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Sant'Ambrogio di Torino, Italy

Masala G.,Cancer Research and Prevention Institute ISPO | Assedi M.,Cancer Research and Prevention Institute ISPO | Bendinelli B.,Cancer Research and Prevention Institute ISPO | Ermini I.,Cancer Research and Prevention Institute ISPO | And 11 more authors.
Breast Cancer Research and Treatment | Year: 2012

The role of fruit and vegetables in breast cancer (BC) development has long been debated. A large variety of vegetables and fruit are consumed by Mediterranean populations, a favourable setting for evaluating the effects of these foods. The association between vegetables and fruit consumption, overall and by specific types, and BC risk was studied in the Italian section of the European Prospective Investigation into Cancer and Nutrition study. Over 31,000 women, aged 36-64 years, recruited in five Italian centers between 1993 and 1998, were available for analyses with dietary and lifestyle information and anthropometric measurements. After a median follow-up of 11.25 years, 1,072 invasive and in situ incident BC cases were identified. Cox proportional hazard models (adjusted for education, anthropometry, reproductive history, hormone replacement therapy, physical activity, alcohol consumption and smoking habits) showed an inverse association between consumption of all vegetables and BC risk (highest vs. lowest quintile HR 0.65; 95% CI 0.53-0.81, P for trend = 0.003). According to subtypes of vegetables, an inverse association emerged for increasing consumption of leafy vegetables (highest vs. lowest quintile HR 0.70; 95% CI 0.57-0.86, P for trend = 0.0001) and fruiting vegetables (highest vs. lowest quintile HR 0.75; 95% CI 0.60-0.94, P for trend = 0.01). An inverse association also emerged with increasing consumption of raw tomatoes (P for trend = 0.03). In contrast, no association of fruit, overall or by subtypes, with BC risk was found. In this Mediterranean population, a clear protective role of increasing vegetables consumption, mainly leafy and fruiting vegetables, on BC risk emerged. © Springer Science+Business Media, LLC. 2011. Source

Baussano I.,International Agency for Research on Cancer | Lazzarato F.,University of Turin | Ronco G.,Center for Cancer Prevention Piemonte | Dillner J.,Karolinska Institutet | Franceschi S.,International Agency for Research on Cancer
International Journal of Cancer | Year: 2013

Human papillomavirus (HPV) vaccination of a birth cohort of girls in the 9-13 age range is recommended as a priority, but decreases in HPV vaccine cost may make catch-up of a few additional cohorts more attractive not only in high-income countries. We assessed the reduction in HPV16 and 18 infections that could be achieved in a medium- (Poland) and a low-income (Guinea) country by adding one-time catch-up of 12- to 19-year-old girls to the vaccination of 11-year-old girls. According to our ad hoc adapted dynamic model of HPV infection transmission, the addition of catch-up was estimated to bring forward the 50% reduction of HPV16/18 prevalence due to vaccination in women ≤35 by as much as 5 years. Catch-up of 12- to 15-year olds reduced the cumulative probability of HPV16/18 infections by age 35 in the relevant cohorts by about 30% in both countries. Catch-up of 16- to 19-year-old girls added little. Regardless of the chosen catch-up strategy, 16 to 20% of HPV16/18 prevention from vaccination was attributable to herd immunity. Assuming a sufficiently low vaccine cost, the addition of a catch-up round is, therefore, worth considering in medium/low-income countries to extend vaccine benefits to less young adolescent girls whose future access to cervical screening is uncertain. What's new? To prevent cervical cancer, the WHO recommends that girls between the ages of 9-13 years be vaccinated against human papillomavirus (HPV). In this study, the authors asked whether vaccinating older girls (12-15 years) as well, in a one-time "catch up" cohort, would provide enough additional benefit to be worthwhile. They found that this strategy brought forward the 50% reduction of HPV16/18 prevalence by as much as 5 years, in both a low-income and a medium-income country. As the cost of HPV vaccine decreases, this strategy may thus become desirable especially in low-income countries. Copyright © 2013 UICC. Source

Hebels D.G.A.J.,Maastricht University | Georgiadis P.,National Hellenic Research Foundation | Keun H.C.,Imperial College London | Athersuch T.J.,Imperial College London | And 15 more authors.
Environmental Health Perspectives | Year: 2013

Background: The suitability for omic analysis of biosamples collected in previous decades and currently stored in biobanks is unknown. Objectives: We evaluated the influence of handling and storage conditions of blood-derived biosamples on transcriptomic, epigenomic (CpG methylation), plasma metabolomic [UPLC-ToFMS (ultra performance liquid chromatography-time-of-flight mass spectrometry)], and wide-target proteomic profiles. Methods: We collected fresh blood samples without RNA preservative in heparin, EDTA, or citrate and held them at room temperature for ≤ 24 hr before fractionating them into buffy coat, erythrocytes, and plasma and freezing the fractions at-80°C or in liquid nitrogen. We developed methodology for isolating RNA from the buffy coats and conducted omic analyses. Finally, we analyzed analogous samples from the EPIC-Italy and Northern Sweden Health and Disease Study biobanks. Results: Microarray-quality RNA could be isolated from buffy coats (including most biobank samples) that had been frozen within 8 hr of blood collection by thawing the samples in RNA preservative. Different anticoagulants influenced the metabolomic, proteomic, and to a lesser extent transcriptomic profiles. Transcriptomic profiles were most affected by the delay (as little as 2 hr) before blood fractionation, whereas storage temperature had minimal impact. Effects on metabolomic and proteomic profiles were noted in samples processed ≥ 8 hr after collection, but no effects were due to storage temperature. None of the variables examined significantly influenced the epigenomic profiles. No systematic influence of tim-in-storage was observed in samples stored over a period of 13-17 years. Conclusions: Most samples currently stored in biobanks are amenable to meaningful omics analysis, provided that they satisfy collection and storage criteria defined in this study. Source

Sieri S.,Fondazione Istituto Nazionale Dei Tumori | Brighenti F.,University of Parma | Agnoli C.,Fondazione Istituto Nazionale Dei Tumori | Grioni S.,Fondazione Istituto Nazionale Dei Tumori | And 12 more authors.
PLoS ONE | Year: 2013

Background:Studies on the association of stroke risk to dietary glycemic index (GI) and glycemic load (GL) have produced contrasting results.Objective:To investigate the relation of dietary GI and GL to stroke risk in the large EPIC-Italy cohort (EPICOR) recruited from widely dispersed geographic areas of Italy.Design:We studied 44099 participants (13,646 men and 30,453 women) who completed a dietary questionnaire. Multivariable Cox modeling estimated adjusted hazard ratios (HRs) of stroke with 95% confidence intervals (95%CI). Over 11 years of follow-up, 355 stroke cases (195 ischemic and 83 hemorrhagic) were identified.Results:Increasing carbohydrate intake was associated with increasing stroke risk (HR = 2.01, 95%CI = 1.04-3.86 highest vs. lowest quintile; p for trend 0.025). Increasing carbohydrate intake from high-GI foods was also significantly associated with increasing stroke risk (HR 1.87, 95%CI = 1.16-3.02 highest vs. lowest, p trend 0.008), while increasing carbohydrate intake from low-GI foods was not. Increasing GL was associated with significantly increasing stroke risk (HR 2.21, 95%CI = 1.16-4.20, highest vs. lowest; p trend 0.015). Dietary carbohydrate from high GI foods was associated with increased both ischemic stroke risk (highest vs. lowest HR 1.92, 95%CI = 1.01-3.66) and hemorrhagic stroke risk (highest vs. lowest HR 3.14, 95%CI = 1.09-9.04). GL was associated with increased both ischemic and hemorrhagic stroke risk (HR 1.44, 95%CI = 1.09-1.92 and HR 1.56, 95%CI = 1.01-2.41 respectively, continuous variable).Conclusions:In this Italian cohort, high dietary GL and carbohydrate from high GI foods consumption increase overall risk of stroke. © 2013 Sieri et al. Source

Elks C.E.,Institute of Metabolic Science | Ong K.K.,Institute of Metabolic Science | Scott R.A.,Institute of Metabolic Science | Van Der Schouw Y.T.,University Utrecht | And 40 more authors.
Diabetes Care | Year: 2013

OBJECTIVE-Younger age at menarche, a marker of pubertal timing in girls, is associated with higher risk of later type 2 diabetes.We aimed to confirmthis association and to examine whether it is explained by adiposity. RESEARCH DESIGN AND METHODSdThe prospective European Prospective Investigation into Cancer andNutrition (EPIC)-InterAct case-cohort study consists of 12,403 incident type 2 diabetes cases and a stratified subcohort of 16,154 individuals from26 research centers across eight European countries.We tested the association between age at menarche and incident type 2 diabetes using Prentice-weighted Cox regression in 15,168 women (n = 5,995 cases). Models were adjusted in a sequential manner for potential confounding and mediating factors, including adult BMI. RESULTS-Mean menarcheal age ranged from 12.6 to 13.6 years across InterAct countries. Each year latermenarche was associated with 0.32 kg/m2 lower adult BMI. Women in the earliest menarche quintile (8-11 years, n = 2,418) had 70%higher incidence of type 2 diabetes compared with those in the middle quintile (13 years, n = 3,634), adjusting for age at recruitment, research center, and a range of lifestyle and reproductive factors (hazard ratio [HR], 1.70; 95% CI, 1.49- 1.94; P < 0.001). Adjustment for BMI partially attenuated this association (HR, 1.42; 95% CI, 1.18-1.71; P < 0.001). Later menarche beyond the median age was not protective against type 2 diabetes. CONCLUSIONS-Women with history of earlymenarche have higher risk of type 2 diabetes in adulthood. Less than half of this association appears to be mediated by higher adult BMI, suggesting that early pubertal development also may directly increase type 2 diabetes risk. © 2013 by the American Diabetes Association. Source

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