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Pediatr Blood Cancer ; 43(5): 568-70, 2004 Oct.
Article in English | MEDLINE | ID: mdl-15382274

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. PROCEDURE: 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. RESULTS AND 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.


Subject(s)
Leukemia, Myeloid/genetics , NAD(P)H Dehydrogenase (Quinone)/genetics , Polymorphism, Genetic , Precursor Cell Lymphoblastic Leukemia-Lymphoma/genetics , Acute Disease , Adolescent , Child , Child, Preschool , Female , Genotype , Humans , Infant , Leukemia, Myeloid/etiology , Male , Polymerase Chain Reaction , Polymorphism, Restriction Fragment Length , Precursor Cell Lymphoblastic Leukemia-Lymphoma/etiology
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