Paolo Vineis

Human Genetics Foundation Torino, Torino, Piedmont, Italy

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Publications (731)4284.85 Total impact

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    ABSTRACT: Cancer research is drawing on the human genome project to develop new molecular-targeted treatments. This is an exciting but insufficient response to the growing, global burden of cancer, particularly as the projected increase in new cases in the coming decades is increasingly falling on developing countries. The world is not able to treat its way out of the cancer problem. However, the mechanistic insights from basic science can be harnessed to better understand cancer causes and prevention, thus underpinning a complementary public health approach to cancer control. This manuscript focuses on how new knowledge about the molecular and cellular basis of cancer, and the associated high-throughput laboratory technologies for studying those pathways, can be applied to population-based epidemiological studies, particularly in the context of large prospective cohorts with associated biobanks to provide an evidence base for cancer prevention. This integrated approach should allow a more rapid and informed translation of the research into educational and policy interventions aimed at risk reduction across a population. © The Author 2014. Published by Oxford University Press. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com.
    Journal of the National Cancer Institute. 01/2015; 107(1).
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    ABSTRACT: There is limited evidence on the association between dietary folate intake and the risk of breast cancer (BC) by hormone receptor expression in the tumors. We investigated the relationship between dietary folate and BC risk using data from the European Prospective Investigation into Cancer and Nutrition (EPIC). A total of 367993 women age 35 to 70 years were recruited in 10 European countries. During a median follow-up of 11.5 years, 11575 women with BC were identified. Dietary folate intake was estimated from country-specific dietary questionnaires. Cox proportional hazards regression models were used to quantify the association between dietary variables and BC risk. BC tumors were classified by receptor status. Subgroup analyses were performed by menopausal status and alcohol intake. Intake of other B vitamins was considered. All statistical tests were two-sided. A borderline inverse association was observed between dietary folate and BC risk (hazard ratio comparing top vs bottom quintile [HRQ5-Q1] = 0.92, 95% CI = 0.83 to 1.01, P trend = .037). In premenopausal women, we observed a statistically significant trend towards lower risk in estrogen receptor-negative BC (HRQ5-Q1 = 0.66, 95% CI = 0.45 to 0.96, P trend = .042) and progesterone receptor-negative BC (HRQ5-Q1 = 0.70, 95% CI = 0.51 to 0.97, P trend = .021). No associations were found in postmenopausal women. A 14% reduction in BC risk was observed when comparing the highest with the lowest dietary folate tertiles in women having a high (>12 alcoholic drinks/week) alcohol intake (HRT3-T1 = 0.86, 95% CI = 0.75 to 0.98, P interaction = .035). Higher dietary folate intake may be associated with a lower risk of sex hormone receptor-negative BC in premenopausal women. © The Author 2014. Published by Oxford University Press. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com.
    Journal of the National Cancer Institute. 01/2015; 107(1).
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    ABSTRACT: The etiology of renal cell carcinoma (RCC) is only partially understood, but a metabolic component appears likely. We investigated biomarkers of one-carbon metabolism and RCC onset and survival.
    Journal of the National Cancer Institute. 12/2014; 106(12).
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    ABSTRACT: It has recently been demonstrated that memory B cells can reenter and reengage germinal center (GC) reactions, opening the possibility that multi-hit lymphomagenesis gradually occurs throughout life during successive immunological challenges. Here, we investigated this scenario in follicular lymphoma (FL), an indolent GC-derived malignancy. We developed a mouse model that recapitulates the FL hallmark t(14;18) translocation, which results in constitutive activation of antiapoptotic protein B cell lymphoma 2 (BCL2) in a subset of B cells, and applied a combination of molecular and immunofluorescence approaches to track normal and t(14;18)+ memory B cells in human and BCL2-overexpressing B cells in murine lymphoid tissues. BCL2-overexpressing B cells required multiple GC transits before acquiring FL-associated developmental arrest and presenting as GC B cells with constitutive activation-induced cytidine deaminase (AID) mutator activity. Moreover, multiple reentries into the GC were necessary for the progression to advanced precursor stages of FL. Together, our results demonstrate that protracted subversion of immune dynamics contributes to early dissemination and progression of t(14;18)+ precursors and shapes the systemic presentation of FL patients.
    The Journal of clinical investigation. 11/2014; 124(12):5337.
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    ABSTRACT: Fish is a source of important nutrients and may play a role in preventing heart diseases and other health outcomes. However, studies of overall mortality and causespecific mortality related to fish consumption are inconclusive. We examined the rate of overall mortality, as well as mortality from ischaemic heart disease and cancer in relation to the intake of total fish, lean fish, and fatty fish in a large prospective cohort including ten European countries. More than 500,000 men and women completed a dietary questionnaire in 1992–1999 and were followed up for mortality until the end of 2010. 32,587 persons were reported dead since enrolment. Hazard ratios and their 99 % confidence interval were estimated using Cox proportional hazard regression models. Fish consumption was examined using quintiles based on reported consumption, using moderate fish consumption (third quintile) as reference, and as continuous variables, using ncrements of 10 g/day. All analyses were adjusted for possible confounders. No association was seen for fish consumption and overall or cause-specific mortality for both the categorical and the continuous analyses, but there seemed to be a U-shaped trend (p\0.000) with fatty fish consumption and total mortality and with total fish consumption and cancer mortality (p = 0.046).
    European Journal of Epidemiology 11/2014; · 5.12 Impact Factor
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    ABSTRACT: A carbohydrate-rich diet, resulting in high blood glucose and insulin, has been hypothesized as involved in colorectal cancer etiology. We investigated dietary glycemic index (GI) and glycemic load (GL), in relation to colorectal cancer, in the prospectively recruited EPIC-Italy cohort. After a median 11.7 years, 421 colorectal cancers were diagnosed among 47,749 recruited adults. GI and GL were estimated from validated food frequency questionnaires. Multivariable Cox modeling estimated hazard ratios (HRs) for associations between colorectal cancer and intakes of total, high GI and low GI carbohydrate, and GI and GL. The adjusted HR of colorectal cancer for highest vs. lowest GI quartile was 1.35; 95% CI 1.03-1.78; p trend 0.031. Increasing high GI carbohydrate intake was also significantly associated with increasing colorectal cancer risk (HR 1.45; 95% CI 1.04-2.03; p trend 0.034); while increasing low GI carbohydrate was associated with reducing risk (HR 0.73; 95% CI 0.54-0.98; p trend 0.033). High dietary GI, and high GI carbohydrate, were associated with increased risks of cancer at all colon sites (HR 1.37; 95% CI 1.00-1.88, HR 1.80;95% CI 1.22-2.65, respectively); whereas high GI carbohydrate and high GL, were associated with increased risk of proximal colon cancer (HR 1.94; 95% CI 1.18-3.16, HR 2.01; 95% CI 1.08-3.74, respectively). After stratification for waist-to-hip ratio (WHR), cancer was significantly associated with GI, and high GI carbohydrate, in those with high WHR. These findings suggest that high dietary GI, and high carbohydrate intake from high GI foods, are associated with increased risk of colorectal cancer. This article is protected by copyright. All rights reserved.
    International Journal of Cancer 11/2014; · 6.20 Impact Factor
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    ABSTRACT: Background The ¿25x25¿ strategy to tackle the global challenge of non-communicable diseases takes a traditional approach, concentrating on a few diseases and their immediate risk factors. Discussion: We propose elements of a comprehensive strategy to address NCDs that takes account of the evolving social, economic, environmental and health care contexts, while developing mechanisms to respond effectively to local patterns of disease. Principles that underpin the comprehensive strategy include: (a) a balance between measures that address health at the individual and population level; (b) the need to identify evidence-based feasible and effective approaches tailored to low and middle income countries rather than exporting questionable strategies developed in high income countries; (c) developing primary health care as a universal framework to support prevention and treatment; (d) ensuring the ability to respond in real time to the complex adaptive behaviours of the global food, tobacco, alcohol and transport industries; (e) integrating evidence-based, cost-effective, and affordable approaches within the post-2015 sustainable development agenda; (f) determination of a set of priorities based on the NCD burden within each country, taking account of what it can afford, including the level of available development assistance; and (g) change from a universal ¿one-size fits all¿ approach of relatively simple prevention oriented approaches to more comprehensive multi-sectoral and development-oriented approaches which address both health systems and the determinants of NCD risk factors.SummaryThe 25x25 is approach is absolutely necessary but insufficient to tackle the the NCD disease burden of mortality and morbidity. A more comprehensive approach is recommended.
    Globalization and Health 10/2014; 10(1):74. · 1.49 Impact Factor
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    ABSTRACT: Observational studies have suggested that the risks of non-communicable diseases in voluntary migrants become similar to those in the host population after one or more generations, supporting the hypothesis that these diseases have a predominantly environmental (rather than inherited) origin. However, no study has been conducted thus far to identify alterations at the molecular level that might mediate these changes in disease risk after migration.
    International journal of epidemiology. 10/2014;
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    ABSTRACT: A genome-wide association study (GWAS) of bladder cancer identified a genetic marker rs8102137 within the 19q12 region as a novel susceptibility variant. This marker is located upstream of the CCNE1 gene, which encodes cyclin E, a cell-cycle protein. We performed genetic fine-mapping analysis of the CCNE1 region using data from two bladder cancer GWAS (5,942 cases and 10,857 controls). We found that the original GWAS marker rs8102137 represents a group of 47 linked SNPs (with r(2) ≥ 0.7) associated with increased bladder cancer risk. From this group, we selected a functional promoter variant rs7257330, which showed strong allele-specific binding of nuclear proteins in several cell lines. In both GWASs, rs7257330 was associated only with aggressive bladder cancer, with a combined per-allele OR = 1.18 [95% confidence interval (CI), 1.09-1.27, P = 4.67 × 10(-5)] versus OR = 1.01 (95% CI, 0.93-1.10, P = 0.79) for nonaggressive disease, with P = 0.0015 for case-only analysis. Cyclin E protein expression analyzed in 265 bladder tumors was increased in aggressive tumors (P = 0.013) and, independently, with each rs7257330-A risk allele (Ptrend = 0.024). Overexpression of recombinant cyclin E in cell lines caused significant acceleration of cell cycle. In conclusion, we defined the 19q12 signal as the first GWAS signal specific for aggressive bladder cancer. Molecular mechanisms of this genetic association may be related to cyclin E overexpression and alteration of cell cycle in carriers of CCNE1 risk variants. In combination with established bladder cancer risk factors and other somatic and germline genetic markers, the CCNE1 variants could be useful for inclusion into bladder cancer risk prediction models. Cancer Res; 74(20); 5808-18. ©2014 AACR.
    Cancer Research 10/2014; 74(20):5808-18. · 9.28 Impact Factor
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    ABSTRACT: Acrylamide, classified in 1994 by IARC as 'probably carcinogenic' to humans, was discovered in 2002 in some heat-treated, carbohydrate-rich foods. The association between dietary acrylamide intake and epithelial ovarian cancer risk (EOC) has been previously studied in one case-control and three prospective cohort studies which obtained inconsistent results, and could not further examine histological subtypes other than serous EOC. The present study was carried out in the European Prospective Investigation into Cancer and Nutrition (EPIC) sub-cohort of women (n=325,006). Multivariate Cox proportional hazards models were used to assess the association between questionnaire-based acrylamide intake and EOC risk. Acrylamide was energy-adjusted using the residual method, and was evaluated both as a continuous variable (per 10µg/day) and in quintiles; when subgroups by histological EOC subtypes were analyzed, acrylamide intake was evaluated in quartiles. During a mean follow-up of 11 years, 1,191 incident EOC cases were diagnosed. At baseline, the median acrylamide intake in EPIC was 21.3 μg/day. No associations, and no evidence for a dose-response were observed between energy-adjusted acrylamide intake and EOC risk (HR10µg/day:1.02, 95%CI:0.96-1.09; HRQ5vsQ1:0.97, 95%CI:0.76-1.23). No differences were seen when invasive EOC subtypes (582 serous, 118 endometrioid, and 79 mucinous tumors) were analyzed separately. This study did not provide evidence that acrylamide intake, based on food intake questionnaires, was associated with risk for EOC in EPIC. Additional studies with more reliable estimates of exposure based on biomarkers may be needed.
    10/2014;
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    ABSTRACT: Genome-wide association studies (GWASs) of follicular lymphoma (FL) have previously identified human leukocyte antigen (HLA) gene variants. To identify additional FL susceptibility loci, we conducted a large-scale two-stage GWAS in 4,523 case subjects and 13,344 control subjects of European ancestry. Five non-HLA loci were associated with FL risk: 11q23.3 (rs4938573, p = 5.79 × 10(-20)) near CXCR5; 11q24.3 (rs4937362, p = 6.76 × 10(-11)) near ETS1; 3q28 (rs6444305, p = 1.10 × 10(-10)) in LPP; 18q21.33 (rs17749561, p = 8.28 × 10(-10)) near BCL2; and 8q24.21 (rs13254990, p = 1.06 × 10(-8)) near PVT1. In an analysis of the HLA region, we identified four linked HLA-DRβ1 multiallelic amino acids at positions 11, 13, 28, and 30 that were associated with FL risk (pomnibus = 4.20 × 10(-67) to 2.67 × 10(-70)). Additional independent signals included rs17203612 in HLA class II (odds ratio [ORper-allele] = 1.44; p = 4.59 × 10(-16)) and rs3130437 in HLA class I (ORper-allele = 1.23; p = 8.23 × 10(-9)). Our findings further expand the number of loci associated with FL and provide evidence that multiple common variants outside the HLA region make a significant contribution to FL risk.
    The American Journal of Human Genetics 10/2014; 95(4):462-71. · 11.20 Impact Factor
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    ABSTRACT: Previous epidemiological studies suggest an inverse association between allergies, marked by elevated IgE levels, and non-Hodgkin lymphoma (NHL) risk. The evidence, however, is inconsistent and prospective data are sparse. We examined the association between pre-diagnostic total (low: <20; intermediate: 20 to 100; high >100 kU/l) and specific IgE (negative: <0.35; positive ≥0.35 kU/I) concentrations against inhalant antigens and lymphoma risk in a study nested within the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. 1021 incident cases and matched controls of NHL, multiple myeloma (MM) and Hodgkin lymphoma (HL) with a mean follow-up time of 7 years were investigated. Multivariate adjusted odds ratios (ORs) with 95% confidence intervals (CI) were calculated by conditional logistic regression. Specific IgE was not associated with the risk of MM, B-NHL and B-NHL subtypes. In contrast, total IgE levels were inversely associated with the risk of MM (high level: OR=0.40 [95%CI=0.21-0.79]) and B-NHL (intermediate level: OR=0.68 [95%CI=0.53-0.88]; high level: OR=0.62 [95%CI=0.44-0.86]), largely on the basis of a strong inverse association with chronic lymphocytic leukaemia (CLL) (intermediate level: OR=0.49 [95%CI=0.30-0.80]; high level: OR=0.13 [95%CI=0.05-0.35]) risk. The inverse relationship for CLL remained significant for those diagnosed 5 years after baseline. The findings of this large prospective study demonstrated significantly lower prediagnostic total IgE levels among CLL and MM cases compared to matched controls. This corresponds to the clinical immunodeficiency state often observed in CLL patients prior to diagnosis. No support for an inverse association between prediagnostic levels of specific IgE and NHL risk was found.
    Carcinogenesis 09/2014; · 5.64 Impact Factor
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    ABSTRACT: Diffuse large B cell lymphoma (DLBCL) is the most common lymphoma subtype and is clinically aggressive. To identify genetic susceptibility loci for DLBCL, we conducted a meta-analysis of 3 new genome-wide association studies (GWAS) and 1 previous scan, totaling 3,857 cases and 7,666 controls of European ancestry, with additional genotyping of 9 promising SNPs in 1,359 cases and 4,557 controls. In our multi-stage analysis, five independent SNPs in four loci achieved genome-wide significance marked by rs116446171 at 6p25.3 (EXOC2; P = 2.33 × 10(-21)), rs2523607 at 6p21.33 (HLA-B; P = 2.40 × 10(-10)), rs79480871 at 2p23.3 (NCOA1; P = 4.23 × 10(-8)) and two independent SNPs, rs13255292 and rs4733601, at 8q24.21 (PVT1; P = 9.98 × 10(-13) and 3.63 × 10(-11), respectively). These data provide substantial new evidence for genetic susceptibility to this B cell malignancy and point to pathways involved in immune recognition and immune function in the pathogenesis of DLBCL.
    Nature genetics. 09/2014;
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    ABSTRACT: Background: Shorter telomere length (TL) has been reported to be associated with increased risk of early death in elder individuals. Telomere shortening has been also related to chromosomal instability, that may possibly contribute to the development of several types of digestive or urogenital system cancers and smoking-related tumors. Therefore, we investigated the impact of TL on bladder cancer survival. Methods: TL was measured in leukocyte DNA from whole peripheral blood using quantitative real-time PCR in 463 bladder cancer patients from a total 726 cases who were followed for up to 18 years. Results: Patients with muscle-invasive tumor/any grade had shorter telomere than patients with non-muscle-invasive tumor/high-grade and with non-muscle-invasive tumor/non high-grade (TL reference 0.7±0.2; vs. respectively, 0.8±0.2, P=3.4x10-2 and 0.8±0.2, P=3.6x10-2). Moreover, patients in the lowest quartiles of TL were associated with decreased survival after diagnosis (log-rank test, P=3.9x10-4). A Cox regression adjusted by age, cancer aggressiveness, BCG, radical cystectomy, radiotherapy and chemotherapy showed an independent effect of TL on bladder cancer survival (HR=3.9; 95% CI, 1.7-9.1; P=1.2x10-3). Conclusions: Our results suggest that leukocyte TL is only partly related to tumor aggressiveness and that shorter telomeres act as independent prognostic predictor of survival in bladder cancer patients. TL information may allow to better select therapeutic approaches in patients with the same stage and grade. Impact: Blood leukocyte TL levels could provide an additional non-invasive prognostic marker to better predict survival and personalize therapies in bladder cancer patients.
    09/2014;
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    ABSTRACT: Prospective studies examining the association between coffee and tea consumption and gastric cancer risk have shown inconsistent results. We investigated the association between coffee (total, caffeinated and decaffeinated) and tea consumption and the risk of gastric cancer by anatomical site and histological type in the EPIC study. Coffee and tea consumption was assessed by dietary questionnaires at baseline. Adjusted hazard ratios (HRs) were calculated using Cox regression models. During 11.6 years of follow up, 683 gastric adenocarcinoma cases were identified among 477,312 participants. We found no significant association between overall gastric cancer risk and consumption of total coffee (HR 1.09, 95%-CI: 0.84-1.43; quartile 4 vs. non/quartile 1), caffeinated coffee (HR 1.14, 95%-CI: 0.82-1.59; quartile 4 vs. non/quartile 1), decaffeinated coffee (HR 1.07, 95%-CI: 0.75-1.53; tertile 3 vs. non/tertile 1) and tea (HR 0.81, 95%-CI: 0.59-1.09; quartile 4 vs. non/quartile 1). When stratified by anatomical site, we observed a significant positive association between gastric cardia cancer risk and total coffee consumption per increment of 100mL/day (HR 1.06, 95%-CI: 1.03-1.11). Similarly, a significant positive association was observed between gastric cardia cancer risk and caffeinated coffee consumption (HR 1.98, 95%-CI: 1.16-3.36, P-trend=0.06; quartile 3 vs. non/quartile 1) and per increment of 100mL/day (HR 1.09, 95%-CI: 1.04-1.14). In conclusion, consumption of total, caffeinated and decaffeinated coffee and tea is not associated with overall gastric cancer risk. However, total and caffeinated coffee consumption may be associated with an increased risk of gastric cardia cancer. Further prospective studies are needed to rule out chance or confounding. © 2014 Wiley Periodicals, Inc.
    International journal of cancer. Journal international du cancer. 09/2014;
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    ABSTRACT: Inverse associations of coffee and/or tea in relation to hepatocellular carcinoma (HCC) risk have been consistently identified in studies conducted mostly in Asia where consumption patterns of such beverages differ from Europe. In the European Prospective Investigation into Cancer and nutrition (EPIC), we identified 201 HCC cases among 486,799 men/women, after a median follow-up of 11 years. We calculated adjusted hazard ratios (HR) for HCC incidence in relation to quintiles/categories of coffee/tea intakes. We found that increased coffee and tea intakes were consistently associated with lower HCC risk. The inverse associations were substantial, monotonic and statistically significant. Coffee consumers in the highest compared to the lowest quintile had lower HCC risk by 72% (HR: 0.28; 95% confidence intervals (CI): 0.16 to 0.50, P-trend <0.001). The corresponding association of tea with HCC risk was 0.41 (95% CI: 0.22 to 0.78, P-trend=0.003). There was no compelling evidence of heterogeneity of these associations across strata of important HCC risk factors, including hepatitis B or hepatitis C status (available in a nested case-control study). The inverse, monotonic associations of coffee intake with HCC were apparent for caffeinated (P-trend=0.009), but not decaffeinated (P-trend=0.45) coffee for which, however, data were available for a fraction of subjects. Results from this multi-centre, European cohort study strengthen the existing evidence regarding the inverse association between coffee/tea and HCC risk. Given the apparent lack of heterogeneity of these associations by HCC risk factors and that coffee/tea are universal exposures, our results could have important implications for high HCC risk subjects. © 2014 Wiley Periodicals, Inc.
    International journal of cancer. Journal international du cancer. 09/2014;
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    ABSTRACT: DNA methylation is a well-characterized epigenetic modification that plays an important role in the regulation of gene expression. There is growing evidence on the involvement of epigenetic mechanisms in disease onset, including cancer. Environmental factors seem to induce changes in DNA methylation affecting human health. However, little is known about basal methylation levels in healthy people and about the correlation between environmental factors and different methylation profiles. We investigated the effect of seasonality on basal methylation by testing methylation levels in the long interspersed nucleotide element-1 (LINE-1) and in two cancer-related genes (RASSF1A and MGMT) of 88 healthy male heavy smokers involved in an Italian randomized study; at enrolment the subjects donated a blood sample collected in different months. Methylation analyses were performed by pyrosequencing. Mean methylation percentage was higher in spring and summer for the LINE1, RASSF1A and MGMT genes (68.26%, 2.35%, and 9.52% respectively) compared with autumn and winter (67.43%, 2.17%, and 8.60% respectively). In particular, LINE-1 was significantly hypomethylated (p = 0.04 or 0.05 depending on the CpG island involved) in autumn and winter compared with spring and summer. Seasonality seems to be a modifier of methylation levels and this observation should be taken into account in future analyses.
    PLoS ONE 09/2014; 9(9):e106846. · 3.53 Impact Factor
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    ABSTRACT: MicroRNAs (miRNAs), a class of small non-coding RNAs, are fundamental for the post-transcriptional regulation of gene expression. Altered expression of miRNAs has been detected in cancers, not only in primary tissue but also in easily obtainable specimens like plasma and stools. miRNA expression is known to be modulated by diet (micro and macronutrients, phytochemicals) and possibly by other lifestyle factors; however, such influence has not yet been exhaustively explored in humans. In the present study, we analysed the expression levels of a panel of seven human miRNAs in plasma and stool samples of a group of 24 healthy individuals characterised by different dietary habits (eight vegans, eight vegetarians and eight subjects with omnivorous diet, all groups with similar age and sex distribution). The dual aim of the study was to identify possible differences in miRNA expression due to diet (or other lifestyle factors recorded from questionnaires) and to compare results in both types of specimens. miR-92a was differentially expressed in both plasma and stool samples and with the same trend, among the three groups with different diets (P = 0.0002 and P = 0.02, respectively, with expression levels of vegans>vegetarians>omnivores). miR-92a was also associated with low body mass index (P = 0.04 and P = 0.05, respectively) in both types of specimens, and with several dietary factors. Other analysed miRNAs (miR-16, miR-21, mir-34a and miR-222) were associated with dietary and lifestyle factors, but not consistently in both stool and plasma. Our pilot study provides the first evidence of miRNA modulation by diet and other factors, that can be detected consistently in both plasma and stools samples.
    Mutagenesis 09/2014; 29(5):385-91. · 3.50 Impact Factor
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    ABSTRACT: Normal renal function is essential for vitamin D metabolism, but it is unclear whether circulating vitamin D is associated with risk of renal cell carcinoma (RCC). We assessed whether 25-hydroxyvitamin D3 (25(OH)D3) was associated with risk of RCC and death after RCC diagnosis in the European Prospective Investigation into Cancer and Nutrition (EPIC). EPIC recruited 385,747 participants with blood samples between 1992 and 2000. The current study included 560 RCC cases, 557 individually matched controls, and 553 additional controls. Circulating 25(OH)D3 was assessed by mass spectrometry. Conditional and unconditional logistic regression models were used to calculate odds ratios and 95% confidence intervals. Death after RCC diagnosis was assessed using Cox proportional hazards models and flexible parametric survival models. A doubling of 25(OH)D3 was associated with 28% lower odds of RCC after adjustment for season of and age at blood collection, sex, and country of recruitment (odds ratio = 0.72, 95% confidence interval: 0.60, 0.86; P = 0.0004). This estimate was attenuated somewhat after additional adjustment for smoking status at baseline, circulating cotinine, body mass index (weight (kg)/height (m)2), and alcohol intake (odds ratio = 0.82, 95% confidence interval: 0.68, 0.99; P = 0.038). There was also some indication that both low and high 25(OH)D3 levels were associated with higher risk of death from any cause among RCC cases.
    American Journal of Epidemiology. 09/2014;
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    ABSTRACT: Evidence of a protective effect of several antioxidants and other nutrients on pancreatic cancer risk is inconsistent. The aim of this study was to investigate the association for prediagnostic plasma levels of carotenoids, vitamin C, retinol and tocopherols with risk of pancreatic cancer in a case-control study nested within the European Prospective Investigation into Cancer and nutrition (EPIC). 446 incident exocrine pancreatic cancer cases were matched to 446 controls by age at blood collection, study center, sex, date and time of blood collection, fasting status and hormone use. Plasma carotenoids (α- and β-carotene, lycopene, β-cryptoxanthin, canthaxanthin, zeaxanthin and lutein), α- and γ-tocopherol and retinol were measured by reverse phase high-performance liquid chromatography and plasma vitamin C by a colorimetric assay. Incidence Rate Ratios (IRRs) with 95% confidence intervals (95%CI) for pancreatic cancer risk were estimated using a conditional logistic regression analysis, adjusted for smoking status, smoking duration and intensity, waist circumference, cotinine levels and diabetes status. Inverse associations with pancreatic cancer risk were found for plasma β-carotene (IRR highest versus lowest quartile 0.52, 95%CI 0.31-0.88, p for trend=0.02), zeaxanthin (IRR highest versus lowest quartile 0.53, 95%CI 0.30-0.94, p for trend=0.06) and α-tocopherol (IRR highest versus lowest quartile 0.62, 95%CI 0.39-0.99, p for trend=0.08. For α- and β-carotene, lutein, sum of carotenoids and γ-tocopherol, heterogeneity between geographical regions was observed. In conclusion, our results show that higher plasma concentrations of β-carotene, zeaxanthin and α-tocopherol may be inversely associated with risk of pancreatic cancer, but further studies are warranted. © 2014 Wiley Periodicals, Inc.
    International Journal of Cancer 08/2014; · 6.20 Impact Factor

Publication Stats

20k Citations
4,284.85 Total Impact Points

Institutions

  • 2010–2014
    • Human Genetics Foundation Torino
      Torino, Piedmont, Italy
    • State University of New York Downstate Medical Center
      Brooklyn, New York, United States
    • University of Salzburg
      Salzburg, Salzburg, Austria
    • Radboud University Medical Centre (Radboudumc)
      Nymegen, Gelderland, Netherlands
  • 2004–2014
    • Imperial College London
      • • Department of Epidemiology and Biostatistics
      • • Department of Primary Care and Public Health
      Londinium, England, United Kingdom
    • Maastricht University
      Maestricht, Limburg, Netherlands
    • University of Florence
      • Dipartimento di Scienze Biomediche, Sperimentali e Cliniche
      Florence, Tuscany, Italy
    • IMIM Hospital del Mar Medical Research Institute
      Barcino, Catalonia, Spain
  • 2013
    • University of Malaya
      Kuala Lumpor, Kuala Lumpur, Malaysia
  • 2012–2013
    • Brown University
      • • Department of Epidemiology
      • • Division of Biology and Medicine
      Providence, RI, United States
    • University of Zurich
      • Epidemiology and Prevention of Cancer
      Zürich, ZH, Switzerland
    • Mount Sinai School of Medicine
      • Tisch Cancer Institute
      Manhattan, NY, United States
    • University of Texas MD Anderson Cancer Center
      • Division of Cancer Prevention & Population Sciences
      Houston, TX, United States
  • 2011–2013
    • University of São Paulo
      • • Departmento de Epidemologia (FSP) (São Paulo)
      • • Faculdade de Saúde Pública (FSP) (São Paulo)
      Ribeirão Preto, Estado de Sao Paulo, Brazil
    • Helmholtz Zentrum München
      • Institute of Epidemiology II
      München, Bavaria, Germany
    • King's College London
      • Institute of Psychiatry
      London, ENG, United Kingdom
    • National Research Council
      Roma, Latium, Italy
    • University of Southern California
      • Department of Preventive Medicine
      Los Angeles, CA, United States
    • The London School of Economics and Political Science
      • Department of Statistics
      London, ENG, United Kingdom
  • 2009–2013
    • Universiteit Utrecht
      • • Division of Environmental Epidemiology
      • • Institute for Risk Assessment Sciences (IRAS)
      Utrecht, Provincie Utrecht, Netherlands
    • Centers for Disease Control and Prevention
      • National Center for Chronic Disease Prevention and Health Promotion
      Druid Hills, GA, United States
    • CREAL Center for Research in Environmental Epidemiology
      Barcino, Catalonia, Spain
  • 2006–2013
    • Danish Cancer Society
      København, Capital Region, Denmark
    • Istituto Scientifico Romagnolo per lo Studio e la Cura dei Tumori
      Meldola, Emilia-Romagna, Italy
  • 2005–2013
    • University Medical Center Utrecht
      • • Department of Gastroenterology and Hepatology
      • • Julius Center for Health Sciences and Primary Care
      Utrecht, Utrecht, Netherlands
  • 2002–2013
    • Catalan Institute of Oncology
      • • Cancer Epidemiology Research Programme (PREC)
      • • Translational Research Laboratory
      Badalona, Catalonia, Spain
    • German Institute of Human Nutrition
      • Department of Epidemiology
      Potsdam, Brandenburg, Germany
  • 1982–2013
    • Università degli Studi di Torino
      • • Dipartimento di Scienze Cliniche e Biologiche
      • • Dipartimento di Psicologia
      • • Dipartimento di Biotecnologie Molecolari e Scienze per la Salute
      • • Department of Medical Science
      Torino, Piedmont, Italy
  • 2009–2012
    • National Institute for Public Health and the Environment (RIVM)
      • Centre for Nutrition and Health
      Utrecht, Utrecht, Netherlands
  • 2008–2012
    • Fondazione IRCCS Istituto Nazionale dei Tumori di Milano
      Milano, Lombardy, Italy
    • Hellenic Health Foundation
      Athínai, Attica, Greece
    • University of Leeds
      • Leeds Institute of Molecular Medicine (LIMM)
      Leeds, ENG, United Kingdom
    • Università degli studi di Cagliari
      • Department of Biomedical Science
      Cagliari, Sardinia, Italy
    • Geisel School of Medicine at Dartmouth
      • Department of Community and Family Medicine
      Hanover, New Hampshire, United States
    • Radboud University Nijmegen
      • Department of Epidemiology and Biostatistics
      Nijmegen, Provincie Gelderland, Netherlands
    • Lund University
      • Department of Occupational and Environmental Medicine
      Lund, Skane, Sweden
  • 2004–2012
    • University of Oxford
      • • Nuffield Department of Clinical Medicine
      • • Cancer Epidemiology Unit
      Oxford, ENG, United Kingdom
  • 1990–2012
    • International Agency for Research on Cancer
      • Nutritional Epidemiology Group
      Lyons, Rhône-Alpes, France
  • 2008–2011
    • Imperial Valley College
      Imperial, California, United States
  • 2007–2011
    • University of Cambridge
      • • MRC Epidemiology Unit
      • • Department of Public Health and Primary Care
      Cambridge, ENG, United Kingdom
    • Université Catholique de Lyon
      Lyons, Rhône-Alpes, France
  • 2006–2011
    • German Cancer Research Center
      • Division of Cancer Epidemiology
      Heidelberg, Baden-Wuerttemberg, Germany
  • 2003–2011
    • ISI Foundation
      Torino, Piedmont, Italy
  • 2002–2011
    • National Institutes of Health
      • Division of Cancer Epidemiology and Genetics
      Bethesda, MD, United States
  • 2007–2010
    • University of Bergen
      • Institute of Medicine
      Bergen, Hordaland Fylke, Norway
  • 1989–2010
    • National Cancer Institute (USA)
      • • Division of Cancer Epidemiology and Genetics
      • • Cancer Etiology Branch (CEB)
      Bethesda, MD, United States
  • 2008–2009
    • Umeå University
      • Department of Surgical and Perioperative Sciences
      Umeå, Västerbotten, Sweden
  • 2005–2008
    • University Hospital of Ioannina
      Yannina, Epirus, Greece
  • 2002–2007
    • Mario Negri Institute for Pharmacological Research
      • Department of Environmental Health Sciences
      Milano, Lombardy, Italy
  • 1996–2006
    • University of Milan
      Milano, Lombardy, Italy
    • Autonomous University of Barcelona
      Cerdanyola del Vallès, Catalonia, Spain
    • Università degli Studi del Sannio
      • Department of Biological Sciences
      Benevento, Campania, Italy
  • 1993–2006
    • University of Cincinnati
      • Department of Environmental Health
      Cincinnati, OH, United States
  • 2000–2004
    • Memorial Sloan-Kettering Cancer Center
      • Epidemiology & Biostatistics Group
      New York City, New York, United States
    • Centro di Riferimento per l'Epidemiologia e la Prevenzione Oncologica in Piemonte
      Torino, Piedmont, Italy
  • 1999–2004
    • CRO Centro di Riferimento Oncologico di Aviano
      Aviano, Friuli Venezia Giulia, Italy
    • Regional Environmental Protection Agency, Piedmont, Italy
      Torino, Piedmont, Italy
  • 1999–2003
    • Ospedale San Giovanni Battista, ACISMOM
      Torino, Piedmont, Italy
  • 2001
    • Università degli Studi di Genova
      Genova, Liguria, Italy
    • National Institute of Occupational Health
      Amadavad, Gujarāt, India
    • Malmö University
      Malmö, Skåne, Sweden
  • 1992–1996
    • Istituto per lo Studio e la Prevenzione Oncologica (ISPO)
      Florens, Tuscany, Italy
  • 1994
    • University of Verona
      Verona, Veneto, Italy
  • 1990–1993
    • Istituto Superiore di Sanità
      Roma, Latium, Italy
  • 1988–1993
    • Rhein Main Medical Center
      Wiesbaden, Hesse, Germany
  • 1988–1989
    • Massachusetts Institute of Technology
      • Department of Chemistry
      Cambridge, MA, United States