Imperial College London

ProfessorPaoloVineis

Faculty of MedicineSchool of Public Health

Chair in Environmental Epidemiology
 
 
 
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Contact

 

+44 (0)20 7594 3372p.vineis Website

 
 
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Location

 

511Medical SchoolSt Mary's Campus

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Summary

 

Publications

Publication Type
Year
to

805 results found

Espin-Perez A, Font-Ribera L, van Veldhoven K, Krauskopf J, Portengen L, Chadeau-Hyam M, Vermeulen R, Grimalt JO, Villanueva CM, Vineis P, Kogevinas M, Kleinjans JC, de Kok TMet al., 2018, Blood transcriptional and microRNA responses to short-term exposure to disinfection by-products in a swimming pool, ENVIRONMENT INTERNATIONAL, Vol: 110, Pages: 42-50, ISSN: 0160-4120

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Gulliver J, Morley D, Dunster C, McCrea A, van Nunen E, Tsai M-Y, Probst-Hensch N, Eeftens M, Imboden M, Ducret-Stich R, Naccarati A, Galassi C, Ranzi A, Nieuwenhuijsen M, Curto A, Donaire-Gonzalez D, Cirach M, Vermeulen R, Vineis P, Hoek G, Kelly FJet al., 2018, Land use regression models for the oxidative potential of fine particles (PM2.5) in five European areas., Environ Res, Vol: 160, Pages: 247-255

Oxidative potential (OP) of particulate matter (PM) is proposed as a biologically-relevant exposure metric for studies of air pollution and health. We aimed to evaluate the spatial variability of the OP of measured PM2.5 using ascorbate (AA) and (reduced) glutathione (GSH), and develop land use regression (LUR) models to explain this spatial variability. We estimated annual average values (m-3) of OPAA and OPGSH for five areas (Basel, CH; Catalonia, ES; London-Oxford, UK (no OPGSH); the Netherlands; and Turin, IT) using PM2.5 filters. OPAA and OPGSH LUR models were developed using all monitoring sites, separately for each area and combined-areas. The same variables were then used in repeated sub-sampling of monitoring sites to test sensitivity of variable selection; new variables were offered where variables were excluded (p > .1). On average, measurements of OPAA and OPGSH were moderately correlated (maximum Pearson's maximum Pearson's R = = .7) with PM2.5 and other metrics (PM2.5absorbance, NO2, Cu, Fe). HOV (hold-out validation) R2 for OPAA models was .21, .58, .45, .53, and .13 for Basel, Catalonia, London-Oxford, the Netherlands and Turin respectively. For OPGSH, the only model achieving at least moderate performance was for the Netherlands (R2 = .31). Combined models for OPAA and OPGSH were largely explained by study area with weak local predictors of intra-area contrasts; we therefore do not endorse them for use in epidemiologic studies. Given the moderate correlation of OPAA with other pollutants, the three reasonably performing LUR models for OPAA could be used independently of other pollutant metrics in epidemiological studies.

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Ambatipudi S, Horvath S, Perrier F, Cuenin C, Hernandez-Vargas H, Le Calvez-Kelm F, Durand G, Byrnes G, Ferrari P, Bouaoun L, Sklias A, Chajes V, Overvad K, Seven G, Baglietto L, Clavel-Chapelon F, Kaaks R, Barrdahl M, Boeing H, Trichopoulou A, Lagiou P, Naska A, Masala G, Agnoli C, Polidoro S, Tumino R, Panico S, Dolle M, Peeters PHM, Onland-Moret NC, Sandanger TM, Nost TH, Weiderpass E, Quiros JR, Agudo A, Rodriguez-Barranco M, Castano JMH, Barricarte A, Fernandez AM, Travis RC, Vineis P, Muller DC, Riboli E, Gunter M, Romieu I, Herceg Zet al., 2017, DNA methylome analysis identifies accelerated epigenetic ageing associated with postmenopausal breast cancer susceptibility, EUROPEAN JOURNAL OF CANCER, Vol: 75, Pages: 299-307, ISSN: 0959-8049

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Andersen ZJ, Pedersen M, Weinmayr G, Stafoggia M, Galassi C, Jørgensen JT, Sommar JN, Forsberg B, Olsson D, Oftedal B, Aasvang GM, Schwarze P, Pyko A, Pershagen G, Korek M, De Faire U, Östenson C-G, Fratiglioni L, Eriksen KT, Poulsen AH, Tjønneland A, Vaclavik Bräuner E, Peeters PH, Bueno-de-Mesquita B, Jaensch A, Nagel G, Lang A, Wang M, Tsai M-Y, Grioni S, Marcon A, Krogh V, Ricceri F, Sacerdote C, Migliore E, Vermeulen R, Sokhi R, Keuken M, de Hoogh K, Beelen R, Vineis P, Cesaroni G, Brunekreef B, Hoek G, Raaschou-Nielsen Oet al., 2017, Long-term Exposure to Ambient Air Pollution and Incidence of Brain Tumor: the European Study of Cohorts for Air Pollution Effects (ESCAPE)., Neuro Oncol

Background: Epidemiological evidence on the association between ambient air pollution and brain tumor risk is sparse and inconsistent. Methods: In 12 cohorts from six European countries, individual estimates of annual mean air pollution levels at the baseline residence were estimated by standardized land-use regression models developed within the ESCAPE and TRANSPHORM projects: particulate matter (PM) ≤ 2.5, ≤ 10, and 2.5-10 μm in diameter (PM2.5, PM10, and PMcoarse), PM2.5 absorbance, nitrogen oxides (NO2 and NOx) and elemental composition of PM. We estimated cohort-specific associations of air pollutant concentrations and traffic intensity with total, malignant and nonmalignant brain tumor, in separate Cox regression models, adjusting for risk factors, and pooled cohort-specific estimates using random-effects meta-analyses. Results: Of 282,194 subjects from 12 cohorts, 466 developed malignant brain tumors during 12 years of follow-up. Six of the cohorts had also data on nonmalignant brain tumor, where among 106,786 subjects, 366 developed brain tumor: 176 nonmalignant and 190 malignant. We found a positive, statistically non-significant association between malignant brain tumor and PM2.5 absorbance (Hazard Ratio and 95% Confidence Interval: 1.67; 0.89-3.14 per 10 -5/m 3), and weak positive or null associations with the other pollutants. Hazard ratio for PM2.5 absorbance (1.01; 0.38-2.71 per 10 -5/m 3) and all other pollutants were lower for nonmalignant than for malignant brain tumors. Conclusion: We found suggestive evidence of an association between long-term exposure to PM2.5 absorbance indicating traffic-related air pollution and malignant brain tumors, and no association with overall or nonmalignant brain tumors.

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Andersen ZJ, Stafoggia M, Weinmayr G, Pedersen M, Galassi C, Jorgensen JT, Oudin A, Forsberg B, Olsson D, Oftedal B, Aasvang GM, Aamodt G, Pyko A, Pershagen G, Korek M, De Faire U, Pedersen NL, Ostenson C-G, Fratiglioni L, Eriksen KT, Tjonneland A, Peeters PH, Bueno-de-Mesquita B, Plusquin M, Key TJ, Jaensch A, Nagel G, Lang A, Wang M, Tsai M-Y, Fournier A, Boutron-Ruault M-C, Baglietto L, Grioni S, Marcon A, Krogh V, Ricceri F, Sacerdote C, Migliore E, Tamayo-Uria I, Amiano P, Dorronsoro M, Vermeulen R, Sokhi R, Keuken M, de Hoogh K, Beelen R, Vineis P, Cesaroni G, Brunekreef B, Hoek G, Raaschou-Nielsen Oet al., 2017, Long-Term Exposure to Ambient Air Pollution and Incidence of Postmenopausal Breast Cancer in 15 European Cohorts within the ESCAPE Project, ENVIRONMENTAL HEALTH PERSPECTIVES, Vol: 125, ISSN: 0091-6765

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Baglietto L, Ponzi E, Haycock P, Hodge A, Assumma MB, Jung C-H, Chung J, Fasanelli F, Guida F, Campanella G, Chadeau-Hyam M, Grankvist K, Johansson M, Ala U, Provero P, Wong EM, Joo J, English DR, Kazmi N, Lund E, Faltus C, Kaaks R, Risch A, Barrdahl M, Sandanger TM, Southey MC, Giles GG, Johansson M, Vineis P, Polidoro S, Relton CL, Severi Get al., 2017, DNA methylation changes measured in pre-diagnostic peripheral blood samples are associated with smoking and lung cancer risk, INTERNATIONAL JOURNAL OF CANCER, Vol: 140, Pages: 50-61, ISSN: 0020-7136

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Barrera-Gomez J, Agier L, Portengen L, Chadeau-Hyam M, Giorgis-Allemand L, Siroux V, Robinson O, Vlaanderen J, Gonzalez JR, Nieuwenhuijsen M, Vineis P, Vrijheid M, Vermeulen R, Slama R, Basagana Xet al., 2017, A systematic comparison of statistical methods to detect interactions in exposome-health associations, ENVIRONMENTAL HEALTH, Vol: 16, ISSN: 1476-069X

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Bernatsky S, Velásquez García HA, Spinelli JJ, Gaffney P, Smedby KE, Ramsey-Goldman R, Wang SS, Adami H-O, Albanes D, Angelucci E, Ansell SM, Asmann YW, Becker N, Benavente Y, Berndt SI, Bertrand KA, Birmann BM, Boeing H, Boffetta P, Bracci PM, Brennan P, Brooks-Wilson AR, Cerhan JR, Chanock SJ, Clavel J, Conde L, Cotenbader KH, Cox DG, Cozen W, Crouch S, De Roos AJ, de Sanjose S, Di Lollo S, Diver WR, Dogan A, Foretova L, Ghesquières H, Giles GG, Glimelius B, Habermann TM, Haioun C, Hartge P, Hjalgrim H, Holford TR, Holly EA, Jackson RD, Kaaks R, Kane E, Kelly RS, Klein RJ, Kraft P, Kricker A, Lan Q, Lawrence C, Liebow M, Lightfoot T, Link BK, Maynadie M, McKay J, Melbye M, Molina TJ, Monnereau A, Morton LM, Nieters A, North KE, Novak AJ, Offit K, Purdue MP, Rais M, Riby J, Roman E, Rothman N, Salles G, Severi G, Severson RK, Skibola CF, Slager SL, Smith A, Smith MT, Southey MC, Staines A, Teras LR, Thompson CA, Tilly H, Tinker LF, Tjonneland A, Turner J, Vajdic CM, Vermeulen RCH, Vijai J, Vineis P, Virtamo J, Wang Z, Weinstein S, Witzig TE, Zelenetz A, Zeleniuch-Jacquotte A, Zhang Y, Zheng T, Zucca M, Clarke AEet al., 2017, Lupus-related single nucleotide polymorphisms and risk of diffuse large B-cell lymphoma., Lupus Sci Med, Vol: 4, ISSN: 2053-8790

Objective: Determinants of the increased risk of diffuse large B-cell lymphoma (DLBCL) in SLE are unclear. Using data from a recent lymphoma genome-wide association study (GWAS), we assessed whether certain lupus-related single nucleotide polymorphisms (SNPs) were also associated with DLBCL. Methods: GWAS data on European Caucasians from the International Lymphoma Epidemiology Consortium (InterLymph) provided a total of 3857 DLBCL cases and 7666 general-population controls. Data were pooled in a random-effects meta-analysis. Results: Among the 28 SLE-related SNPs investigated, the two most convincingly associated with risk of DLBCL included the CD40 SLE risk allele rs4810485 on chromosome 20q13 (OR per risk allele=1.09, 95% CI 1.02 to 1.16, p=0.0134), and the HLA SLE risk allele rs1270942 on chromosome 6p21.33 (OR per risk allele=1.17, 95% CI 1.01 to 1.36, p=0.0362). Of additional possible interest were rs2205960 and rs12537284. The rs2205960 SNP, related to a cytokine of the tumour necrosis factor superfamily TNFSF4, was associated with an OR per risk allele of 1.07, 95% CI 1.00 to 1.16, p=0.0549. The OR for the rs12537284 (chromosome 7q32, IRF5 gene) risk allele was 1.08, 95% CI 0.99 to 1.18, p=0.0765. Conclusions: These data suggest several plausible genetic links between DLBCL and SLE.

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Boccardi M, Gallo V, Yasui Y, Vineis P, Padovani A, Mosimann U, Giannakopoulos P, Gold G, Dubois B, Jack CR, Winblad B, Frisoni GB, Albanese Eet al., 2017, The biomarker-based diagnosis of Alzheimer's disease. 2-lessons from oncology, NEUROBIOLOGY OF AGING, Vol: 52, Pages: 141-152, ISSN: 0197-4580

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Carayol M, Leitzmann MF, Ferrari P, Zamora-Ros R, Achaintre D, Stepien M, Schmidt JA, Travis RC, Overvad K, Tjonneland A, Hansen L, Kaaks R, Kuehn T, Boein H, Bachlechner U, Trichoroulou A, Bamia C, Palli D, Agnoli C, Tumino R, Vineis P, Panico S, Quiros JR, Sanchez-Cantalejo E, Huerta JM, Ardanaz E, Arriola L, Agudo A, Nilsson J, Melander E, Bueno-de-Mesquita B, Peeters PH, Wareham N, Khaw K-T, Jenab M, Key TJ, Scalbert A, Rinaldi Set al., 2017, Blood Metabolic Signatures of Body Mass Index: A Targeted Metabolomics Study in the EPIC Cohort, JOURNAL OF PROTEOME RESEARCH, Vol: 16, Pages: 3137-3146, ISSN: 1535-3893

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Chatziioannou A, Georgiadis P, Hebels DG, Liampa I, Valavanis I, Bergdahl IA, Johansson A, Palli D, Chadeau-Hyam M, Siskos AP, Keun H, Botsivali M, de Kok TMCM, Perez AE, Kleinjans JCS, Vineis P, Kyrtopoulos SAet al., 2017, Blood-based omic profiling supports female susceptibility to tobacco smoke-induced cardiovascular diseases, SCIENTIFIC REPORTS, Vol: 7, ISSN: 2045-2322

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Dossus L, Franceschi S, Biessy C, Navionis A-S, Travis RC, Weiderpass E, Scalbert A, Romieu I, Tjønneland A, Olsen A, Overvad K, Boutron-Ruault M-C, Bonnet F, Fournier A, Fortner RT, Kaaks R, Aleksandrova K, Trichopoulou A, La Vecchia C, Peppa E, Tumino R, Panico S, Palli D, Agnoli C, Vineis P, Bueno-de-Mesquita B, Peeters PH, Skeie G, Zamora-Ros R, Chirlaque M-D, Ardanaz E, Sánchez M-J, Quirós JR, Dorronsoro M, Sandström M, Nilsson LM, Schmidt JA, Khaw K-T, Tsilidis KK, Aune D, Riboli E, Rinaldi Set al., 2017, Adipokines and inflammation markers and risk of differentiated thyroid carcinoma: The EPIC study., Int J Cancer

Other than the influence of ionizing radiation and benign thyroid disease, little is known about the risk factors for differentiated thyroid cancer (TC) which is an increasing common cancer worldwide. Consistent evidence shows that body mass is positively associated with TC risk. As excess weight is a state of chronic inflammation, we investigated the relationship between concentrations of leptin, adiponectin, C-reactive protein, interleukin(IL)-6, IL-10 and TNF-α and the risk of TC. A case-control study was nested within the European Prospective Investigation into Cancer and Nutrition (EPIC) study and included 475 first primary incident TC cases (399 women and 76 men) and 1,016 matched cancer-free cohort participants. Biomarkers were measured in serum samples using validated and highly sensitive commercially available immunoassays. Odds ratios (ORs) of TC by levels of each biomarker were estimated using conditional logistic regression models, adjusting for BMI and alcohol consumption. Adiponectin was inversely associated with TC risk among women (ORT3vs.T1 =0.69, 95%CI: 0.49-0.98, Ptrend =0.04) but not among men (ORT3vs.T1 =1.36, 95%CI: 0.67-2.76, Ptrend =0.37). Increasing levels of IL-10 were positively associated with TC risk in both genders and significantly so in women (ORT3vs.T1 =1.59, 95%CI: 1.13-2.25, Ptrend =0.01) but not in men (ORT3vs.T1 =1.78, 95%CI: 0.80-3.98, Ptrend =0.17). Leptin, CRP, IL-6 and TNF-α were not associated with TC risk in either gender. These results indicate a positive association of TC risk with IL-10 and a negative association with adiponectin that is probably restricted to women. Inflammation may play a role in TC in combination with or independently of excess weight. This article is protected by copyright. All rights reserved.

JOURNAL ARTICLE

Duell EJ, Lujan-Barroso L, Sala N, McElyea SD, Overvad K, Tjonneland A, Olsen A, Weiderpass E, Busund L-T, Moi L, Muller D, Vineis P, Aune D, Matullo G, Naccarati A, Panico S, Tagliabue G, Tumino R, Palli D, Kaaks R, Katzke VA, Boeing H, Bueno-de-Mesquita HBA, Peeters PH, Trichopoulou A, Lagiou P, Kotanidou A, Travis RC, Wareham N, Khaw K-T, Quiros JR, Rodriguez-Barranco M, Dorronsoro M, Chirlaque M-D, Ardanaz E, Severi G, Boutron-Ruault M-C, Rebours V, Brennan P, Gunter M, Scelo G, Cote G, Sherman S, Korc Met al., 2017, Plasma microRNAs as biomarkers of pancreatic cancer risk in a prospective cohort study, INTERNATIONAL JOURNAL OF CANCER, Vol: 141, Pages: 905-915, ISSN: 0020-7136

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Ek WE, Tobi EW, Ahsan M, Lampa E, Ponzi E, Kyrtopoulos SA, Georgiadis P, Lumey LH, Heijmans BT, Botsivali M, Bergdahl IA, Karlsson T, Rask-Andersen M, Palli D, Ingelsson E, Hedman AK, Nilsson LM, Vineis P, Lind L, Flanagan JM, Johansson Aet al., 2017, Tea and coffee consumption in relation to DNA methylation in four European cohorts, HUMAN MOLECULAR GENETICS, Vol: 26, Pages: 3221-3231, ISSN: 0964-6906

JOURNAL ARTICLE

Fehringer G, Brenner DR, Zhang Z-F, Lee Y-CA, Matsuo K, Ito H, Lan Q, Vineis P, Johansson M, Overvad K, Riboli E, Trichopoulou A, Sacerdote C, Stucker I, Boffetta P, Brennan P, Christiani DC, Hong Y-C, Landi MT, Morgenstern H, Schwartz AG, Wenzlaff AS, Rennert G, McLaughlin JR, Harris CC, Olivo-Marston S, Orlow I, Park BJ, Zauderer M, Barros Dios JM, Ruano Ravina A, Siemiatycki J, Koushik A, Lazarus P, Fernandez-Somoano A, Tardon A, Le Marchand L, Brenner H, Saum K-U, Duell EJ, Andrew AS, Szeszenia-Dabrowska N, Lissowska J, Zaridze D, Rudnai P, Fabianova E, Mates D, Foretova L, Janout V, Bencko V, Holcatova I, Pesatori AC, Consonni D, Olsson A, Straif K, Hung RJet al., 2017, Alcohol and lung cancer risk among never smokers: A pooled analysis from the international lung cancer consortium and the SYNERGY study, INTERNATIONAL JOURNAL OF CANCER, Vol: 140, Pages: 1976-1984, ISSN: 0020-7136

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Fiorito G, Polidoro S, Dugue P-A, Kivimaki M, Ponzi E, Matullo G, Guarrera S, Assumma MB, Georgiadis P, Kyrtopoulos SA, Krogh V, Palli D, Panico S, Sacerdote C, Tumino R, Chadeau-Hyam M, Stringhini S, Severi G, Hodge AM, Giles GG, Marioni R, Linner RK, O'Halloran AM, Kenny RA, Layte R, Baglietto L, Robinson O, McCrory C, Milne RL, Vineis Pet al., 2017, Social adversity and epigenetic aging: a multi-cohort study on socioeconomic differences in peripheral blood DNA methylation, SCIENTIFIC REPORTS, Vol: 7, ISSN: 2045-2322

JOURNAL ARTICLE

Fiorito G, Vlaanderen J, Polidoro S, Gulliver J, Galassi C, Ranzi A, Krogh V, Grioni S, Agnoli C, Sacerdote C, Panico S, Tsai M-Y, Probst-Hensch N, Hoek G, Herceg Z, Vermeulen R, Ghantous A, Vineis P, Naccarati A, EXPOsOMICS consortiumet al., 2017, Oxidative stress and inflammation mediate the effect of air pollution on cardio- and cerebrovascular disease: A prospective study in nonsmokers., Environ Mol Mutagen

Air pollution is associated with a broad range of adverse health effects, including mortality and morbidity due to cardio- and cerebrovascular diseases (CCVD), but the molecular mechanisms involved are not entirely understood. This study aims to investigate the involvement of oxidative stress and inflammation in the causal chain, and to identify intermediate biomarkers that are associated retrospectively with the exposure and prospectively with the disease. We designed a case-control study on CCVD nested in a cohort of 18,982 individuals from the EPIC-Italy study. We measured air pollution, inflammatory biomarkers, and whole-genome DNA methylation in blood collected up to 17 years before the diagnosis. The study sample includes all the incident CCVD cases among former- and never-smokers, with available stored blood sample, that arose in the cohort during the follow-up. We identified enrichment of altered DNA methylation in "ROS/Glutathione/Cytotoxic granules" and "Cytokine signaling" pathways related genes, associated with both air pollution (multiple comparisons adjusted p for enrichment ranging from 0.01 to 0.03 depending on pollutant) and with CCVD risk (P = 0.04 and P = 0.03, respectively). Also, Interleukin-17 was associated with higher exposure to NO2 (P = 0.0004), NOx (P = 0.0005), and CCVD risk (OR = 1.79; CI 1.04-3.11; P = 0.04 comparing extreme tertiles). Our findings indicate that chronic exposure to air pollution can lead to oxidative stress, which in turn activates a cascade of inflammatory responses mainly involving the "Cytokine signaling" pathway, leading to increased risk of CCVD. Inflammatory proteins and DNA methylation alterations can be detected several years before CCVD diagnosis in blood samples, being promising preclinical biomarkers. Environ. Mol. Mutagen., 2017. © 2017 Wiley Periodicals, Inc.

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Frisoni GB, Boccardi M, Barkhof F, Blennow K, Cappa S, Chiotis K, Demonet J-F, Garibotto V, Giannakopoulos P, Gietl A, Hansson O, Herholz K, Jack CR, Nobili F, Nordberg A, Snyder HM, Ten Kate M, Varrone A, Albanese E, Becker S, Bossuyt P, Carrillo MC, Cerami C, Dubois B, Gallo V, Giacobini E, Gold G, Hurst S, Loenneborg A, Lovblad K-O, Mattsson N, Molinuevo J-L, Monsch AU, Mosimann U, Padovani A, Picco A, Porteri C, Ratib O, Saint-Aubert L, Scerri C, Scheltens P, Schott JM, Sonni I, Teipel S, Vineis P, Visser PJ, Yasui Y, Winblad Bet al., 2017, Strategic roadmap for an early diagnosis of Alzheimer's disease based on biomarkers, LANCET NEUROLOGY, Vol: 16, Pages: 661-676, ISSN: 1474-4422

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Georgiadis P, Liampa I, Hebels DG, Krauskopf J, Chatziioannou A, Valavanis I, de Kok TMCM, Kleinjans JCS, Bergdahl IA, Melin B, Spaeth F, Palli D, Vermeulen RCH, Vlaanderen J, Chadeau-Hyam M, Vineis P, Kyrtopoulos SAet al., 2017, Evolving DNA methylation and gene expression markers of B-cell chronic lymphocytic leukemia are present in pre-diagnostic blood samples more than 10 years prior to diagnosis, BMC GENOMICS, Vol: 18, ISSN: 1471-2164

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Gunter MJ, Murphy N, Cross AJ, Dossus L, Dartois L, Fagherazzi G, Kaaks R, Kuehn T, Boeing H, Aleksandrova K, Tjonneland A, Olsen A, Overvad K, Larsen SC, Redondo Cornejo ML, Agudo A, Sanchez Perez MJ, Altzibar JM, Navarro C, Ardanaz E, Khaw K-T, Butterworth A, Bradbury KE, Trichopoulou A, Lagiou P, Trichopoulos D, Palli D, Grioni S, Vineis P, Panico S, Tumino R, Bueno-de-Mesquita B, Siersema P, Leenders M, Beulens JWJ, Uiterwaal CU, Wallstrom P, Nilsson LM, Landberg R, Weiderpass E, Skeie G, Braaten T, Brennan P, Licaj I, Muller DC, Sinha R, Wareham N, Riboli Eet al., 2017, Coffee Drinking and Mortality in 10 European Countries A Multinational Cohort Study, ANNALS OF INTERNAL MEDICINE, Vol: 167, Pages: 236-+, ISSN: 0003-4819

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Herceg Z, Ghantous A, Wild CP, Sklias A, Casati L, Duthie SJ, Fry R, Issa J-P, Kellermayer R, Koturbash I, Kondo Y, Lepeule J, Lima SCS, Marsit CJ, Rakyan V, Saffery R, Taylor JA, Teschendorff AE, Ushijima T, Vineis P, Walker CL, Waterland RA, Wiemels J, Ambatipudi S, Degli Esposti D, Hernandez-Vargas Het al., 2017, Roadmap for investigating epigenome deregulation and environmental origins of cancer., Int J Cancer

The interaction between the (epi)genetic makeup of an individual and his/her environmental exposure record (exposome) is accepted as a determinant factor for a significant proportion of human malignancies. Recent evidence has highlighted the key role of epigenetic mechanisms in mediating gene-environment interactions and translating exposures into tumorigenesis. There is also growing evidence that epigenetic changes may be risk factor-specific ("fingerprints") that should prove instrumental in the discovery of new biomarkers in cancer. Here, we review the state of the science of epigenetics associated with environmental stimuli and cancer risk, highlighting key developments in the field. Critical knowledge gaps and research needs are discussed and advances in epigenomics that may help in understanding the functional relevance of epigenetic alterations. Key elements required for causality inferences linking epigenetic changes to exposure and cancer are discussed and how these alterations can be incorporated in carcinogen evaluation and in understanding mechanisms underlying epigenome deregulation by the environment.

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Jay R, Brennan P, Brenner, Overvad K, Olsen A, Tjønneland A, Boutron-Ruault MC, Clavel-Chapelon F, Fagherazzi, Katzke V, Kühn T, Boeing H, Bergmann MM, Steffen A, Naska A, Trichopoulou A, Trichopoulos D, Saieva C, Grioni S, Panico S, Tumino R, Vineis P, Bueno-de-Mesquita HB, Peeters PH, Hjartåker A, Weiderpass E, Arriola L, Molina-Montes E, Duell EJ, Santiuste C, Alonso de la Torre R, Barricarte Gurrea A, Stocks T, Johansson M, Ljungberg B, Wareham N, Khaw KT, Travis RC, Cross AJ, Murphy N, Riboli E, Scelo Get al., 2017, Alcohol consumption and the risk of renal cancers in the European Prospective Investigation into Cancer and Nutrition (EPIC). Wozniak MB, Brennan P, Brenner DR, Overvad K, Olsen A, Tjønneland A, Boutron-Ruault MC, Clavel-Chapelon F, Fagherazzi G, Katzke V, Kühn T, Boeing H, Bergmann MM, Steffen A, Naska A, Trichopoulou A, Trichopoulos D, Saieva C, Grioni S, Panico S, Tumino R, Vineis P, Bueno-de-Mesquita HB, Peeters PH, Hjartåker A, Weiderpass E, Arriola L, Molina-Montes E, Duell EJ, Santiuste C, Alonso de la Torre R, Barricarte Gurrea A, Stocks T, Johansson M, Ljungberg B, Wareham N, Khaw KT, Travis RC, Cross AJ, Murphy N, Riboli E, Scelo G.Int J Cancer. 2015 Oct 15;137(8):1953-66. [Epub 2015 Apr 28]. doi: 10.1002/ijc.29559., Urol Oncol, Vol: 35

Epidemiologic studies have reported that moderate alcohol consumption is inversely associated with the risk of renal cancer. However, there is no information available on the associations in renal cancer subsites. From 1992 to 2010, 477,325 men and women in the European Prospective Investigation into Cancer and Nutrition cohort were followed for incident renal cancers (n = 931). Baseline and lifetime alcohol consumption was assessed by country-specific, validated dietary questionnaires. Information on past alcohol consumption was collected by lifestyle questionnaires. Hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated from Cox proportional hazard models. In multivariate analysis, total alcohol consumption at baseline was inversely associated with renal cancer; the HR and 95% CI for the increasing categories of total alcohol consumption at recruitment vs. the light drinkers category were 0.78 (0.62-0.99), 0.82 (0.64-1.04), 0.70 (0.55-0.90), and 0.91 (0.63-1.30), respectively, (ptrend = 0.001). A similar relationship was observed for average lifetime alcohol consumption and for all renal cancer subsites combined or for renal parenchyma subsite. The trend was not observed in hypertensive individuals and not significant in smokers. In conclusion, moderate alcohol consumption was associated with a decreased risk of renal cancer.

JOURNAL ARTICLE

Kelly RS, Kiviranta H, Bergdahl IA, Palli D, Johansson A-S, Botsivali M, Vineis P, Vermeulen R, Kyrtopoulos SA, Chadeau-Hyam Met al., 2017, Prediagnostic plasma concentrations of organochlorines and risk of B-cell non-Hodgkin lymphoma in envirogenomarkers: a nested case-control study, ENVIRONMENTAL HEALTH, Vol: 16, ISSN: 1476-069X

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Kelly-Irving M, Delpierre C, Vineis P, 2017, Beyond bad luck: induced mutations and hallmarks of cancer, LANCET ONCOLOGY, Vol: 18, Pages: 999-1000, ISSN: 1470-2045

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