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Articles by D Consonni
Total Records ( 2 ) for D Consonni
  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.

  G Sottilotta , S. M Siboni , C Latella , V Oriana , E Romeo , R Santoro , D Consonni and V. Trapani Lombardo

Introduction: Elevated homocysteine (Hcy) is associated with the risk of deep vein thrombosis, pulmonary embolism, ischemic heart disease, and stroke. Several studies have suggested that hyperhomocysteinemia (HHcy) may predispose to retinal vein thrombosis (RVT) development. The aim of this study is to investigate the relationship between Hcy, C677T methylenetetrahydrofolate reductase (MTHFR) genotype, and RVT in patients compared with controls.

Materials and Methods: We evaluated the Hcy plasma level of 3114 consecutive participants in 2 Italian centers during a 2-year period. Hyperhomocysteinemia was found in 99 patients and 136 healthy participants. Of the 99 patients, 20 had RVT with a high prevalence of HHcy in the RVT subgroup (20.2%). This result suggested a possible relationship between HHcy and RVT development. We investigated 105 consecutive patients with recent diagnosis of RVT, and we compared them with 226 healthy controls to evaluate whether HHcy may be a risk factor for RVT.

Results: the prevalence of HHcy was higher in patients compared with controls (34.3% vs 14.2%; P < .001). The MTHFR C677T genotype was found in 69 of 105 (65.7%) patients with RVT (heterozygosity: 40 of 105 and homozygosity: 29 of 105). The control group showed the presence of MTHFR C677T genotype in 169 of 226 participants (74.8%; heterozygosity: 100 of 226 and homozygosity: 69 of 226) without difference between the 2 groups (P = .08).

Conclusion: our study suggests that HHcy is a possible risk factor for RVT development, while no association was found between RVT and the C677T MTHFR genotype.

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