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Pancreatic Neoplasms: HELP
Articles by Miren Dorronsoro
Based on 16 articles published since 2010
(Why 16 articles?)
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Between 2010 and 2020, M. Dorronsoro wrote the following 16 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Article Dietary folate intake and pancreatic cancer risk: Results from the European prospective investigation into cancer and nutrition. 2019

Park, Jin Young / Bueno-de-Mesquita, H Bas / Ferrari, Pietro / Weiderpass, Elisabete / de Batlle, Jordi / Tjønneland, Anne / Kyro, Cecilie / Rebours, Vinciane / Boutron-Ruault, Marie-Christine / Mancini, Francesca Romana / Katzke, Verena / Kühn, Tilman / Boeing, Heiner / Trichopoulou, Antonia / La Vecchia, Carlo / Kritikou, Maria / Masala, Giovanna / Pala, Valeria / Tumino, Rosario / Panico, Salvatore / Peeters, Petra H / Skeie, Guri / Merino, Susana / Duell, Eric J / Rodríguez-Barranco, Miguel / Dorronsoro, Miren / Chirlaque, Maria-Dolores / Ardanaz, Eva / Gylling, Björn / Schneede, Jörn / Ericson, Ulrika / Sternby, Hanna / Khaw, Kay-Tee / Bradbury, Kathryn E / Huybrechts, Inge / Aune, Dagfinn / Vineis, Paolo / Slimani, Nadia. ·International Agency for Research on Cancer, Lyon, France. · National Institute for Public Health and the Environment (RIVM), Bilthoven, The Netherlands. · Department of Gastroenterology and Hepatology, University Medical Centre, Utrecht, The Netherlands. · School of Public Health, Imperial College London, London, United Kingdom. · Department of Community Medicine, Faculty of Health Sciences, University of Tromsø, Tromsø, Norway. · Cancer Registry of Norway, Institute of Population-Based Cancer Research, Oslo, Norway. · Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden. · Genetic Epidemiology Group, Folkhälsan Research Center, Helsinki, Finland. · Group of Translational Research in Respiratory Medicine, IRBLleida, Hospital Universitari Arnau de Vilanova and Santa Maria, Lleida, Spain. · Centro de Investigación Biomédica en Red de Enfermedades Respiratorias (CIBERES), Madrid, Spain. · Danish Cancer Society Research Center, Copenhagen, Denmark. · Pancreatology Unit, Beaujon Hospital, Clichy, France. · INSERM-UMR 1149, University Paris 7, France. · CESP, INSERM U1018, University of Paris-Sud, UVSQ, Université Paris-Saclay, France. · Gustave Roussy, Villejuif, France. · German Cancer Research Center (DKFZ), Division of Cancer Epidemiology, Heidelberg, Germany. · Department of Epidemiology, German Institute of Human Nutrition (DIfE) Potsdam-Rehbrücke, Germany. · Hellenic Health Foundation, Athens, Greece. · Department of Clinical Sciences and Community Health, Università degli Studi di Milano, Milan, Italy. · Cancer Risk Factors and Life-Style Epidemiology Unit, Institute for Cancer Research, Prevention and Clinical Network-ISPRO, Florence, Italy. · Epidemiology and Prevention Unit, IRCCS Foundation National Cancer Institute, Milan, Italy. · Cancer Registry and Histopathology Department, 'Civic-M.P. Arezzo' Hospital, ASP Ragusa, Italy. · Department of Clinical Medicine and Surgery, Federico II University, Naples, Italy. · Department of Epidemiology, Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht. · Public Health Directorate, Asturias, Spain. · Unit of Nutrition and Cancer, Cancer Epidemiology Research Program, Catalan Institute of Oncology-IDIBELL, L'Hospitalet de Llobregat, Barcelona, Spain. · Escuela Andaluza de Salud Pública, Instituto de Investigación Biosanitaria ibs.GRANADA, Hospitales Universitarios de Granada/Universidad de Granada, Granada, Spain. · CIBER de Epidemiología y Salud Pública (CIBERESP), Madrid, Spain. · Dirección de Salud Pública y Adicciones, Gobierno Vasco, Vitoria, Spain. · Instituto de Investigación Sanitaria Biodonostia, San Sebastián, Spain. · Department of Epidemiology, Regional Health Council, IMIB-Arrixaca, Murcia, Spain. · Department of Health and Social Sciences, Universidad de Murcia, Murcia, Spain. · Navarra Public Health Institute, Pamplona, Spain. · IdiSNA, Navarra Institute for Health Research, Pamplona, Spain. · Department of Medical Biosciences, Pathology, Umeå University, Umeå, Sweden. · Department of Clinical Pharmacology, Pharmacology and Clinical Neurosciences, Umeå University, Umeå, Sweden. · Diabetes and Cardiovascular disease, Genetic Epidemiology, Department of Clinical Sciences in Malmö, Lund University, Sweden. · Department of Surgery, Institution of Clinical Sciences Malmö, Lund University, Sweden. · Department of Public Health and Primary Care, University of Cambridge, Cambridge, United Kingdom. · Cancer Epidemiology Unit, Nuffield Department of Population Health, University of Oxford, United Kingdom. · Bjørknes University College, Oslo, Norway. · IIGM Foundation, Turin, Italy. ·Int J Cancer · Pubmed #30178496.

ABSTRACT: Pancreatic cancer (PC) has an exceptionally low survival rate and primary prevention strategies are limited. Folate plays an important role in one-carbon metabolism and has been associated with the risk of several cancers, but not consistently with PC risk. We aimed to investigate the association between dietary folate intake and PC risk, using the standardised folate database across 10 European countries. A total of 477,206 participants were followed up for 11 years, during which 865 incident primary PC cases were recorded. Folate intake was energy-adjusted using the residual method. Hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated using Cox proportional hazards models. In multivariable analyses stratified by age, sex, study centre and adjusted for energy intake, smoking status, BMI, educational level, diabetes status, supplement use and dietary fibre intake, we found no significant association between folate intake and PC risk: the HR of PC risk for those in the highest quartile of folate intake (≥353 μg/day) compared to the lowest (<241 μg/day) was 0.81 (95% CI: 0.51, 1.31; p

2 Article Lifetime and baseline alcohol intakes and risk of pancreatic cancer in the European Prospective Investigation into Cancer and Nutrition study. 2018

Naudin, Sabine / Li, Kuanrong / Jaouen, Tristan / Assi, Nada / Kyrø, Cecilie / Tjønneland, Anne / Overvad, Kim / Boutron-Ruault, Marie-Christine / Rebours, Vinciane / Védié, Anne-Laure / Boeing, Heiner / Kaaks, Rudolf / Katzke, Verena / Bamia, Christina / Naska, Androniki / Trichopoulou, Antonia / Berrino, Franco / Tagliabue, Giovanna / Palli, Domenico / Panico, Salvatore / Tumino, Rosario / Sacerdote, Carlotta / Peeters, Petra H / Bueno-de-Mesquita, H B As / Weiderpass, Elisabete / Gram, Inger Torhild / Skeie, Guri / Chirlaque, Maria-Dolores / Rodríguez-Barranco, Miguel / Barricarte, Aurelio / Quirós, Jose Ramón / Dorronsoro, Miren / Johansson, Ingegerd / Sund, Malin / Sternby, Hanna / Bradbury, Kathryn E / Wareham, Nick / Riboli, Elio / Gunter, Marc / Brennan, Paul / Duell, Eric J / Ferrari, Pietro. ·Nutritional Methodology and Biostatistics Group, International Agency for Research on Cancer, Lyon, France. · Danish Cancer Society Research Center, Copenhagen, Denmark. · Section for Epidemiology, Department of Public Health, Aarhus University, Aarhus, Denmark. · CESP, INSERM U1018, University of Paris-Sud, UVSQ, University of Paris-Saclay, Villejuif, France. · Institut Gustave Roussy, Villejuif, France. · Pancreatology Unit, Beaujon Hospital, Clichy, France. · INSERM U1149, University Paris 7, Paris, France. · Department of Epidemiology, German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE), Potsdam, Germany. · Division of Cancer Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany. · Hellenic Health Foundation, Athens, Greece. · Unit of Nutritional Epidemiology and Nutrition in Public Health, Department of Hygiene, Epidemiology and Medical Statistics, School of Medicine, WHO Collaborating Center for Nutrition and Health, National and Kapodistrian University of Athens, Athens, Greece. · Department of Preventive & Predictive Medicine, Fondazione IRCCS Istituto Nazionale dei Tumori, Milan, Italy. · Lombardy Cancer Registry Unit, Fondazione IRCCS Istituto Nazionale dei Tumori, Milan, Italy. · Cancer Risk Factors and Life-Style Epidemiology Unit, Cancer Research and Prevention Institute (ISPO), Florence, Italy. · Department of Clinical and Experimental Medicine, University Federico II, Naples, Italy. · Cancer Registry and Histopathology Department, Civic M.P.Arezzo Hospital, Ragusa, Italy, Ragusa, Italy. · Unit of Cancer Epidemiology, Hospital and Center for Cancer Prevention (CPO), Città della Salute e della Scienza University, Turin, Italy. · Department of Epidemiology, Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Utrecht, The Netherlands. · Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, London, United Kingdom. · Department for Determinants of Chronic Diseases (DCD), National Institute for Public Health and the Environment (RIVM), Bilthoven, The Netherlands. · Department of Social & Preventive Medicine, Faculty of Medicine, University of Malaya, Kuala, Malaysia, Lumpur. · Department of Community Medicine, Faculty of Health Sciences, University of Tromsø, The Arctic University of Norway, Tromsø, Norway. · Department of Research, Cancer Registry of Norway, Institute of Population-Based Cancer Research, Oslo, Norway. · Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden. · Genetic Epidemiology Group, Folkhälsan Research Center, Helsinki, Finland. · Department of Epidemiology, Regional Health Council, IMIB-Arrixaca, Murcia, Spain. · CIBER of Epidemiology and Public Health (CIBERESP), Madrid, Spain. · Department of Health and Social Sciences, University of Murcia, Murcia, Spain. · Biosanitary Investigation Institute (IBS) of Granada, University Hospital and University of Granada, Granada, Spain. · Navarra Public Health Institute, Pamplona, Spain. · Navarra Institute for Health Research (IdiSNA), Pamplona, Spain. · Public Health Directorate, Asturias, Spain. · Subdirección de Salud Pública de Gipuzkoa, Gobierno Vasco, San Sebastian, Spain. · Department of Odontology, Cariology, Umeå University, Umeå, Sweden. · Department of Surgical and Perioperative Sciences, Umeå University, Umeå, Sweden. · Department of Surgery, Institution of Clinical Sciences Malmö, Lund University, Malmö, Sweden. · Cancer Epidemiology Unit, Nuffield Department of Population Health, University of Oxford, Oxford, United Kingdom. · MRC Epidemiology Unit, University of Cambridge School of Clinical Medicine, Cambridge Biomedical Campus, Cambridge, United Kingdom. · School of Public Health, Imperial College London, London, United Kingdom. · Nutrition and Epidemiology Group, International Agency for Research on Cancer, Lyon, France. · Genetic Epidemiology Group, International Agency for Research on Cancer, Lyon, France. · Unit of Nutrition and Cancer, Catalan Institute of Oncology (ICO-Idibell), Barcelona, Spain. ·Int J Cancer · Pubmed #29524225.

ABSTRACT: Recent evidence suggested a weak relationship between alcohol consumption and pancreatic cancer (PC) risk. In our study, the association between lifetime and baseline alcohol intakes and the risk of PC was evaluated, including the type of alcoholic beverages and potential interaction with smoking. Within the European Prospective Investigation into Cancer and Nutrition (EPIC) study, 1,283 incident PC (57% women) were diagnosed from 476,106 cancer-free participants, followed up for 14 years. Amounts of lifetime and baseline alcohol were estimated through lifestyle and dietary questionnaires, respectively. Cox proportional hazard models with age as primary time variable were used to estimate PC hazard ratios (HR) and their 95% confidence interval (CI). Alcohol intake was positively associated with PC risk in men. Associations were mainly driven by extreme alcohol levels, with HRs comparing heavy drinkers (>60 g/day) to the reference category (0.1-4.9 g/day) equal to 1.77 (95% CI: 1.06, 2.95) and 1.63 (95% CI: 1.16, 2.29) for lifetime and baseline alcohol, respectively. Baseline alcohol intakes from beer (>40 g/day) and spirits/liquors (>10 g/day) showed HRs equal to 1.58 (95% CI: 1.07, 2.34) and 1.41 (95% CI: 1.03, 1.94), respectively, compared to the reference category (0.1-2.9 g/day). In women, HR estimates did not reach statistically significance. The alcohol and PC risk association was not modified by smoking status. Findings from a large prospective study suggest that baseline and lifetime alcohol intakes were positively associated with PC risk, with more apparent risk estimates for beer and spirits/liquors than wine intake.

3 Article Circulating concentrations of vitamin D in relation to pancreatic cancer risk in European populations. 2018

van Duijnhoven, Fränzel J B / Jenab, Mazda / Hveem, Kristian / Siersema, Peter D / Fedirko, Veronika / Duell, Eric J / Kampman, Ellen / Halfweeg, Anouk / van Kranen, Henk J / van den Ouweland, Jody M W / Weiderpass, Elisabete / Murphy, Neil / Langhammer, Arnulf / Ness-Jensen, Eivind / Olsen, Anja / Tjønneland, Anne / Overvad, Kim / Cadeau, Claire / Kvaskoff, Marina / Boutron-Ruault, Marie-Christine / Katzke, Verena A / Kühn, Tilman / Boeing, Heiner / Trichopoulou, Antonia / Kotanidou, Anastasia / Kritikou, Maria / Palli, Domenico / Agnoli, Claudia / Tumino, Rosario / Panico, Salvatore / Matullo, Giuseppe / Peeters, Petra / Brustad, Magritt / Olsen, Karina Standahl / Lasheras, Cristina / Obón-Santacana, Mireia / Sánchez, María-José / Dorronsoro, Miren / Chirlaque, Maria-Dolores / Barricarte, Aurelio / Manjer, Jonas / Almquist, Martin / Renström, Frida / Ye, Weimin / Wareham, Nick / Khaw, Kay-Tee / Bradbury, Kathryn E / Freisling, Heinz / Aune, Dagfinn / Norat, Teresa / Riboli, Elio / Bueno-de-Mesquita, H B As. ·National Institute for Public Health and the Environment (RIVM), Bilthoven, The Netherlands. · Division of Human Nutrition, Wageningen University & Research, Wageningen, The Netherlands. · International Agency for Research on Cancer (IARC-WHO), Lyon, France. · HUNT Research Centre, Department of Public Health and General Practice, Norwegian University of Science and Technology, Levanger, Norway. · Department of Gastroenterology and Hepatology, University Medical Center Utrecht, The Netherlands. · Department of Gastroenterology and Hepatology, Radboud University Medical Center, Nijmegen, The Netherlands. · Department of Epidemiology, Rollins School of Public Health, Winship Cancer Institute, Emory University, Atlanta, GA. · Unit of Nutrition and Cancer, Cancer Epidemiology Research Program, Catalan Institute of Oncology (ICO-IDIBELL), L'Hospitalet de Llobregat, Barcelona, Spain. · Department of Clinical Chemistry, Canisius Wilhelmina Hospital, Nijmegen, The Netherlands. · Department of Community Medicine, Faculty of Health Sciences, University of Tromsø, The Arctic University of Norway, Tromsø, Norway. · Cancer Registry of Norway, Institute for Population-based Cancer Research, Oslo, Norway. · Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden. · Genetic Epidemiology Group, Folkhälsan Research Center, Helsinki, Finland. · Danish Cancer Society Research Center, Copenhagen, Denmark. · Section for Epidemiology, Department of Public Health, Aarhus University, Aarhus C, Denmark. · Université Paris-Saclay, Université Paris-Sud, UVSQ, CESP, INSERM, Villejuif, France. · Gustave Roussy, Villejuif, F-94805, France. · Division of Cancer Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany. · Department of Epidemiology, German Institute for Human Nutrition Potsdam-Rehbrücke, Nuthetal, Germany. · Hellenic Health Foundation, Athens, Greece. · WHO Collaborating Center for Nutrition and Health, Unit of Nutritional Epidemiology and Nutrition in Public Health, Dept. of Hygiene, Epidemiology and Medical Statistics, University of Athens Medical School, Greece. · Department of Critical Care Medicine and Pulmonary Services, University of Athens Medical School, Evangelismos Hospital, Athens, Greece. · Molecular and Nutritional Epidemiology Unit, Cancer Research and Prevention Institute-ISPO, Florence, Italy. · Epidemiology and Prevention Unit, Fondazione IRCCS Istituto Nazionale dei Tumori, Milano, Italy. · Cancer Registry and Histopathology Unit, "Civic - M.P.Arezzo" Hospital, ASP Ragusa, (Italy). · Dipartimento di medicina clinica e chirurgia, Federico II university, Naples, Italy. · Department of Medical Sciences, University of Torino, Torino, Italy. · Italian Institute for Genomic Medicine (IIGM/HuGeF), Torino, Italy. · Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Utrecht, The Netherlands. · Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, United Kingdom. · Oviedo University, Asturias, Spain. · Escuela Andaluza de Salud Pública. Instituto de Investigación Biosanitaria ibs.GRANADA. Hospitales Universitarios de Granada/Universidad de Granada, Granada, Spain. · CIBER de Epidemiología y Salud Pública (CIBERESP), Spain. · Public Health Direction and Biodonostia-Ciberesp, Basque Regional Health Department, San Sebastian, Spain. · Department of Epidemiology, Regional Health Council, IMIB-Arrixaca, Murcia, Spain. · Department of Health and Social Sciences, Universidad de Murcia, Murcia, Spain. · Navarra Public Health Institute, Pamplona, Spain. · Navarra Institute for Health Research (IdiSNA) Pamplona, Spain. · Department of Surgery, Lund University, Skåne University Hospital Malmö, Malmö, Sweden. · Department of Surgery, Endocrine-Sarcoma unit, Skane University Hospital, Lund, Sweden. · Genetic and Molecular Epidemiology Unit, Department of Clinical Sciences, Lund University, Malmö, Sweden. · Department of Biobank Research, Umeå University, Umeå, Sweden. · The Medical Biobank at Umeå University, Umeå, Sweden. · MRC Epidemiology Unit, University of Cambridge, Cambridge, United Kingdom. · University of Cambridge, Cambridge, United Kingdom. · Cancer Epidemiology Unit, Nuffield Department of Population Health, University of Oxford, Oxford, United Kingdom. · Department of Social and Preventive Medicine, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia. ·Int J Cancer · Pubmed #29114875.

ABSTRACT: Evidence from in vivo, in vitro and ecological studies are suggestive of a protective effect of vitamin D against pancreatic cancer (PC). However, this has not been confirmed by analytical epidemiological studies. We aimed to examine the association between pre-diagnostic circulating vitamin D concentrations and PC incidence in European populations. We conducted a pooled nested case-control study within the European Prospective Investigation into Cancer and Nutrition (EPIC) and the Nord-Trøndelag Health Study's second survey (HUNT2) cohorts. In total, 738 primary incident PC cases (EPIC n = 626; HUNT2 n = 112; median follow-up = 6.9 years) were matched to 738 controls. Vitamin D [25(OH)D

4 Article Plasma microRNAs as biomarkers of pancreatic cancer risk in a prospective cohort study. 2017

Duell, Eric J / Lujan-Barroso, Leila / Sala, Núria / Deitz McElyea, Samantha / Overvad, Kim / Tjonneland, Anne / Olsen, Anja / Weiderpass, Elisabete / Busund, Lill-Tove / Moi, Line / Muller, David / Vineis, Paolo / Aune, Dagfinn / Matullo, Giuseppe / Naccarati, Alessio / Panico, Salvatore / Tagliabue, Giovanna / Tumino, Rosario / Palli, Domenico / Kaaks, Rudolf / Katzke, Verena A / Boeing, Heiner / Bueno-de-Mesquita, H B As / Peeters, Petra H / Trichopoulou, Antonia / Lagiou, Pagona / Kotanidou, Anastasia / Travis, Ruth C / Wareham, Nick / Khaw, Kay-Tee / Ramon Quiros, Jose / Rodríguez-Barranco, Miguel / Dorronsoro, Miren / Chirlaque, María-Dolores / Ardanaz, Eva / Severi, Gianluca / Boutron-Ruault, Marie-Christine / Rebours, Vinciane / Brennan, Paul / Gunter, Marc / Scelo, Ghislaine / Cote, Greg / Sherman, Stuart / Korc, Murray. ·Unit of Nutrition and Cancer, Cancer Epidemiology Research Program, Catalan Institute of Oncology (ICO-IDIBELL), Barcelona, Spain. · Department of Medicine, Indiana University School of Medicine, Indianapolis, IN. · Department of Public Health, Section for Epidemiology, Aarhus University, Aarhus C, Denmark. · Danish Cancer Society Research Center, Copenhagen, Denmark. · Department of Research, Cancer Registry of Norway, Institute of Population-Based Cancer Research, Oslo, Norway. · Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden. · Department of Community Medicine, University of Tromsø, The Arctic University of Norway, Tromsø, Norway. · Genetic Epidemiology Group, Folkhälsan Research Center, Helsinki, Finland. · Department of Clinical Pathology, University Hospital of North Norway, Tromso, Norway. · Department of Medical Biology, UiT The Arctic University of Norway, Tromso, Norway. · School of Public Health, Epidemiology & Biostatistics, Imperial College London, London, United Kingdom. · Human Genetics Foundation (HuGeF), Turin, Italy. · Department of Medical Sciences, University of Turin, Turin, Italy. · Dipartimento di Medicina Clinica e Chirurgia, Federico II University, Naples, Italy. · Lombardy Cancer Registry Unit, Fondazione IRCCS Istituto Nazionale dei Tumori, Milano, Italy. · Cancer Registry and Histopathology Unit, "Civic - M.P, Arezzo" Hospital, ASP, Ragusa, Italy. · Cancer Risk Factors and Life-Style Epidemiology Unit, Cancer Research and Prevention Institute-ISPO, Florence, Italy. · Division of Cancer Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany. · Department of Epidemiology, German Institute of Human Nutrition, Potsdam-Rehbruecke, Nuthetal, Germany. · Dt. for Determinants of Chronic Diseases (DCD), National Institute for Public Health and the Environment (RIVM), Bilthoven, The Netherlands. · Dt. of Epidemiology and Biostatistics, The School of Public Health, Imperial College London, London, United Kingdom. · Dt. of Social & Preventive Medicine, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia. · Dept of Epidemiology, Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Utrecht, The Netherlands. · MRC-PHE Centre for Environment and Health, Dept of Epidemiology and Biostatistics, School of Public Health, Imperial College, London, United Kingdom. · Hellenic Health Foundation, Athens, Greece. · WHO Collaborating Center for Nutrition and Health, Unit of Nutritional Epidemiology and Nutrition in Public Health, Dept. of Hygiene, Epidemiology and Medical Statistics, School of Medicine, National and Kapodistrian University of Athens, Greece. · Department of Epidemiology, Harvard School of Public Health, Boston, MA. · Department of Critical Care Medicine & Pulmonary Services, University of Athens Medical School, Evangelismos Hospital, Athens, Greece. · Cancer Epidemiology Unit, Nuffield Department of Population Health, University of Oxford, Oxford, United Kingdom. · MRC Epidemiology Unit, University of Cambridge, Cambridge, United Kingdom. · Public Health Directorate, Asturias, Spain. · Andalusian School of Public Health, Research Insititute Biosanitary Granada, University Hospital Granada/University of Granada, Granada. · CIBER Epidemiology and Public Health (CIBERESP), Madrid, Spain. · Basque Regional Health Department, San Sebatian, Spain. · Department of Epidemiology, Murcia Regional Health Authority, Murcia, Spain. · Navarra Public Health Institute, Pamplona, Spain. · IdiSNA, Navarra Institute for Health Research, Pamplona, Spain. · Université Paris-Saclay, Université Paris-Sud, UVSQ, CESP, INSERM, Villejuif, France. · Gustave Roussy, Villejuif, France. · Beaujon Hospital, Pancreatology Unit, Clichy, France. · INSERM, University Paris, France. · International Agency for Research on Cancer (IARC), Lyon, France. · Medical University of South Carolina, Charleston, SC. · Departments of Medicine and Biochemistry & Molecular Biology, Indiana University School of Medicine, Indianapolis, IN. · Pancreatic Cancer Signature Center, Indiana University Melvin and Bren Simon Cancer Center, Indianapolis, IN. ·Int J Cancer · Pubmed #28542740.

ABSTRACT: Noninvasive biomarkers for early pancreatic ductal adenocarcinoma (PDAC) diagnosis and disease risk stratification are greatly needed. We conducted a nested case-control study within the Prospective Investigation into Cancer and Nutrition (EPIC) cohort to evaluate prediagnostic microRNAs (miRs) as biomarkers of subsequent PDAC risk. A panel of eight miRs (miR-10a, -10b, -21-3p, -21-5p, -30c, -106b, -155 and -212) based on previous evidence from our group was evaluated in 225 microscopically confirmed PDAC cases and 225 controls matched on center, sex, fasting status and age/date/time of blood collection. MiR levels in prediagnostic plasma samples were determined by quantitative RT-PCR. Logistic regression was used to model levels and PDAC risk, adjusting for covariates and to estimate area under the receiver operating characteristic curves (AUC). Plasma miR-10b, -21-5p, -30c and -106b levels were significantly higher in cases diagnosed within 2 years of blood collection compared to matched controls (all p-values <0.04). Based on adjusted logistic regression models, levels for six miRs (miR-10a, -10b, -21-5p, -30c, -155 and -212) overall, and for four miRs (-10a, -10b, -21-5p and -30c) at shorter follow-up time between blood collection and diagnosis (≤5 yr, ≤2 yr), were statistically significantly associated with risk. A score based on the panel showed a linear dose-response trend with risk (p-value = 0.0006). For shorter follow-up (≤5 yr), AUC for the score was 0.73, and for individual miRs ranged from 0.73 (miR-212) to 0.79 (miR-21-5p).

5 Article Sweet-beverage consumption and risk of pancreatic cancer in the European Prospective Investigation into Cancer and Nutrition (EPIC). 2016

Navarrete-Muñoz, Eva M / Wark, Petra A / Romaguera, Dora / Bhoo-Pathy, Nirmala / Michaud, Dominique / Molina-Montes, Esther / Tjønneland, Anne / Olsen, Anja / Overvad, Kim / Boutron-Ruault, Marie-Christine / Clavel-Chapelon, Françoise / Fagherazzi, Guy / Katzke, Verena A / Kühn, Tilman / Steffen, Annika / Trichopoulou, Antonia / Klinaki, Eleni / Papatesta, Eleni-Maria / Masala, Giovanna / Krogh, Vittorio / Tumino, Rosario / Naccarati, Alessio / Mattiello, Amalia / Peeters, Petra H / Rylander, Charlotta / Parr, Christine L / Skeie, Guri / Weiderpass, Elisabete / Quirós, J Ramón / Duell, Eric J / Dorronsoro, Miren / Huerta, José María / Ardanaz, Eva / Wareham, Nick / Khaw, Kay-Tee / Travis, Ruth C / Key, Tim / Stepien, Magdalena / Freisling, Heinz / Riboli, Elio / Bueno-de-Mesquita, H Bas. ·Department of Public Health, Faculty of Medicine, Miguel Hernández University, Alicante, Spain; The Spanish Biomedical Research Centre in Epidemology and Public Health (CIBERESP), Health Institute Carlos III, Madrid, Spain; · Global eHealth Unit, Department of Primary Care and Public Health. · Department of Epidemiology and Biostatistics, and The Spanish Biomedical Research Centre in Physiopathology of Obesity and Nutrition (CIBEROBN), Health Institute Carlos III, Madrid, Spain; Medical Research Institute of Palma, University Hospital Son Espases, Palma de Mallorca, Spain; mariaadoracion.romaguera@ssib.es. · Julius Centre University of Malaya, Department of Social and Preventive Medicine, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia; · Department of Public Health and Community Medicine, Tufts University School of Medicine, Boston, MA; · The Spanish Biomedical Research Centre in Epidemology and Public Health (CIBERESP), Health Institute Carlos III, Madrid, Spain; Andalusian School of Public Health. Biomedical Research Institute of Granada; University Hospital of Granada/Granada University, Granada, Spain; · Diet, Genes and Environment, Danish Cancer Society Research Center, Copenhagen Ø, Denmark; · Department of Public Health, Section for Epidemiology, Aarhus University, Aarhus C, Denmark; · Centre for Research in Epidemiology and Population Health, U1018, Nutrition, Hormones and Women's Health team, National Institute for Health and Medical Research, Villejuif, France; UMRS 1018, Université Paris Sud, Villejuif, France; Institut Gustave Roussy, Villejuif, France; · Division of Cancer Epidemiology, German Cancer Research Center, Heidelberg, Germany; · Department of Epidemiology, German Institute of Human Nutrition, Potsdam-Rehbrücke, Nuthetal, Germany; · Hellenic Health Foundation, Athens, Greece; Bureau of Epidemiologic Research, Academy of Athens, Athens, Greece; · Hellenic Health Foundation, Athens, Greece; · Molecular and Nutritional Epidemiology Unit, Cancer Research and Prevention Institute-ISPO, Florence, Italy; · Epidemiology and Prevention Unit. Fondazione IRCCS Istituto Nazionale dei Tumori, Milan, Italy; · Cancer Registry and Histopathology Unit, "Civic - M.P. Arezzo" Hospital, ASP Ragusa, Italy; · Human Genetics Foundation,Torino, Molecular and Genetic Epidemiology Unit, Torino, Italy; · Dipartamento di Medicina Clinica e Chirurgia, Federico II University of Naples, Naples, Italy; · MRC-PHE Centre for Environment and Health, Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, London, United Kingdom; Department of Epidemiology, Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Netherlands; · Department of Community Medicine, University of Tromsø-the Arctic University of Norway, Tromsø, Norway; · Department of Chronic Diseases, Division of Epidemiology, Norwegian Institute of Public Health, Oslo, Norway; · Department of Community Medicine, University of Tromsø-the Arctic University of Norway, Tromsø, Norway; Department of Research, Cancer Registry of Norway, Oslo, Norway; Department of Medical Epidemiology and Biostatistics, Karolinska Institute, Stockholm, Sweden; Samfundet Folkhälsan, Helsinki, Finland; · Public Health Directorate, Asturias, Spain; · Unit of Nutrition and Cancer, Cancer Epidemiology Research Program, Bellvitge Biomedical Research Institute, Catalan Institute of Oncology, Barcelona, Spain; · The Spanish Biomedical Research Centre in Epidemology and Public Health (CIBERESP), Health Institute Carlos III, Madrid, Spain; Public Health Direction Biodonostia Basque Regional Health Department, San Sebastian, Spain; · The Spanish Biomedical Research Centre in Epidemology and Public Health (CIBERESP), Health Institute Carlos III, Madrid, Spain; Department of Epidemiology, Murcia Regional Health Council, IMIB-Arrixaca, Murcia, Spain; · The Spanish Biomedical Research Centre in Epidemology and Public Health (CIBERESP), Health Institute Carlos III, Madrid, Spain; Navarre Public Health Institute, Pamplona, Spain; · Medical Research Council Epidemiology Unit. · Department of Public Health and Primary Care, and Clinical Gerontology Unit, School of Clinical Medicine, University of Cambridge, Cambridge, United Kingdom; · Cancer Epidemiology Unit, Nuffield Department of Population Health, University of Oxford, Oxford, United Kingdom; · Nutrition and Metabolism Section, International Agency for Research on Cancer, Lyon, France; · Department for Determinants of Chronic Diseases, National Institute for Public Health and the Environment, Bilthoven, Netherlands; and. · Department of Epidemiology and Biostatistics, and. · Department of Epidemiology and Biostatistics, and Julius Centre University of Malaya, Department of Social and Preventive Medicine, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia; Department for Determinants of Chronic Diseases, National Institute for Public Health and the Environment, Bilthoven, Netherlands; and Department of Gastroenterology and Hepatology, University Medical Center, Utrecht, Netherlands. ·Am J Clin Nutr · Pubmed #27510540.

ABSTRACT: BACKGROUND: The consumption of sweet beverages has been associated with greater risk of type 2 diabetes and obesity, which may be involved in the development of pancreatic cancer. Therefore, it has been hypothesized that sweet beverages may increase pancreatic cancer risk as well. OBJECTIVE: We examined the association between sweet-beverage consumption (including total, sugar-sweetened, and artificially sweetened soft drink and juice and nectar consumption) and pancreatic cancer risk. DESIGN: The study was conducted within the European Prospective Investigation into Cancer and Nutrition cohort. A total of 477,199 participants (70.2% women) with a mean age of 51 y at baseline were included, and 865 exocrine pancreatic cancers were diagnosed after a median follow-up of 11.60 y (IQR: 10.10-12.60 y). Sweet-beverage consumption was assessed with the use of validated dietary questionnaires at baseline. HRs and 95% CIs were obtained with the use of multivariable Cox regression models that were stratified by age, sex, and center and adjusted for educational level, physical activity, smoking status, and alcohol consumption. Associations with total soft-drink consumption were adjusted for juice and nectar consumption and vice versa. RESULTS: Total soft-drink consumption (HR per 100 g/d: 1.03; 95% CI: 0.99, 1.07), sugar-sweetened soft-drink consumption (HR per 100 g/d: 1.02; 95% CI: 0.97, 1.08), and artificially sweetened soft-drink consumption (HR per 100 g/d: 1.04; 95% CI: 0.98, 1.10) were not associated with pancreatic cancer risk. Juice and nectar consumption was inversely associated with pancreatic cancer risk (HR per 100 g/d: 0.91; 95% CI: 0.84, 0.99); this association remained statistically significant after adjustment for body size, type 2 diabetes, and energy intake. CONCLUSIONS: Soft-drink consumption does not seem to be associated with pancreatic cancer risk. Juice and nectar consumption might be associated with a modest decreased pancreatic cancer risk. Additional studies with specific information on juice and nectar subtypes are warranted to clarify these results.

6 Article Plasma carotenoids, vitamin C, retinol and tocopherols levels and pancreatic cancer risk within the European Prospective Investigation into Cancer and Nutrition: a nested case-control study: plasma micronutrients and pancreatic cancer risk. 2015

Jeurnink, Suzanne M / Ros, Martine M / Leenders, Max / van Duijnhoven, Franzel J B / Siersema, Peter D / Jansen, Eugene H J M / van Gils, Carla H / Bakker, Marije F / Overvad, Kim / Roswall, Nina / Tjønneland, Anne / Boutron-Ruault, Marie-Christine / Racine, Antoine / Cadeau, Claire / Grote, Verena / Kaaks, Rudolf / Aleksandrova, Krasimira / Boeing, Heiner / Trichopoulou, Antonia / Benetou, Vasiliki / Valanou, Elisavet / Palli, Domenico / Krogh, Vittorio / Vineis, Paolo / Tumino, Rosario / Mattiello, Amalia / Weiderpass, Elisabete / Skeie, Guri / Castaño, José María Huerta / Duell, Eric J / Barricarte, Aurelio / Molina-Montes, Esther / Argüelles, Marcial / Dorronsoro, Mire / Johansen, Dorthe / Lindkvist, Björn / Sund, Malin / Crowe, Francesca L / Khaw, Kay-Tee / Jenab, Mazda / Fedirko, Veronika / Riboli, E / Bueno-de-Mesquita, H B. ·Department of Gastroenterology and Hepatology, University Medical Center Utrecht, the Netherlands; National Institute for Public Health and the Environment (RIVM), Bilthoven, the Netherlands. ·Int J Cancer · Pubmed #25175624.

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%CIs) 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 vs. lowest quartile 0.52, 95%CI 0.31-0.88, p for trend = 0.02), zeaxanthin (IRR highest vs. lowest quartile 0.53, 95%CI 0.30-0.94, p for trend = 0.06) and α-tocopherol (IRR highest vs. 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.

7 Article Leukocyte telomere length in relation to pancreatic cancer risk: a prospective study. 2014

Campa, Daniele / Mergarten, Björn / De Vivo, Immaculata / Boutron-Ruault, Marie-Christine / Racine, Antoine / Severi, Gianluca / Nieters, Alexandra / Katzke, Verena A / Trichopoulou, Antonia / Yiannakouris, Nikos / Trichopoulos, Dimitrios / Boeing, Heiner / Quirós, J Ramón / Duell, Eric J / Molina-Montes, Esther / Huerta, José María / Ardanaz, Eva / Dorronsoro, Miren / Khaw, Kay-Tee / Wareham, Nicholas / Travis, Ruth C / Palli, Domenico / Pala, Valeria / Tumino, Rosario / Naccarati, Alessio / Panico, Salvatore / Vineis, Paolo / Riboli, Elio / Siddiq, Afshan / Bueno-de-Mesquita, H B / Peeters, Petra H / Nilsson, Peter M / Sund, Malin / Ye, Weimin / Lund, Eiliv / Jareid, Mie / Weiderpass, Elisabete / Duarte-Salles, Talita / Kong, So Yeon / Stepien, Magdalena / Canzian, Federico / Kaaks, Rudolf. ·Division of Cancer Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany. · Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts. Program in Genetic Epidemiology and Statistical Genetics, Harvard School of Public Health, Boston, Massachusetts. · Institut National de la Santé et de la Recherche Médicale (INSERM), Centre for research in Epidemiology and Population Health (CESP), U1018, Nutrition, Hormones, and Women's Health team, Villejuif, France. Univ Paris Sud, UMRS 1018, Villejuif, France. IGR, Villejuif, France. · Human Genetics Foundation (HuGeF), Torino, Italy. · Center for Chronic Immunodeficiency, University Medical Center Freiburg, Freiburg, Germany. · Hellenic Health Foundation, Athens, Greece. Bureau of Epidemiologic Research, Academy of Athens, Athens, Greece. · Hellenic Health Foundation, Athens, Greece. Harokopio University of Athens, Greece. · Hellenic Health Foundation, Athens, Greece. Bureau of Epidemiologic Research, Academy of Athens, Athens, Greece. Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts. · Department of Epidemiology, German Institute of Human Nutrition Potsdam-Rehbrücke, Nuthetal, Germany. · Public Health Directorate, Asturias, Spain. · Unit of Nutrition, Environment, and Cancer, Cancer Epidemiology Research Program, Bellvitge Biomedical Research Institute (IDIBELL), Catalan Institute of Oncology (ICO), Barcelona, Spain. · Escuela Andaluza de Salud Pública, Instituto de Investigación Biosanitaria de Granada (Granada.ibs), Granada, Spain. CIBER Epidemiology and Public Health CIBERESP, Madrid, Spain. · CIBER Epidemiology and Public Health CIBERESP, Madrid, Spain. Department of Epidemiology, Murcia Regional Health Council, Murcia, Spain. · CIBER Epidemiology and Public Health CIBERESP, Madrid, Spain. Navarre Public Health Institute, Pamplona, Spain. · Public Health Direction and Biodonostia-Ciberesp Basque Regional Health Department, San Sebastian, Spain. · University of Cambridge, School of Clinical Medicine, Cambridge, United Kingdom. · Cancer Epidemiology Unit, University of Oxford, Oxford, United Kingdom. · Molecular and Nutritional Epidemiology Unit, Cancer Research and Prevention Institute, ISPO, Florence, Italy. · Epidemiology and Prevention Unit Fondazione IRCCS Istituto Nazionale dei Tumori, Milan, Italy. · Cancer Registry and Histopathology Unit, "Civic - M.P. Arezzo" Hospital, ASP Ragusa, Ragusa, Italy. · Dipartimento Di Medicina Clinica e Chirurgia Federico II University, Naples, Italy. · Division of Epidemiology, Public Health and Primary Care, Imperial College, London, United Kingdom. · Department of Genomics of Common Disease, School of Public Health, Imperial College London, London, United Kingdom. · National Institute for Public Health and the Environment (RIVM), Bilthoven, the Netherlands. Department of Gastroenterology and Hepatology, University Medical Centre, Utrecht, the Netherlands. The School of Public Health, Imperial College London, London, United Kingdom. · Department of Epidemiology, Julius Center for Health Sciences and Primary Care, University Medical Center, Utrecht, the Netherlands. · Lund University, Department of Clinical Sciences, Skåne University Hospital, Malmö Sweden. · Department of Surgical and Perioperative Sciences, Umeå University, Umeå, Sweden. · Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden. The Medical Biobank at Umeå University, Umeå, Sweden. · Department of Community Medicine, Faculty of Health Sciences, University of Tromso, The Arctic University of Norway, Tromsø, Norway. · Department of Community Medicine, Faculty of Health Sciences, University of Tromso, The Arctic University of Norway, Tromsø, Norway. Department of Research, Cancer Registry of Norway, Oslo, Norway. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden. Samfundet Folkhälsan, Helsinki, Finland. · International Agency for Research on Cancer (IARC-WHO), Lyon, France. · Genomic Epidemiology Group, German Cancer Research Center (DKFZ), Heidelberg, Germany. · Division of Cancer Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany. r.kaaks@dkfz.de. ·Cancer Epidemiol Biomarkers Prev · Pubmed #25103821.

ABSTRACT: BACKGROUND: Several studies have examined leukocyte telomere length (LTL) as a possible predictor for cancer at various organ sites. The hypothesis originally motivating many of these studies was that shorter telomeres would be associated with an increase in cancer risk; the results of epidemiologic studies have been inconsistent, however, and suggested positive, negative, or null associations. Two studies have addressed the association of LTL in relation to pancreatic cancer risk and the results are contrasting. METHODS: We measured LTL in a prospective study of 331 pancreatic cancer cases and 331 controls in the context of the European Prospective Investigation into Cancer and Nutrition (EPIC). RESULTS: We observed that the mean LTL was higher in cases (0.59 ± 0.20) than in controls (0.57 ± 0.17), although this difference was not statistically significant (P = 0.07), and a basic logistic regression model showed no association of LTL with pancreas cancer risk. When adjusting for levels of HbA1c and C-peptide, however, there was a weakly positive association between longer LTL and pancreatic cancer risk [OR, 1.13; 95% confidence interval (CI), 1.01-1.27]. Additional analyses by cubic spline regression suggested a possible nonlinear relationship between LTL and pancreatic cancer risk (P = 0.022), with a statistically nonsignificant increase in risk at very low LTL, as well as a significant increase at high LTL. CONCLUSION: Taken together, the results from our study do not support LTL as a uniform and strong predictor of pancreatic cancer. IMPACT: The results of this article can provide insights into telomere dynamics and highlight the complex relationship between LTL and pancreatic cancer risk.

8 Article Intake of coffee, decaffeinated coffee, or tea does not affect risk for pancreatic cancer: results from the European Prospective Investigation into Nutrition and Cancer Study. 2013

Bhoo-Pathy, Nirmala / Uiterwaal, Cuno S P M / Dik, Vincent K / Jeurnink, Suzanne M / Bech, Bodil H / Overvad, Kim / Halkjær, Jytte / Tjønneland, Anne / Boutron-Ruault, Marie-Christine / Fagherazzi, Guy / Racine, Antoine / Katzke, Verena A / Li, Kuanrong / Boeing, Heiner / Floegel, Anna / Androulidaki, Anna / Bamia, Christina / Trichopoulou, Antonia / Masala, Giovanna / Panico, Salvatore / Crosignani, Paolo / Tumino, Rosario / Vineis, Paolo / Peeters, Petra H M / Gavrilyuk, Oxana / Skeie, Guri / Weiderpass, Elisabete / Duell, Eric J / Arguelles, Marcial / Molina-Montes, Esther / Navarro, Carmen / Ardanaz, Eva / Dorronsoro, Miren / Lindkvist, Björn / Wallström, Peter / Sund, Malin / Ye, Weimin / Khaw, Kay-Tee / Wareham, Nick / Key, Timothy J / Travis, Ruth C / Duarte-Salles, Talita / Freisling, Heinz / Licaj, Idlir / Gallo, Valentina / Michaud, Dominique S / Riboli, Elio / Bueno-De-Mesquita, H Bas. ·Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Utrecht, The Netherlands; Department of Social and Preventive Medicine, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia; National Clinical Research Centre, Kuala Lumpur Hospital, Kuala Lumpur, Malaysia. ·Clin Gastroenterol Hepatol · Pubmed #23756220.

ABSTRACT: BACKGROUND & AIMS: Few modifiable risk factors have been implicated in the etiology of pancreatic cancer. There is little evidence for the effects of caffeinated coffee, decaffeinated coffee, or tea intake on risk of pancreatic cancer. We investigated the association of total coffee, caffeinated coffee, decaffeinated coffee, and tea consumption with risk of pancreatic cancer. METHODS: This study was conducted within the European Prospective Investigation into Nutrition and Cancer cohort, comprising male and female participants from 10 European countries. Between 1992 and 2000, there were 477,312 participants without cancer who completed a dietary questionnaire and were followed up to determine pancreatic cancer incidence. Coffee and tea intake was calibrated with a 24-hour dietary recall. Adjusted hazard ratios (HRs) were computed using multivariable Cox regression. RESULTS: During a mean follow-up period of 11.6 y, 865 first incidences of pancreatic cancers were reported. When divided into fourths, neither total intake of coffee (HR, 1.03; 95% confidence interval [CI], 0.83-1.27; high vs low intake), decaffeinated coffee (HR, 1.12; 95% CI, 0.76-1.63; high vs low intake), nor tea were associated with risk of pancreatic cancer (HR, 1.22, 95% CI, 0.95-1.56; high vs low intake). Moderately low intake of caffeinated coffee was associated with an increased risk of pancreatic cancer (HR, 1.33; 95% CI, 1.02-1.74), compared with low intake. However, no graded dose response was observed, and the association attenuated after restriction to histologically confirmed pancreatic cancers. CONCLUSIONS: Based on an analysis of data from the European Prospective Investigation into Nutrition and Cancer cohort, total coffee, decaffeinated coffee, and tea consumption are not related to the risk of pancreatic cancer.

9 Article Menstrual and reproductive factors in women, genetic variation in CYP17A1, and pancreatic cancer risk in the European prospective investigation into cancer and nutrition (EPIC) cohort. 2013

Duell, Eric J / Travier, Noémie / Lujan-Barroso, Leila / Dossus, Laure / Boutron-Ruault, Marie-Christine / Clavel-Chapelon, Françoise / Tumino, Rosario / Masala, Giovanna / Krogh, Vittorio / Panico, Salvatore / Ricceri, Fulvio / Redondo, Maria Luisa / Dorronsoro, Miren / Molina-Montes, Esther / Huerta, José M / Barricarte, Aurelio / Khaw, Kay-Tee / Wareham, Nick J / Allen, Naomi E / Travis, Ruth / Siersema, Peter D / Peeters, Petra H M / Trichopoulou, Antonia / Fragogeorgi, Eirini / Oikonomou, Eleni / Boeing, Heiner / Schuetze, Madlen / Canzian, Federico / Lukanova, Annekatrin / Tjønneland, Anne / Roswall, Nina / Overvad, Kim / Weiderpass, Elisabete / Gram, Inger Torhild / Lund, Eiliv / Lindkvist, Björn / Johansen, Dorthe / Ye, Weimin / Sund, Malin / Fedirko, Veronika / Jenab, Mazda / Michaud, Dominique S / Riboli, Elio / Bueno-de-Mesquita, H Bas. ·Unit of Nutrition, Environment and Cancer, Catalan Institute of Oncology, Bellvitge Biomedical Research Institute (IDIBELL), Barcelona, Spain. eduell@iconcologia.net ·Int J Cancer · Pubmed #23015357.

ABSTRACT: Menstrual and reproductive factors and exogenous hormone use have been investigated as pancreatic cancer risk factors in case-control and cohort studies, but results have been inconsistent. We conducted a prospective examination of menstrual and reproductive factors, exogenous hormone use and pancreatic cancer risk (based on 304 cases) in 328,610 women from the EPIC cohort. Then, in a case-control study nested within the EPIC cohort, we examined 12 single nucleotide polymorphisms (SNPs) in CYP17A1 (an essential gene in sex steroid metabolism) for association with pancreatic cancer in women and men (324 cases and 353 controls). Of all factors analyzed, only younger age at menarche (<12 vs. 13 years) was moderately associated with an increased risk of pancreatic cancer in the full cohort; however, this result was marginally significant (HR = 1.44; 95% CI = 0.99-2.10). CYP17A1 rs619824 was associated with HRT use (p value = 0.037) in control women; however, none of the SNPs alone, in combination, or as haplotypes were associated with pancreatic cancer risk. In conclusion, with the possible exception of an early age of menarche, none of the menstrual and reproductive factors, and none of the 12 common genetic variants we evaluated at the CYP17A1 locus makes a substantial contribution to pancreatic cancer susceptibility in the EPIC cohort.

10 Article Plasma antibodies to oral bacteria and risk of pancreatic cancer in a large European prospective cohort study. 2013

Michaud, Dominique S / Izard, Jacques / Wilhelm-Benartzi, Charlotte S / You, Doo-Ho / Grote, Verena A / Tjønneland, Anne / Dahm, Christina C / Overvad, Kim / Jenab, Mazda / Fedirko, Veronika / Boutron-Ruault, Marie Christine / Clavel-Chapelon, Françoise / Racine, Antoine / Kaaks, Rudolf / Boeing, Heiner / Foerster, Jana / Trichopoulou, Antonia / Lagiou, Pagona / Trichopoulos, Dimitrios / Sacerdote, Carlotta / Sieri, Sabina / Palli, Domenico / Tumino, Rosario / Panico, Salvatore / Siersema, Peter D / Peeters, Petra H M / Lund, Eiliv / Barricarte, Aurelio / Huerta, José-María / Molina-Montes, Esther / Dorronsoro, Miren / Quirós, J Ramón / Duell, Eric J / Ye, Weimin / Sund, Malin / Lindkvist, Björn / Johansen, Dorthe / Khaw, Kay-Tee / Wareham, Nick / Travis, Ruth C / Vineis, Paolo / Bueno-de-Mesquita, H Bas / Riboli, Elio. ·Department of Epidemiology, Division of Biology and Medicine, Brown University, Providence, Rhode Island, USA. ·Gut · Pubmed #22990306.

ABSTRACT: OBJECTIVE: Examine the relationship between antibodies to 25 oral bacteria and pancreatic cancer risk in a prospective cohort study. DESIGN: We measured antibodies to oral bacteria in prediagnosis blood samples from 405 pancreatic cancer cases and 416 matched controls, nested within the European Prospective Investigation into Cancer and Nutrition study. Analyses were conducted using conditional logistic regression and additionally adjusted for smoking status and body mass index. RESULTS: Individuals with high levels of antibodies against Porphyromonas gingivalis ATTC 53978, a pathogenic periodontal bacteria, had a twofold higher risk of pancreatic cancer than individuals with lower levels of these antibodies (OR 2.14; 95% CI 1.05 to 4.36; >200 ng/ml vs ≤200 ng/ml). To explore the association with commensal (non-pathogenic) oral bacteria, we performed a cluster analysis and identified two groups of individuals, based on their antibody profiles. A cluster with overall higher levels of antibodies had a 45% lower risk of pancreatic cancer than a cluster with overall lower levels of antibodies (OR 0.55; 95% CI 0.36 to 0.83). CONCLUSIONS: Periodontal disease might increase the risk for pancreatic cancer. Moreover, increased levels of antibodies against specific commensal oral bacteria, which can inhibit growth of pathogenic bacteria, might reduce the risk of pancreatic cancer. Studies are needed to determine whether oral bacteria have direct effects on pancreatic cancer pathogenesis or serve as markers of the immune response.

11 Article Inflammation marker and risk of pancreatic cancer: a nested case-control study within the EPIC cohort. 2012

Grote, V A / Kaaks, R / Nieters, A / Tjønneland, A / Halkjær, J / Overvad, K / Skjelbo Nielsen, M R / Boutron-Ruault, M C / Clavel-Chapelon, F / Racine, A / Teucher, B / Becker, S / Pischon, T / Boeing, H / Trichopoulou, A / Cassapa, C / Stratigakou, V / Palli, D / Krogh, V / Tumino, R / Vineis, P / Panico, S / Rodríguez, L / Duell, E J / Sánchez, M-J / Dorronsoro, M / Navarro, C / Gurrea, A B / Siersema, P D / Peeters, P H M / Ye, W / Sund, M / Lindkvist, B / Johansen, D / Khaw, K-T / Wareham, N / Allen, N E / Travis, R C / Fedirko, V / Jenab, M / Michaud, D S / Chuang, S-C / Romaguera, D / Bueno-de-Mesquita, H B / Rohrmann, S. ·Division of Cancer Epidemiology (c020), German Cancer Research Center (DKFZ), Im Neuenheimer Feld 581, Heidelberg 69120, Germany. ·Br J Cancer · Pubmed #22617158.

ABSTRACT: BACKGROUND: Established risk factors for pancreatic cancer include smoking, long-standing diabetes, high body fatness, and chronic pancreatitis, all of which can be characterised by aspects of inflammatory processes. However, prospective studies investigating the relation between inflammatory markers and pancreatic cancer risk are scarce. METHODS: We conducted a nested case-control study within the European Prospective Investigation into Cancer and Nutrition, measuring prediagnostic blood levels of C-reactive protein (CRP), interleukin-6 (IL-6), and soluble receptors of tumour necrosis factor-α (sTNF-R1, R2) in 455 pancreatic cancer cases and 455 matched controls. Odds ratios (ORs) were estimated using conditional logistic regression models. RESULTS: None of the inflammatory markers were significantly associated with risk of pancreatic cancer overall, although a borderline significant association was observed for higher circulating sTNF-R2 (crude OR=1.52 (95% confidence interval (CI) 0.97-2.39), highest vs lowest quartile). In women, however, higher sTNF-R1 levels were significantly associated with risk of pancreatic cancer (crude OR=1.97 (95% CI 1.02-3.79)). For sTNF-R2, risk associations seemed to be stronger for diabetic individuals and those with a higher BMI. CONCLUSION: Prospectively, CRP and IL-6 do not seem to have a role in our study with respect to risk of pancreatic cancer, whereas sTNF-R1 seemed to be a risk factor in women and sTNF-R2 might be a mediator in the risk relationship between overweight and diabetes with pancreatic cancer. Further large prospective studies are needed to clarify the role of proinflammatory proteins and cytokines in the pathogenesis of exocrine pancreatic cancer.

12 Article Concentrations of IGF-I and IGFBP-3 and pancreatic cancer risk in the European Prospective Investigation into Cancer and Nutrition. 2012

Rohrmann, S / Grote, V A / Becker, S / Rinaldi, S / Tjønneland, A / Roswall, N / Grønbæk, H / Overvad, K / Boutron-Ruault, M C / Clavel-Chapelon, F / Racine, A / Teucher, B / Boeing, H / Drogan, D / Dilis, V / Lagiou, P / Trichopoulou, A / Palli, D / Tagliabue, G / Tumino, R / Vineis, P / Mattiello, A / Rodríguez, L / Duell, E J / Molina-Montes, E / Dorronsoro, M / Huerta, J-M / Ardanaz, E / Jeurnink, S / Peeters, P H M / Lindkvist, B / Johansen, D / Sund, M / Ye, W / Khaw, K-T / Wareham, N J / Allen, N E / Crowe, F L / Fedirko, V / Jenab, M / Michaud, D S / Norat, T / Riboli, E / Bueno-de-Mesquita, H B / Kaaks, R. ·Division of Cancer Epidemiology and Prevention, Institute of Social and Preventive Medicine, University of Zurich, Hirschengraben 84, Zürich 8001, Switzerland. sabine.rohrmann@ifspm.uzh.ch ·Br J Cancer · Pubmed #22315049.

ABSTRACT: BACKGROUND: Insulin-like growth factors (IGFs) and their binding proteins (BPs) regulate cell differentiation, proliferation and apoptosis, and may have a role in the aetiology of various cancers. Information on their role in pancreatic cancer is limited and was examined here in a case-control study nested within the European Prospective Investigation into Cancer and Nutrition. METHODS: Serum concentrations of IGF-I and IGFBP-3 were measured using enzyme-linked immunosorbent assays in 422 cases and 422 controls matched on age, sex, study centre, recruitment date, and time since last meal. Conditional logistic regression was used to compute odds ratios (OR) and 95% confidence intervals (CI) adjusted for confounding variables. RESULTS: Neither circulating levels of IGF-I (OR=1.21, 95% CI 0.75-1.93 for top vs bottom quartile, P-trend 0.301), IGFBP-3 (OR=1.00, 95% CI 0.66-1.51, P-trend 0.79), nor the molar IGF-I/IGFBP-3 ratio, an indicator of free IGF-I level (OR=1.22, 95% CI 0.75-1.97, P-trend 0.27), were statistically significantly associated with the risk of pancreatic cancer. In a cross-classification, however, a high concentration of IGF-I with concurrently low levels of IGFBP-3 was related to an increased risk of pancreatic cancer (OR=1.72, 95% CI 1.05-2.83; P-interaction=0.154). CONCLUSION: On the basis of these results, circulating levels of components of the IGF axis do not appear to be the risk factors for pancreatic cancer. However, on the basis of the results of a subanalysis, it cannot be excluded that a relatively large amount of IGF-1 together with very low levels of IGFBP-3 might still be associated with an increase in pancreatic cancer risk.

13 Article The associations of advanced glycation end products and its soluble receptor with pancreatic cancer risk: a case-control study within the prospective EPIC Cohort. 2012

Grote, Verena A / Nieters, Alexandra / Kaaks, Rudolf / Tjønneland, Anne / Roswall, Nina / Overvad, Kim / Nielsen, Michael R Skjelbo / Clavel-Chapelon, Françoise / Boutron-Ruault, Marie Christine / Racine, Antoine / Teucher, Birgit / Lukanova, Annekatrin / Boeing, Heiner / Drogan, Dagmar / Trichopoulou, Antonia / Trichopoulos, Dimitrios / Lagiou, Pagona / Palli, Domenico / Sieri, Sabina / Tumino, Rosario / Vineis, Paolo / Mattiello, Amalia / Argüelles Suárez, Marcial Vicente / Duell, Eric J / Sánchez, María-José / Dorronsoro, Miren / Huerta Castaño, José María / Barricarte, Aurelio / Jeurnink, Suzanne M / Peeters, Petra H M / Sund, Malin / Ye, Weimin / Regner, Sara / Lindkvist, Björn / Khaw, Kay-Tee / Wareham, Nick / Allen, Naomi E / Crowe, Francesca L / Fedirko, Veronika / Jenab, Mazda / Romaguera, Dora / Siddiq, Afshan / Bueno-de-Mesquita, H Bas / Rohrmann, Sabine. ·Division of Cancer Epidemiology c020, German Cancer Research Center (DKFZ), Im Neuenheimer Feld 581, Heidelberg, Germany. ·Cancer Epidemiol Biomarkers Prev · Pubmed #22301828.

ABSTRACT: BACKGROUND: Advanced glycation end products (AGE) and their receptors (RAGE) have been implicated in cancer development through their proinflammatory capabilities. However, prospective data on their association with cancer of specific sites, including pancreatic cancer, are limited. METHODS: Prediagnostic blood levels of the AGE product Nε-(carboxymethyl)lysine (CML) and the endogenous secreted receptor for AGE (esRAGE) were measured using ELISA in 454 patients with exocrine pancreatic cancer and individually matched controls within the European Prospective Investigation into Cancer and Nutrition (EPIC). Pancreatic cancer risk was estimated by calculating ORs with corresponding 95% confidence intervals (CI). RESULTS: Elevated CML levels tended to be associated with a reduction in pancreatic cancer risk [OR = 0.57 (95% CI, 0.32-1.01) comparing highest with lowest quintile), whereas no association was observed for esRAGE (OR = 0.98; 95% CI, 0.62-1.54). Adjustments for body mass index and smoking attenuated the inverse associations of CML with pancreatic cancer risk (OR = 0.78; 95% CI, 0.41-1.49). There was an inverse association between esRAGE and risk of pancreatic cancer for cases that were diagnosed within the first 2 years of follow-up [OR = 0.46 (95% CI, 0.22-0.96) for a doubling in concentration], whereas there was no association among those with a longer follow-up (OR = 1.11; 95% CI, 0.88-1.39; P(interaction) = 0.002). CONCLUSIONS AND IMPACT: Our results do not provide evidence for an association of higher CML or lower esRAGE levels with risk of pancreatic cancer. The role of AGE/RAGE in pancreatic cancer would benefit from further investigations.

14 Article Diabetes mellitus, glycated haemoglobin and C-peptide levels in relation to pancreatic cancer risk: a study within the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. 2011

Grote, V A / Rohrmann, S / Nieters, A / Dossus, L / Tjønneland, A / Halkjær, J / Overvad, K / Fagherazzi, G / Boutron-Ruault, M C / Morois, S / Teucher, B / Becker, S / Sluik, D / Boeing, H / Trichopoulou, A / Lagiou, P / Trichopoulos, D / Palli, D / Pala, V / Tumino, R / Vineis, P / Panico, S / Rodríguez, L / Duell, E J / Molina-Montes, E / Dorronsoro, M / Huerta, J M / Ardanaz, E / Jeurnink, S M / Beulens, J W J / Peeters, P H M / Sund, M / Ye, W / Lindkvist, B / Johansen, D / Khaw, K T / Wareham, N / Allen, N / Crowe, F / Jenab, M / Romieu, I / Michaud, D S / Riboli, E / Romaguera, D / Bueno-de-Mesquita, H B / Kaaks, R. ·Division of Cancer Epidemiology c020, German Cancer Research Center (DKFZ), Im Neuenheimer Feld 581, 69120 Heidelberg, Germany. ·Diabetologia · Pubmed #21953276.

ABSTRACT: AIMS/HYPOTHESIS: There has been long-standing debate about whether diabetes is a causal risk factor for pancreatic cancer or a consequence of tumour development. Prospective epidemiological studies have shown variable relationships between pancreatic cancer risk and blood markers of glucose and insulin metabolism, overall and as a function of lag times between marker measurements (blood donation) and date of tumour diagnosis. METHODS: Pre-diagnostic levels of HbA(1c) and C-peptide were measured for 466 participants with pancreatic cancer and 466 individually matched controls within the European Prospective Investigation into Cancer and Nutrition. Conditional logistic regression models were used to estimate ORs for pancreatic cancer. RESULTS: Pancreatic cancer risk gradually increased with increasing pre-diagnostic HbA(1c) levels up to an OR of 2.42 (95% CI 1.33, 4.39 highest [≥ 6.5%, 48 mmol/mol] vs lowest [≤ 5.4%, 36 mmol/mol] category), even for individuals with HbA(1c) levels within the non-diabetic range. C-peptide levels showed no significant relationship with pancreatic cancer risk, irrespective of fasting status. Analyses showed no clear trends towards increasing hyperglycaemia (as marked by HbA(1c) levels) or reduced pancreatic beta cell responsiveness (as marked by C-peptide levels) with decreasing time intervals from blood donation to cancer diagnosis. CONCLUSIONS/INTERPRETATION: Our data on HbA(1c) show that individuals who develop exocrine pancreatic cancer tend to have moderate increases in HbA(1c) levels, relatively independently of obesity and insulin resistance-the classic and major risk factors for type 2 diabetes. While there is no strong difference by lag time, more data are needed on this in order to reach a firm conclusion.

15 Article No association between educational level and pancreatic cancer incidence in the European Prospective Investigation into Cancer and Nutrition. 2010

van Boeckel, Petra G A / Boshuizen, Hendriek C / Siersema, Peter D / Vrieling, Alina / Kunst, Anton E / Ye, Weimin / Sund, Malin / Michaud, Dominique S / Gallo, Valentina / Spencer, Elizabeth A / Trichopoulou, Antonia / Benetou, Vasiliki / Orfanos, Philippos / Cirera, Lluis / Duell, Eric J / Rohrmann, Sabine / Hemann, Silke / Masala, Giovanni / Manjer, Jonas / Mattiello, Amalia / Lindkvist, Bjorn / Sánchez, María-José / Pala, Valeria / Peeters, Petra H M / Braaten, Tonje / Tjonneland, Anne / Dalton, Susanne Oksbjerg / Larranaga, Nerea / Dorronsoro, Miren / Overvad, Kim / Illner, Anne-Kathrin / Ardanaz, Eva / Marron, M / Straif, K / Riboli, E / Bueno-de-Mesquita, B. ·National Institute for Public Health and the Environment (RIVM), Bilthoven, The Netherlands. p.g.a.vanboeckel@umcutrecht.nl ·Cancer Epidemiol · Pubmed #20829145.

ABSTRACT: INTRODUCTION: Until now, studies examining the relationship between socioeconomic status and pancreatic cancer incidence have been inconclusive. AIM: To prospectively investigate to what extent pancreatic cancer incidence varies according to educational level within the European Prospective Investigation into Cancer and Nutrition (EPIC) study. METHODS: In the EPIC study, socioeconomic status at baseline was measured using the highest level of education attained. Hazard ratios by educational level and a summary index, the relative indices of inequality (RII), were estimated using Cox regression models stratified by age, gender, and center and adjusted for known risk factors. In addition, we conducted separate analyses by age, gender and geographical region. RESULTS: Within the source population of 407, 944 individuals at baseline, 490 first incident primary pancreatic adenocarcinoma cases were identified in 9 European countries. The crude difference in risk of pancreatic cancer according to level of education was small and not statistically significant (RII=1.14, 95% CI 0.80-1.62). Adjustment for known risk factors reduced the inequality estimates to only a small extent. In addition, no statistically significant associations were observed for age groups (adjusted RII(≤ 60 years)=0.85, 95% CI 0.44-1.64, adjusted RII(>60 years)=1.18, 95% CI 0.73-1.90), gender (adjusted RII(male)=1.20, 95% CI 0.68-2.10, adjusted RII(female)=0.96, 95% CI 0.56-1.62) or geographical region (adjusted RII(Northern Europe)=1.14, 95% CI 0.81-1.61, adjusted RII(Middle Europe)=1.72, 95% CI 0.93-3.19, adjusted RII(Southern Europe)=0.75, 95% CI 0.32-1.80). CONCLUSION: Despite large educational inequalities in many risk factors within the EPIC study, we found no evidence for an association between educational level and the risk of developing pancreatic cancer in this European cohort.

16 Article Family history of cancer and risk of pancreatic cancer: a pooled analysis from the Pancreatic Cancer Cohort Consortium (PanScan). 2010

Jacobs, Eric J / Chanock, Stephen J / Fuchs, Charles S / Lacroix, Andrea / McWilliams, Robert R / Steplowski, Emily / Stolzenberg-Solomon, Rachael Z / Arslan, Alan A / Bueno-de-Mesquita, H Bas / Gross, Myron / Helzlsouer, Kathy / Petersen, Gloria / Zheng, Wei / Agalliu, Ilir / Allen, Naomi E / Amundadottir, Laufey / Boutron-Ruault, Marie-Christine / Buring, Julie E / Canzian, Federico / Clipp, Sandra / Dorronsoro, Miren / Gaziano, J Michael / Giovannucci, Edward L / Hankinson, Susan E / Hartge, Patricia / Hoover, Robert N / Hunter, David J / Jacobs, Kevin B / Jenab, Mazda / Kraft, Peter / Kooperberg, Charles / Lynch, Shannon M / Sund, Malin / Mendelsohn, Julie B / Mouw, Tracy / Newton, Christina C / Overvad, Kim / Palli, Domenico / Peeters, Petra H M / Rajkovic, Aleksandar / Shu, Xiao-Ou / Thomas, Gilles / Tobias, Geoffrey S / Trichopoulos, Dimitrios / Virtamo, Jarmo / Wactawski-Wende, Jean / Wolpin, Brian M / Yu, Kai / Zeleniuch-Jacquotte, Anne. ·Department of Epidemiology, American Cancer Society, Atlanta, GA, USA. ejacobs@cancer.org ·Int J Cancer · Pubmed #20049842.

ABSTRACT: A family history of pancreatic cancer has consistently been associated with increased risk of pancreatic cancer. However, uncertainty remains about the strength of this association. Results from previous studies suggest a family history of select cancers (i.e., ovarian, breast and colorectal) could also be associated, although not as strongly, with increased risk of pancreatic cancer. We examined the association between a family history of 5 types of cancer (pancreas, prostate, ovarian, breast and colorectal) and risk of pancreatic cancer using data from a collaborative nested case-control study conducted by the Pancreatic Cancer Cohort Consortium. Cases and controls were from cohort studies from the United States, Europe and China, and a case-control study from the Mayo Clinic. Analyses of family history of pancreatic cancer included 1,183 cases and 1,205 controls. A family history of pancreatic cancer in a parent, sibling or child was associated with increased risk of pancreatic cancer [multivariate-adjusted odds ratios (ORs) = 1.76, 95% confidence interval (CI) = 1.19-2.61]. A family history of prostate cancer was also associated with increased risk (OR = 1.45, 95% CI = 1.12-1.89). There were no statistically significant associations with a family history of ovarian cancer (OR = 0.82, 95% CI = 0.52-1.31), breast cancer (OR = 1.21, 95% CI = 0.97-1.51) or colorectal cancer (OR = 1.17, 95% CI = 0.93-1.47). Our results confirm a moderate sized association between a family history of pancreatic cancer and risk of pancreatic cancer and also provide evidence for an association with a family history of prostate cancer worth further study.