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Articles by M. A Tucker
Total Records ( 3 ) for M. A Tucker
  T. K Lam , M Rotunno , J. H Lubin , S Wacholder , D Consonni , A. C Pesatori , P. A Bertazzi , S. J Chanock , L Burdette , A. M Goldstein , M. A Tucker , N. E Caporaso , A. F Subar and M. T. Landi
 

Epidemiological and mechanistic evidence on the association of quercetin-rich food intake with lung cancer risk and carcinogenesis are inconclusive. We investigated the role of dietary quercetin and the interaction between quercetin and P450 and glutathione S-transferase (GST) polymorphisms on lung cancer risk in 1822 incident lung cancer cases and 1991 frequency-matched controls from the Environment And Genetics in Lung cancer Etiology study. In non-tumor lung tissue from 38 adenocarcinoma patients, we assessed the correlation between quercetin intake and messenger RNA expression of the same P450 and GST metabolic genes. Multivariate odds ratios (ORs) and 95% confidence intervals (CIs) for sex-specific quintiles of intake were calculated using unconditional logistic regression adjusting for putative risk factors. Frequent intake of quercetin-rich foods was inversely associated with lung cancer risk (OR = 0.49; 95% CI: 0.37–0.67; P-trend < 0.001) and did not differ by P450 or GST genotypes, gender or histological subtypes. The association was stronger in subjects who smoked >20 cigarettes per day (OR = 0.35; 95% CI: 0.19–0.66; P-trend = 0.003). Based on a two-sample t-test, we compared gene expression and high versus low consumption of quercetin-rich foods and observed an overall upregulation of GSTM1, GSTM2, GSTT2, and GSTP1 as well as a downregulation of specific P450 genes (P-values < 0.05, adjusted for age and smoking status). In conclusion, we observed an inverse association of quercetin-rich food with lung cancer risk and identified a possible mechanism of quercetin-related changes in the expression of genes involved in the metabolism of tobacco carcinogens in humans. Our findings suggest an interplay between quercetin intake, tobacco smoking, and lung cancer risk. Further research on this relationship is warranted.

  F Demenais , H Mohamdi , V Chaudru , A. M Goldstein , J. A Newton Bishop , D. T Bishop , P. A Kanetsky , N. K Hayward , E Gillanders , D. E Elder , M. F Avril , E Azizi , P van Belle , W Bergman , G Bianchi Scarra , B Bressac de Paillerets , D Calista , C Carrera , J Hansson , M Harland , D Hogg , V Hoiom , E. A Holland , C Ingvar , M. T Landi , J. M Lang , R. M Mackie , G. J Mann , M. E Ming , C. J Njauw , H Olsson , J Palmer , L Pastorino , S Puig , J Randerson Moor , M Stark , H Tsao , M. A Tucker , P van der Velden , X. R Yang , N Gruis and and the Melanoma Genetics Consortium
  Background

Carrying the cyclin-dependent kinase inhibitor 2A (CDKN2A) germline mutations is associated with a high risk for melanoma. Penetrance of CDKN2A mutations is modified by pigmentation characteristics, nevus phenotypes, and some variants of the melanocortin-1 receptor gene (MC1R), which is known to have a role in the pigmentation process. However, investigation of the associations of both MC1R variants and host phenotypes with melanoma risk has been limited.

Methods

We included 815 CDKN2A mutation carriers (473 affected, and 342 unaffected, with melanoma) from 186 families from 15 centers in Europe, North America, and Australia who participated in the Melanoma Genetics Consortium. In this family-based study, we assessed the associations of the four most frequent MC1R variants (V60L, V92M, R151C, and R160W) and the number of variants (1, ≥2 variants), alone or jointly with the host phenotypes (hair color, propensity to sunburn, and number of nevi), with melanoma risk in CDKN2A mutation carriers. These associations were estimated and tested using generalized estimating equations. All statistical tests were two-sided.

Results

Carrying any one of the four most frequent MC1R variants (V60L, V92M, R151C, R160W) in CDKN2A mutation carriers was associated with a statistically significantly increased risk for melanoma across all continents (1.24 x 10–6P ≤ .0007). A consistent pattern of increase in melanoma risk was also associated with increase in number of MC1R variants. The risk of melanoma associated with at least two MC1R variants was 2.6-fold higher than the risk associated with only one variant (odds ratio = 5.83 [95% confidence interval = 3.60 to 9.46] vs 2.25 [95% confidence interval = 1.44 to 3.52]; Ptrend = 1.86 x 10–8). The joint analysis of MC1R variants and host phenotypes showed statistically significant associations of melanoma risk, together with MC1R variants (.0001 ≤ P ≤ .04), hair color (.006 ≤ P ≤ .06), and number of nevi (6.9 x 10–6P ≤ .02).

Conclusion

Results show that MC1R variants, hair color, and number of nevi were jointly associated with melanoma risk in CDKN2A mutation carriers. This joint association may have important consequences for risk assessments in familial settings.

  E. J Wamsley , M. A Tucker , J. D Payne and R. Stickgold
 

Here, we examined the effect of a daytime nap on changes in virtual maze performance across a single day. Participants either took a short nap or remained awake following training on a virtual maze task. Post-training sleep provided a clear performance benefit at later retest, but only for those participants with prior experience navigating in a three-dimensional (3D) environment. Performance improvements in experienced players were correlated with delta-rich stage 2 sleep. Complementing observations that learning-related brain activity is reiterated during post-navigation NREM sleep in rodents, the present data demonstrate that NREM sleep confers a performance advantage for spatial memory in humans.

 
 
 
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