NAD(P)H:quinone oxidoreductase (NQO1) plays an important role in

NAD(P)H:quinone oxidoreductase (NQO1) plays an important role in the detoxification of quinones. C6091 and C465T are 2 common polymorphisms in NQO1 resulting in lower NQO1 activity compared with wild type (CC). We assessed the frequency of C609T (NQO1*2 Proline to Serine) and C465T (NQO1*3; Arginine to Tryptophane) polymorphisms of the NQO1 gene among the Iranian population to determine the association between these polymorphisms and a susceptibility to adult acute myeloid leukemia (AML).

Materials and Methods: Frequencies of N001 gene polymorphisms were determined in 140 AML patients for NQO1*2 and NQO1*3. In addition, 160 www.selleckchem.com/products/ly2835219.html age-sex matched healthy individuals participated in this study as

a control group. Genotyping was done using polymerase chain reaction and restriction fragment length polymorphism (PCR-RFLP) assays.

Results: No significant association was observed between these 2 polymorphisms of NQO1 and the risk

of AML. Odds ratio (OR) for C609T and 04651 were 0.917 (95% CI=0.513-1.639) and 1.976 (95% 01=0.549-7.121), respectively. https://www.selleckchem.com/products/liproxstatin-1.html Men showed a higher incidence of C609T and C465T NQO1 than women. The majority of patients with a mutant allele were diagnosed as M3 sub type of French-American-British (FAB) classification.

Conclusions: Our findings suggest that the NQO1 C609T and C465T gene variants do not have a major influence on the susceptibility to adult AML. Interestingly, we found a higher incidence of the T allele in NQO1*2 than NQO1*3 in the control and patient groups. Further studies are required to validate these findings across different populations.”
“While genetics clearly influences dental caries risk, few caries genes have been discovered and validated. Recent studies have suggested differential genetic factors for primary dentition caries and permanent dentition caries, as well as for pit-and-fissure(PF) and smooth- (SM) surface caries. We performed separate GWAS for caries in Transmembrane Transporters inhibitor permanent-dentition PF surfaces (1,017

participants, adjusted for age, sex, and the presence of Streptococcus mutans) and SM surfaces (1,004 participants, adjusted for age, education group, and the presence of Streptococcus mutans) in self-reported whites (ages 14 to 56 yrs). Caries scores were derived based on visual assessment of each surface of each tooth; more than 1.2 million SNPs were either successfully genotyped or imputed and were tested for association. Two homologous genes were suggestively associated: BCOR (Xp11.4) in PF-surface caries (p value = 1.8E-7), and BCORL1 (Xq26.1) in SM-surface caries (p value = 1.0E-5). BCOR mutations cause oculofaciocardiodental syndrome, a Mendelian disease involving multiple dental anomalies. Associations of other plausible cariogenesis genes were also observed for PF-surface caries (e. g., INHBA, p value = 6.5E-6) and for SM-surface caries (e. g., CXCR1 and CXCR2, p value = 1.9E-6).

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