NAD(p)h: Quinone oxidoreductase 1 genetic polymorphism and its association to acute leukemia

Cancer has a genetic component and at the level of the cell it can be said to begenetic disease. Most cancer results from interaction between enviroment andgenetics. Individual susceptibility to some of cancers maybe explained partly bygenetic differences in the activation and detoxification of xenobiotics. NAD(P)H:quinone oxidoreductase1(NQO1) detoxifies quinones derived from the oxidationof phenolic metabolites of benzene. NQO1 enzyme activity protects cells fromoxidative stres. A point mutation in codon 187 (C609T) results in complete lossof enzyme activity in homozygus subjects, whereas those with 2 wild-type allelshave normal activity. Low or null enzyme activity may play a role in etiology ofacute leukemiaIn this study, we investigated associations between genetic polymorphism inNQO1 susceptibility to acute leukemia. The distrubition of NQO1 allels weredetermined in 87 healty individuals and 78 patients with acute leukeima. NQO1polymorphism was studied using polymerase chain reaction based restrictionfragment length polymorphism (PCR-RFLP), followed by digestion withrestriction enzyme was used to analyze the mutation in NQO1 gene. Thedistrubtion of wt/wt and mt/mt genotypes were determined as %60,92, %5,75 inthe healthy control population and %62,82, %8,97 in acute leukemia. TheNQO1 C609T allele frequency was not statistically different in acute leukemiain comparison to the controls (OR:1,133; 0,675-1,902; Cl: %95). Thedistribution of NQO1 genotypes acute leukemia was not statistically differentfrom the control group (OR:0,923; 0,492-1,731; Cl: %95). These findings do notsupport the role of NQO1 C609T polymorphism in the ethiology acuteleukemia.