (DETAE), Istanbul University, Istanbul, Turkey.
authors.forename: Sema
authors.initials: S
authors.lastname: Sirma
authors.forename: Leyla
authors.initials: L
authors.lastname: Agaoglu
authors.forename: Inci
authors.initials: I
authors.lastname: Yildiz
authors.forename: Dilara
authors.initials: D
authors.lastname: Cayli
authors.forename: Emrin
authors.initials: E
authors.lastname: Horgusluoglu
authors.forename: Sema
authors.initials: S
authors.lastname: Anak
authors.forename: Lebriz
authors.initials: L
authors.lastname: Yuksel
authors.forename: Aysegul
authors.initials: A
authors.lastname: Unuvar
authors.forename: Tiraje
authors.initials: T
authors.lastname: Celkan
authors.forename: Hilmi
authors.initials: H
authors.lastname: Apak
authors.forename: Zeynep
authors.initials: Z
authors.lastname: Karakas
authors.forename: Omer
authors.initials: O
authors.lastname: Devecioglu
authors.forename: Ugur
authors.initials: U
authors.lastname: Ozbek
mesh_terms: D000208:Acute Disease; D000293:Adolescent; D002648:Child; D002675:Child, Preschool; D005260:Female; D005838:Genotype; D006801:Humans; D007223:Infant; D007951:Leukemia, Myeloid / Q000209:etiology / Q000235:genetics*; D008297:Male; D016660:NAD(P)H Dehydrogenase (Quinone) / Q000235:genetics*; D016133:Polymerase Chain Reaction; D011110:Polymorphism, Genetic; D012150:Polymorphism, Restriction Fragment Length; D054198:Precursor Cell Lymphoblastic Leukemia-Lymphoma / Q000209:etiology / Q000235:genetics*
chemical_list: D016660:NAD(P)H Dehydrogenase (Quinone); C447479:NQO1 protein, human