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Pancreatic Neoplasms: HELP
Articles by Weimin Ye
Based on 20 articles published since 2010
(Why 20 articles?)
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Between 2010 and 2020, Weimin Ye wrote the following 20 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Article Methodological issues in a prospective study on plasma concentrations of persistent organic pollutants and pancreatic cancer risk within the EPIC cohort. 2019

Gasull, Magda / Pumarega, José / Kiviranta, Hannu / Rantakokko, Panu / Raaschou-Nielsen, Ole / Bergdahl, Ingvar A / Sandanger, Torkjel Manning / Goñi, Fernando / Cirera, Lluís / Donat-Vargas, Carolina / Alguacil, Juan / Iglesias, Mar / Tjønneland, Anne / Overvad, Kim / Mancini, Francesca Romana / Boutron-Ruault, Marie-Christine / Severi, Gianluca / Johnson, Theron / Kühn, Tilman / Trichopoulou, Antonia / Karakatsani, Anna / Peppa, Eleni / Palli, Domenico / Pala, Valeria / Tumino, Rosario / Naccarati, Alessio / Panico, Salvatore / Verschuren, Monique / Vermeulen, Roel / Rylander, Charlotta / Nøst, Therese Haugdahl / Rodríguez-Barranco, Miguel / Molinuevo, Amaia / Chirlaque, María-Dolores / Ardanaz, Eva / Sund, Malin / Key, Tim / Ye, Weimin / Jenab, Mazda / Michaud, Dominique / Matullo, Giuseppe / Canzian, Federico / Kaaks, Rudolf / Nieters, Alexandra / Nöthlings, Ute / Jeurnink, Suzanne / Chajes, Veronique / Matejcic, Marco / Gunter, Marc / Aune, Dagfinn / Riboli, Elio / Agudo, Antoni / Gonzalez, Carlos Alberto / Weiderpass, Elisabete / Bueno-de-Mesquita, Bas / Duell, Eric J / Vineis, Paolo / Porta, Miquel. ·Hospital del Mar Institute of Medical Research (IMIM), Barcelona, Catalonia, Spain; Universitat Autònoma de Barcelona, Barcelona, Catalonia, Spain; CIBER de Epidemiología y Salud Pública (CIBERESP), Madrid, Spain. · Hospital del Mar Institute of Medical Research (IMIM), Barcelona, Catalonia, Spain; CIBER de Epidemiología y Salud Pública (CIBERESP), Madrid, Spain. · National Institute for Health and Welfare, Department of Health Security, Kuopio, Finland. · Danish Cancer Society Research Center, Copenhagen, Denmark. · Department of Biobank Research, Umeå University, Umeå, Sweden; Occupational and Environmental Medicine, Department of Public Health and Clinical Medicine, Umeå University, Umeå, Sweden. · Department of Community Medicine, UiT-The Arctic University of Norway, Tromsø, Norway. · CIBER de Epidemiología y Salud Pública (CIBERESP), Madrid, Spain; Biodonostia Health Research Institute; Public Health Laboratory in Gipuzkoa, Basque Government, San Sebastian, Spain. · CIBER de Epidemiología y Salud Pública (CIBERESP), Madrid, Spain; Department of Epidemiology, Murcia Regional Health Council, IMIB - Arrixaca, Murcia, Spain. · Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden. · CIBER de Epidemiología y Salud Pública (CIBERESP), Madrid, Spain; Universidad de Huelva, Huelva, Spain. · Department of Pathology, Hospital del Mar (PSMar), Barcelona, Spain. · Section for Epidemiology, Department of Public Health, Aarhus University, Aarhus, Denmark. · CESP, Faculté de Médecine - Univ. Paris-Sud, Faculté de Médecine - UVSQ, INSERM, Université Paris-Saclay, Villejuif, France; Gustave Roussy, Villejuif, France. · Division of Cancer Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany. · Hospital del Mar Institute of Medical Research (IMIM), Barcelona, Catalonia, Spain. · Hellenic Health Foundation, Athens, Greece. · Hellenic Health Foundation, Athens, Greece; 2nd Pulmonary Medicine Department, School of Medicine, National and Kapodistrian University of Athens, "ATTIKON" University Hospital, Haidari, Greece. · Cancer Risk Factors and Life-Style Epidemiology Unit, Institute for Cancer Research, Prevention and Clinical Network - ISPRO, Florence, Italy. · Epidemiology and Prevention Unit, Fondazione IRCCS Istituto Nazionale dei Tumori, Milan, Italy. · Cancer Registry and Histopathology Department, "Civic - M.P. Arezzo" Hospital, ASP Ragusa, Italy. · Molecular and Genetic Epidemiology Unit, Italian Institute for Genomic Medicine (IIGM), Turin, Italy. · Dipartimento di Medicina Clinica e Chirurgia, Federico II University, Naples, Italy. · Centre for Nutrition, Prevention and Health Services, National Institute for Public Health and the Environment (RIVM), Bilthoven, the Netherlands. · Institute for Risk Assessment Sciences (IRAS), Utrecht University, Utrecht, The Netherlands. · CIBER de Epidemiología y Salud Pública (CIBERESP), Madrid, Spain; Escuela Andaluza de Salud Pública. Instituto de Investigación Biosanitaria, Granada, Hospitales Universitarios de Granada/Universidad de Granada, Granada, Spain. · CIBER de Epidemiología y Salud Pública (CIBERESP), Madrid, Spain; Department of Epidemiology, Murcia Regional Health Council, IMIB - Arrixaca, Murcia, Spain; Department of Health and Social Sciences, University of Murcia, Murcia, Spain. · CIBER de Epidemiología y Salud Pública (CIBERESP), Madrid, Spain; Navarra Public Health Institute, Pamplona, Spain; IdiSNA, Navarra Institute for Health Research, Pamplona, Spain. · Department of Surgical and Perioperative Sciences, Umeå University, Umeå, Sweden. · Cancer Epidemiology Unit, Nuffield Department of Population Health, University of Oxford, Oxford, United Kingdom. · Department of Biobank Research, Umeå University, Umeå, Sweden; Department of Medical Epidemiology and Biostatistics Karolinska Institutet, Stockholm, Sweden. · Nutrition and Metabolism Section, International Agency for Research on Cancer (IARC), Lyon, France. · Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, London, United Kingdom. · Department Medical Sciences, University of Torino, Italian Institute for Genomic Medicine -IIGM/HuGeF, Torino, Italy. · Genomic Epidemiology Group, German Cancer Research Center (DKFZ), Heidelberg, Germany. · Center for Chronic Immunodeficiency, Molecular Epidemiology, University Medical Center Freiburg, Freiburg, Germany. · Department of Nutrition and Food Sciences, University of Bonn, Bonn, Germany. · Department of Gastroenterology and Hepatology, University Medical Center Utrecht, Utrecht, the Netherlands; National Institute for Public Health and the Environment (RIVM), Bilthoven, the Netherlands. · Unit of Nutrition and Cancer, Catalan Institute of Oncology (ICO-Idibell), Barcelona, Spain. · Department of Community Medicine, UiT-The Arctic University of Norway, Tromsø, Norway; Department of Medical Epidemiology and Biostatistics Karolinska Institutet, Stockholm, Sweden; Cancer Registry of Norway, Institute of Population-Based Cancer Research, Oslo, Norway; Genetic Epidemiology Group, Folkhälsan Research Center, Faculty of Medicine, University of Helsinki, Helsinki, Finland. · Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, London, United Kingdom; National Institute for Public Health and the Environment (RIVM), Bilthoven, the Netherlands; Department of Social & Preventive Medicine, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia. · Molecular and Genetic Epidemiology Unit, Italian Institute for Genomic Medicine (IIGM), Turin, Italy; Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, London, United Kingdom. · Hospital del Mar Institute of Medical Research (IMIM), Barcelona, Catalonia, Spain; Universitat Autònoma de Barcelona, Barcelona, Catalonia, Spain; CIBER de Epidemiología y Salud Pública (CIBERESP), Madrid, Spain. Electronic address: mporta@imim.es. ·Environ Res · Pubmed #30529143.

ABSTRACT: BACKGROUND: The use of biomarkers of environmental exposure to explore new risk factors for pancreatic cancer presents clinical, logistic, and methodological challenges that are also relevant in research on other complex diseases. OBJECTIVES: First, to summarize the main design features of a prospective case-control study -nested within the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort- on plasma concentrations of persistent organic pollutants (POPs) and pancreatic cancer risk. And second, to assess the main methodological challenges posed by associations among characteristics and habits of study participants, fasting status, time from blood draw to cancer diagnosis, disease progression bias, basis of cancer diagnosis, and plasma concentrations of lipids and POPs. Results from etiologic analyses on POPs and pancreatic cancer risk, and other analyses, will be reported in future articles. METHODS: Study subjects were 1533 participants (513 cases and 1020 controls matched by study centre, sex, age at blood collection, date and time of blood collection, and fasting status) enrolled between 1992 and 2000. Plasma concentrations of 22 POPs were measured by gas chromatography - triple quadrupole mass spectrometry (GC-MS/MS). To estimate the magnitude of the associations we calculated multivariate-adjusted odds ratios by unconditional logistic regression, and adjusted geometric means by General Linear Regression Models. RESULTS: There were differences among countries in subjects' characteristics (as age, gender, smoking, lipid and POP concentrations), and in study characteristics (as time from blood collection to index date, year of last follow-up, length of follow-up, basis of cancer diagnosis, and fasting status). Adjusting for centre and time of blood collection, no factors were significantly associated with fasting status. Plasma concentrations of lipids were related to age, body mass index, fasting, country, and smoking. We detected and quantified 16 of the 22 POPs in more than 90% of individuals. All 22 POPs were detected in some participants, and the smallest number of POPs detected in one person was 15 (median, 19) with few differences by country. The highest concentrations were found for p,p'-DDE, PCBs 153 and 180 (median concentration: 3371, 1023, and 810 pg/mL, respectively). We assessed the possible occurrence of disease progression bias (DPB) in eight situations defined by lipid and POP measurements, on one hand, and by four factors: interval from blood draw to index date, tumour subsite, tumour stage, and grade of differentiation, on the other. In seven of the eight situations results supported the absence of DPB. CONCLUSIONS: The coexistence of differences across study centres in some design features and participant characteristics is of relevance to other multicentre studies. Relationships among subjects' characteristics and among such characteristics and design features may play important roles in the forthcoming analyses on the association between plasma concentrations of POPs and pancreatic cancer risk.

2 Article Pancreatic cancer and autoimmune diseases: An association sustained by computational and epidemiological case-control approaches. 2019

Gomez-Rubio, Paulina / Piñero, Janet / Molina-Montes, Esther / Gutiérrez-Sacristán, Alba / Marquez, Mirari / Rava, Marta / Michalski, Christoph W / Farré, Antoni / Molero, Xavier / Löhr, Matthias / Perea, José / Greenhalf, William / O'Rorke, Michael / Tardón, Adonina / Gress, Thomas / Barberá, Victor M / Crnogorac-Jurcevic, Tatjana / Muñoz-Bellvís, Luís / Domínguez-Muñoz, Enrique / Balsells, Joaquim / Costello, Eithne / Yu, Jingru / Iglesias, Mar / Ilzarbe, Lucas / Kleeff, Jörg / Kong, Bo / Mora, Josefina / Murray, Liam / O'Driscoll, Damian / Poves, Ignasi / Lawlor, Rita T / Ye, Weimin / Hidalgo, Manuel / Scarpa, Aldo / Sharp, Linda / Carrato, Alfredo / Real, Francisco X / Furlong, Laura I / Malats, Núria / Anonymous2240962. ·Genetic and Molecular Epidemiology Group, Spanish National Cancer Research Center CNIO, Madrid, Spain. · Centro de Investigación Biomédica en Red en Oncología (CIBERONC), Enfermedades Hepáticas y Digestivas (CIBERHD), and Epidemiología y Salud Pública (CIBERESP), Barcelona, Spain. · Research Program on Biomedical Informatics (GRIB), Hospital del Mar Research Institute (IMIM), Universidad Pompeu Fabra (UPF), Barcelona, Spain. · Department of Surgery, Technical University of Munich, Munich, Germany. · Department of Surgery, University of Heidelberg, Heidelberg, Germany. · Department of Gastroenterology, Hospital de la Santa Creu i Sant Pau, Barcelona, Spain. · Hospital Universitaru Vall d'Hebron, Exocrine Pancreas Research Unit and Vall d'Hebron Research Institute (VHIR), Barcelona, Spain. · Universitat Auntònoma de Barcelona, Campus de la UAB, Barcelona, Spain. · Department of Clinical Science, Intervention and Technology (CLINTEC), Karolinska Institutet and University Hospital, Stockholm, Sweden. · Department of Surgery, University Hospital 12 de Octubre, Madrid, Spain. · Department of Molecular and Clinical Cancer Medicine, The Royal Liverpool University Hospital, Liverpool, United Kingdom. · Centre for Public Health, Queen's University Belfast, Belfast, United Kingdom. · Department of Medicine, Instituto Universitario de Oncología del Principado de Asturias, Oviedo, Spain. · Department of Gastroenterology, University Hospital of Giessen and Marburg, Marburg, Germany. · Laboratorio de Genética Molecular, Hospital General Universitario de Elche, Elche, Spain. · Centre for Molecular Oncology, John Vane Science Centre, Barts Cancer Institute, Queen Mary University of London, London, United Kingdom. · General and Digestive Surgery Department, Hospital Universitario de Salamanca, Salamanca, Spain. · Department of Gastroenterology, Hospital Clínico Universitario de Santiago de Compostela, Santiago de Compostela, Spain. · Department of Gastroenterology, Hospital del Mar/Parc de Salut Mar, Barcelona, Spain. · Department of Visceral, Vascular and Endocrine Surgery, Martin-Luther-University Halle-Wittenberg, Halle, (Saale), Germany. · Cancer Data Registrars, National Cancer Registry Ireland, Cork, Ireland. · ARC-Net Centre for Applied Research on Cancer, Department of Pathology and Diagnostics, University Hospital Trust of Verona, Verona, Italy. · Department of Medical Epidemiology and Biostatistics, Karolinska Institutet and University Hospital, Sweden. · Hospital Madrid-Norte-Sanchinarro and Spanish National Cancer Research Centre (CNIO), Madrid, Spain. · Rosenberg Clinical Cancer Center, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA. · Institute of Health and Society, Newcastle University, Newcastle upon Tyne, United Kingdom. · Department of Oncology, Hospital Ramón y Cajal, Madrid, Spain. · Epithelial Carcinogenesis Group, Spanish National Cancer Research Centre (CNIO), Madrid, Spain. · Departament de Ciències Experimentals i de la Salut, Universitat Pompeu Fabra, Barcelona, Spain. · PanGenEU Study Investigators (Additional file 1: Annex S1). ·Int J Cancer · Pubmed #30229903.

ABSTRACT: Deciphering the underlying genetic basis behind pancreatic cancer (PC) and its associated multimorbidities will enhance our knowledge toward PC control. The study investigated the common genetic background of PC and different morbidities through a computational approach and further evaluated the less explored association between PC and autoimmune diseases (AIDs) through an epidemiological analysis. Gene-disease associations (GDAs) of 26 morbidities of interest and PC were obtained using the DisGeNET public discovery platform. The association between AIDs and PC pointed by the computational analysis was confirmed through multivariable logistic regression models in the PanGen European case-control study population of 1,705 PC cases and 1,084 controls. Fifteen morbidities shared at least one gene with PC in the DisGeNET database. Based on common genes, several AIDs were genetically associated with PC pointing to a potential link between them. An epidemiologic analysis confirmed that having any of the nine AIDs studied was significantly associated with a reduced risk of PC (Odds Ratio (OR) = 0.74, 95% confidence interval (CI) 0.58-0.93) which decreased in subjects having ≥2 AIDs (OR = 0.39, 95%CI 0.21-0.73). In independent analyses, polymyalgia rheumatica, and rheumatoid arthritis were significantly associated with low PC risk (OR = 0.40, 95%CI 0.19-0.89, and OR = 0.73, 95%CI 0.53-1.00, respectively). Several inflammatory-related morbidities shared a common genetic component with PC based on public databases. These molecular links could shed light into the molecular mechanisms underlying PC development and simultaneously generate novel hypotheses. In our study, we report sound findings pointing to an association between AIDs and a reduced risk of PC.

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 Mediterranean diet and risk of pancreatic cancer in the European Prospective Investigation into Cancer and Nutrition cohort. 2017

Molina-Montes, Esther / Sánchez, María-José / Buckland, Genevieve / Bueno-de-Mesquita, H B As / Weiderpass, Elisabete / Amiano, Pilar / Wark, Petra A / Kühn, Tilman / Katzke, Verena / Huerta, José María / Ardanaz, Eva / Quirós, José Ramón / Affret, Aurélie / His, Mathilde / Boutron-Ruault, Marie-Christine / Peeters, Petra H / Ye, Weimin / Sund, Malin / Boeing, Heiner / Iqbal, Khalid / Ohlsson, Bodil / Sonestedt, Emily / Tjønneland, Anne / Petersen, Kristina En / Travis, Ruth C / Skeie, Guri / Agnoli, Claudia / Panico, Salvatore / Palli, Domenico / Tumino, Rosario / Sacerdote, Carlotta / Freisling, Heinz / Huybrechts, Inge / Overvad, Kim / Trichopoulou, Antonia / Bamia, Christina / Vasilopoulou, Effie / Wareham, Nick / Khaw, Kay-Tee / Cross, Amanda J / Ward, Heather A / Riboli, Elio / Duell, Eric J. ·Genetic and Molecular Epidemiology Group, Spanish National Cancer Research Center (CNIO), Madrid, Spain. · Andalusian School of Public Health, Instituto de Investigación Biosanitaria ibs.GRANADA. Hospitales Universitarios de Granada/Universidad de Granada, Granada, Spain. · CIBER Epidemiología y Salud Pública, CIBERESP, Madrid, Spain. · Unit of Nutrition and Cancer, Cancer Epidemiology Research Programme, Catalan Institute of Oncology (ICO-IDIBELL), Barcelona, Spain. · Department for Determinants of Chronic Diseases (DCD), National Institute for Public Health and the Environment (RIVM), Bilthoven, The Netherlands. · Department of Gastroenterology and Hepatology, University Medical Centre, Utrecht, The Netherlands. · Department of Epidemiology and Biostatistics, The School of Public Health, Imperial College London, London, UK. · Department of Social & Preventive Medicine, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia. · 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 Institute, Stockholm, Sweden. · Genetic Epidemiology Group, Folkhälsan Research Center, Helsinki, Finland. · Public Health Division of Gipuzkoa, BioDonostia Research Institute, San Sebastián, Spain. · Global eHealth Unit, Department of Primary Care and Public Health, The School of Public Health, Imperial College London, London, UK. · Division of Cancer Epidemiology, German Cancer Research Center (DFKZ), Heidelberg, Germany. · Department of Epidemiology, Murcia Regional Health Council, IMIB-Arrixaca, Murcia, Spain. · Navarra Public Health Institute, Pamplona, Spain. · IdiSNA, Navarra Institute for Health Research, Pamplona, Spain. · Public Health Directorate, Asturias, Spain. · Université Paris-Saclay, Université Paris-Sud, UVSQ, CESP Generations and Health Team, INSERM, Villejuif, France. · Gustave Roussy, Villejuif F-94805, France. · Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Utrecht, The Netherlands. · Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden. · The Medical Biobank at Umeå University, Umeå, Sweden. · Department of Epidemiology, German Institute of Human Nutrition Potsdam-Rehbruecke, Nuthetal, Germany. · Department of Internal Medicine, Skane University Hospital, Malmö, Sweden. · Department of Clinical Sciences, Lund University, Malmö, Sweden. · Danish Cancer Society Research Center, Unit of Diet, Genes and Environment, Copenhagen, Denmark. · Cancer Epidemiology Unit, Nuffield Department of Population Health, University of Oxford, Oxford, UK. · Epidemiology and Prevention Unit Fondazione IRCCS Istituto Nazionale dei Tumori, Milan, Italy. · Dipartimento di Medicina Clinica e Chirurgia, Federico II University, Naples, Italy. · Molecular and Nutritional Epidemiology Unit, Cancer Research and Prevention Institute-ISPO, Florence, Italy. · Cancer Registry and Histopathology Unit, 'Civic-M.P.Arezzo' Hospital, ASP Ragusa, Ragusa, Italy. · Unit of Cancer Epidemiology, Citta' della Salute e della Scienza Hospital, University of Turin and Centre for Cancer Prevention (CPO), Turin, Italy. · Section of Nutrition and Metabolism, International Agency for Research on Cancer (IARC-WHO), Lyon, France. · Department of Public Health, Section of Epidemiology, Aarhus University, Aarhus, Denmark. · Hellenic Health Foundation, Athens, Greece. · WHO Collaborating Center for Nutrition and Health, Unit of Nutritional Epidemiology and Nutrition in Public Health, Department of Hygiene, Epidemiology and Medical Statistics, University of Athens Medical School, Athens, Greece. · Medical Research Council (MCR), Epidemiology Unit, Cambridge, UK. · University of Cambridge, School of Clinical Medicine, Cambridge, UK. ·Br J Cancer · Pubmed #28170373.

ABSTRACT: BACKGROUND: The Mediterranean diet (MD) has been proposed as a means for cancer prevention, but little evidence has been accrued regarding its potential to prevent pancreatic cancer. We investigated the association between the adherence to the MD and pancreatic cancer risk within the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. METHODS: Over half a million participants from 10 European countries were followed up for over 11 years, after which 865 newly diagnosed exocrine pancreatic cancer cases were identified. Adherence to the MD was estimated through an adapted score without the alcohol component (arMED) to discount alcohol-related harmful effects. Cox proportional hazards regression models, stratified by age, sex and centre, and adjusted for energy intake, body mass index, smoking status, alcohol intake and diabetes status at recruitment, were used to estimate hazard ratios (HRs) associated with pancreatic cancer and their corresponding 95% confidence intervals (CIs). RESULTS: Adherence to the arMED score was not associated with risk of pancreatic cancer (HR high vs low adherence=0.99; 95% CI: 0.77-1.26, and HR per increments of two units in adherence to arMED=1.00; 95% CI: 0.94-1.06). There was no convincing evidence for heterogeneity by smoking status, body mass index, diabetes or European region. There was also no evidence of significant associations in analyses involving microscopically confirmed cases, plausible reporters of energy intake or other definitions of the MD pattern. CONCLUSIONS: A high adherence to the MD is not associated with pancreatic cancer risk in the EPIC study.

5 Article Helicobacter pylori infection, chronic corpus atrophic gastritis and pancreatic cancer risk in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort: A nested case-control study. 2017

Huang, Jiaqi / Zagai, Ulrika / Hallmans, Göran / Nyrén, Olof / Engstrand, Lars / Stolzenberg-Solomon, Rachael / Duell, Eric J / Overvad, Kim / Katzke, Verena A / Kaaks, Rudolf / Jenab, Mazda / Park, Jin Young / Murillo, Raul / Trichopoulou, Antonia / Lagiou, Pagona / Bamia, Christina / Bradbury, Kathryn E / Riboli, Elio / Aune, Dagfinn / Tsilidis, Konstantinos K / Capellá, Gabriel / Agudo, Antonio / Krogh, Vittorio / Palli, Domenico / Panico, Salvatore / Weiderpass, Elisabete / Tjønneland, Anne / Olsen, Anja / Martínez, Begoña / Redondo-Sanchez, Daniel / Chirlaque, Maria-Dolores / Hm Peeters, Petra / Regnér, Sara / Lindkvist, Björn / Naccarati, Alessio / Ardanaz, Eva / Larrañaga, Nerea / Boutron-Ruault, Marie-Christine / Rebours, Vinciane / Barré, Amélie / Bueno-de-Mesquita, H B As / Ye, Weimin. ·Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Solna, Sweden. · Department of Public Health and Clinical Nutrition, Umeå University, Umeå, Sweden. · Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden. · Metabolic Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, MD. · Unit of Nutrition and Cancer, Cancer Epidemiology Research Program, Catalan Institute of Oncology (ICO-IDIBELL), Barcelona, Spain. · Department of Public Health, Section for Epidemiology, Aarhus University, Aarhus, Denmark. · Division of Cancer Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany. · Prevention and Implementation Group, Section of Early Detection and Prevention, Section of Nutrition and Metabolism, International Agency for Research on Cancer, Lyon, France. · Hellenic Health Foundation, Athens, Greece. · WHO Collaborating Center for Nutrition and Health, Unit of Nutritional Epidemiology and Nutrition in Public Health, Department of Hygiene, Epidemiology and Medical Statistics, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece. · Department of Epidemiology, Harvard T. H. Chan School of Public Health, Boston, MA. · Cancer Epidemiology Unit, Nuffield Department of Population Health, University of Oxford, Oxford, United Kingdom. · Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, London, United Kingdom. · Department of Hygiene and Epidemiology, University of Ioannina School of Medicine, Ioannina, Greece. · Translational Research Laboratory, IDIBELL-Catalan Institute of Oncology, Barcelona, Spain. · Unit of Nutrition and Cancer. Cancer Epidemiology Research Program. Catalan Institute of Oncology-IDIBELL. L'Hospitalet de Llobregat, Barcelona, Spain. · Epidemiology and Prevention Unit, Fondazione IRCCS Istituto Nazionale dei Tumori, Milano, Italy. · Cancer Risk Factors and Life-Style Epidemiology Unit, Cancer Research and Prevention Institute - ISPO, Florence, Italy. · Dipartimento di medicina clinica e chirurgia Federico II, Naples, Italy. · Department of Community Medicine, 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. · Genetic Epidemiology Group, Folkhälsan Research Center, Helsinki, Finland. · Danish Cancer Society Research Center, Copenhagen, Denmark. · Andalusian School of Public Health, Instituto De Investigación Biosanitaria Ibs, Granada, Spain. · CIBER of Epidemiology and Public Health (CIBERESP), Madrid, Spain. · Escuela Andaluza de Salud Pública, Instituto de Investigación Biosanitaria ibs, Granada, Hospitales Universitarios de Granada/Universidad de Granada, Granada, Spain. · Department of Epidemiology, Regional Health Council, IMIB-Arrixaca, Murcia, Spain. · Department of Health and Social Sciences, Universidad de Murcia, Murcia, Spain. · Department of Epidemiology, Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Utrecht, The Netherlands. · Department of Surgery, Institution of Clinical Sciences Malmö, Lund University, Malmö, Sweden. · Department of Medicine, Sahlgrenska University Hospital, Gothenburg, Sweden. · Molecular and Genetic Epidemiology Unit, Human Genetics Foundation, Turin, Italy. · Navarra Public Health Institute, Pamplona, Spain; IdiSNA, Navarra Institute for Health Research, Pamplona, Spain. · Public Health Division of Gipuzkoa, Regional Government of the Basque Country, Spain. · Hormones and Women's Health Team, INSERM, Centre for Research in Epidemiology and Population Health (CESP), U1018, Nutrition, Villejuif, F-94805, France. · Université Paris Sud, UMRS 1018, Villejuif, F-94805, France. · Institut Gustave Roussy, Villejuif, F-94805, France. · Department of Gastroenterology and Pancreatology, Beaujon Hospital, University Paris 7, Clichy, France. · Université Paris Sud and Gastroenterology Unit, Hôpitaux Universitaires Paris Sud, CHU de Bicêtre, AP-HP, Le Kremlin Bicêtre, France. · Department for Determinants of Chronic Diseases (DCD), National Institute for Public Health and the Environment (RIVM), Bilthoven, The Netherlands. · Department of Gastroenterology and Hepatology, University Medical Centre, Utrecht, The Netherlands. · Department of Epidemiology and Biostatistics, The School of Public Health, Imperial College London, London, United Kingdom. · Department of Social & Preventive Medicine, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia. · The Medical Biobank at Umeå University, Umeå, Sweden. ·Int J Cancer · Pubmed #28032715.

ABSTRACT: The association between H. pylori infection and pancreatic cancer risk remains controversial. We conducted a nested case-control study with 448 pancreatic cancer cases and their individually matched control subjects, based on the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort, to determine whether there was an altered pancreatic cancer risk associated with H. pylori infection and chronic corpus atrophic gastritis. Conditional logistic regression models were applied to calculate odds ratios (ORs) and corresponding 95% confidence intervals (CIs), adjusted for matching factors and other potential confounders. Our results showed that pancreatic cancer risk was neither associated with H. pylori seropositivity (OR = 0.96; 95% CI: 0.70, 1.31) nor CagA seropositivity (OR = 1.07; 95% CI: 0.77, 1.48). We also did not find any excess risk among individuals seropositive for H. pylori but seronegative for CagA, compared with the group seronegative for both antibodies (OR = 0.94; 95% CI: 0.63, 1.38). However, we found that chronic corpus atrophic gastritis was non-significantly associated with an increased pancreatic cancer risk (OR = 1.35; 95% CI: 0.77, 2.37), and although based on small numbers, the excess risk was particularly marked among individuals seronegative for both H. pylori and CagA (OR = 5.66; 95% CI: 1.59, 20.19, p value for interaction < 0.01). Our findings provided evidence supporting the null association between H. pylori infection and pancreatic cancer risk in western European populations. However, the suggested association between chronic corpus atrophic gastritis and pancreatic cancer risk warrants independent verification in future studies, and, if confirmed, further studies on the underlying mechanisms.

6 Article Flavonoid and lignan intake and pancreatic cancer risk in the European prospective investigation into cancer and nutrition cohort. 2016

Molina-Montes, Esther / Sánchez, María-José / Zamora-Ros, Raul / Bueno-de-Mesquita, H B As / Wark, Petra A / Obon-Santacana, Mireia / Kühn, Tilman / Katzke, Verena / Travis, Ruth C / Ye, Weimin / Sund, Malin / Naccarati, Alessio / Mattiello, Amalia / Krogh, Vittorio / Martorana, Caterina / Masala, Giovanna / Amiano, Pilar / Huerta, José-María / Barricarte, Aurelio / Quirós, José-Ramón / Weiderpass, Elisabete / Angell Åsli, Lene / Skeie, Guri / Ericson, Ulrika / Sonestedt, Emily / Peeters, Petra H / Romieu, Isabelle / Scalbert, Augustin / Overvad, Kim / Clemens, Matthias / Boeing, Heiner / Trichopoulou, Antonia / Peppa, Eleni / Vidalis, Pavlos / Khaw, Kay-Tee / Wareham, Nick / Olsen, Anja / Tjønneland, Anne / Boutroun-Rualt, Marie-Christine / Clavel-Chapelon, Françoise / Cross, Amanda J / Lu, Yunxia / Riboli, Elio / Duell, Eric J. ·Andalusian School of Public Health, Instituto De Investigación Biosanitaria Ibs, GRANADA, Hospitales Universitarios De Granada/Universidad De Granada, Granada, Spain. · CIBERESP, CIBER Epidemiología Y Salud Pública, Spain. · Section of Nutrition and Metabolism, International Agency for Research on Cancer (IARC), 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. · Department of Epidemiology and Biostatistics, the School of Public Health, Imperial College London, London, United Kingdom. · Department of Social and Preventive Medicine, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia. · Global eHealth Unit, Department of Primary Care and Public Health, the School of Public Health, Imperial College London, London, United Kingdom. · Unit of Nutrition and Cancer, Catalan Institute of Oncology (ICO-Idibell), Barcelona, Spain. · Division of Cancer Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany. · Cancer Epidemiology Unit, Nuffield Department of Population Health, University of Oxford, Oxford, United Kingdom. · Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden. · The Medical Biobank at Umeå University, Umeå, Sweden. · Molecular and Genetic Epidemiology Unit, HuGeF-Human Genetics Foundation, Torino, Italy. · Dipartimento Di Medicina Clinica E Chirurgia, Federico II University, Naples, Italy. · Epidemiology and Prevention Unit Fondazione IRCCS Istituto Nazionale Dei Tumori, Milan, Italy. · Cancer Registry ASP, Ragusa, Italy. · Molecular and Nutritional Epidemiology Unit, Cancer Research and Prevention Institute-ISPO, Florence, Italy. · Public Health Division of Gipuzkoa, BioDonostia Research Institute, San Sebastián, Spain. · Department of Epidemiology, Murcia Regional Health Council, IMIB-Arrixaca, Murcia, Spain. · Public Health Institute of Navarra, Pamplona, Spain. · Public Health Directorate, Asturias, Spain. · 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, Oslo, Norway. · Genetic Epidemiology Group, Folkhälsan Research Center, Helsinki, Finland. · Department of Clinical Sciences in Malmö, Lund University, Lund, Sweden. · Department of Epidemiology, Julius Center for Health Sciences and Primary Care, University Medical Center, Utrecht, The Netherlands. · Department of Public Health, Section for Epidemiology, Aarhus University, Aarhus, Denmark. · Department of Epidemiology, German Institute of Human Nutrition Potsdam-Rehbruecke, Nuthetal, Germany. · Hellenic Health Foundation, Athens, Greece. · WHO Collaborating Center for Nutrition and Health, Unit of Nutritional Epidemiology and Nutrition in Public Health, Department of Hygiene, Epidemiology, and Medical Statistics, University of Athens Medical School, Athens, Greece. · University of Cambridge School of Clinical Medicine, Cambridge, United Kingdom. · Epidemiology Unit, Medical Research Council, Cambridge, United Kingdom. · Danish Cancer Society Research Center, Copenhagen, Denmark. · Inserm, CESP Centre for Research in Epidemiology and Population Health, France. ·Int J Cancer · Pubmed #27184434.

ABSTRACT: Despite the potential cancer preventive effects of flavonoids and lignans, their ability to reduce pancreatic cancer risk has not been demonstrated in epidemiological studies. Our aim was to examine the association between dietary intakes of flavonoids and lignans and pancreatic cancer risk in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. A total of 865 exocrine pancreatic cancer cases occurred after 11.3 years of follow-up of 477,309 cohort members. Dietary flavonoid and lignan intake was estimated through validated dietary questionnaires and the US Department of Agriculture (USDA) and Phenol Explorer databases. Hazard ratios (HR) and 95% confidence intervals (CIs) were calculated using age, sex and center-stratified Cox proportional hazards models, adjusted for energy intake, body mass index (BMI), smoking, alcohol and diabetes status. Our results showed that neither overall dietary intake of flavonoids nor of lignans were associated with pancreatic cancer risk (multivariable-adjusted HR for a doubling of intake = 1.03, 95% CI: 0.95-1.11 and 1.02; 95% CI: 0.89-1.17, respectively). Statistically significant associations were also not observed by flavonoid subclasses. An inverse association between intake of flavanones and pancreatic cancer risk was apparent, without reaching statistical significance, in microscopically confirmed cases (HR for a doubling of intake = 0.96, 95% CI: 0.91-1.00). In conclusion, we did not observe an association between intake of flavonoids, flavonoid subclasses or lignans and pancreatic cancer risk in the EPIC cohort.

7 Article A prospective cohort study on poor oral hygiene and pancreatic cancer risk. 2016

Huang, Jiaqi / Roosaar, Ann / Axéll, Tony / Ye, Weimin. ·Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden. · Department of Dental Medicine, Karolinska Institutet, Stockholm, Sweden. · Maxillofacial Unit, Halmstad Hospital Halland, 30185 Halmstad, Sweden. ·Int J Cancer · Pubmed #26235255.

ABSTRACT: Poor oral hygiene has been proposed to increase the risk for pancreatic cancer. We aim to assess this hypothesis, using number of teeth, dental plaque and oral mucosal lesions examined at baseline as a proxy for oral hygiene. During 1973-74 a population-based prevalence study of oral mucosal lesions was carried out in Uppsala County in central Sweden. We followed the study population through linkages with the Swedish Cancer and Total Population registers. A total of 19,924 participants were included, and 126 pancreatic cancer cases were identified during an average of 28.7 years of follow-up. Hazard ratios (HRs) and their corresponding 95% confidence intervals (CIs) for pancreatic cancer were estimated using Cox proportional hazards regression models. Overall, subjects with fewer teeth at baseline tended to have an increased risk for pancreatic cancer, although the estimates were not statistically significant. Among subjects with more than 10 teeth, those with unacceptable dental plaque had an HR of 2.1 (95% CI: 1.0, 4.7), compared with those without dental plaque after adjustment for potential confounding factors. Individuals with Candida-related or denture-related oral mucosal lesions, or tongue lesions, compared with those without any of the three studied lesions, had a 70, 30 and 80% excess risk of developing pancreatic cancer, respectively. Presence of more than one type of studied lesions further increased the risk for pancreatic cancer. In conclusion, our findings provide evidence to support the hypothesis that poor oral hygiene plays an important role in the development of pancreatic cancer.

8 Article Variant Profiling of Candidate Genes in Pancreatic Ductal Adenocarcinoma. 2015

Huang, Jiaqi / Löhr, Johannes-Matthias / Nilsson, Magnus / Segersvärd, Ralf / Matsson, Hans / Verbeke, Caroline / Heuchel, Rainer / Kere, Juha / Iafrate, A John / Zheng, Zongli / Ye, Weimin. ·Department of Medical Epidemiology and Biostatistics and. · Center for Digestive Diseases, Division of Surgery, CLINTEC, and. · Department of Biosciences and Nutrition and Center for Innovative Medicine (CIMED), Karolinska Institutet, Huddinge, Sweden; · Division of Pathology, Department of Laboratory Medicine, Karolinska Institutet, Stockholm, Sweden; Clinical Pathology/Cytology, Karolinska University Hospital, Stockholm, Sweden; · Department of Pathology, Massachusetts General Hospital, Boston, MA; · Department of Medical Epidemiology and Biostatistics and Department of Pathology, Massachusetts General Hospital, Boston, MA; Current address: Department of Biomedical Sciences, City University of Hong Kong, Hong Kong. zhengzongli@gmail.com weimin.ye@ki.se. · Department of Medical Epidemiology and Biostatistics and zhengzongli@gmail.com weimin.ye@ki.se. ·Clin Chem · Pubmed #26378065.

ABSTRACT: BACKGROUND: Pancreatic ductal adenocarcinoma (PDAC) has a poor prognosis. Variant profiling is crucial for developing personalized treatment and elucidating the etiology of this disease. METHODS: Patients with PDAC undergoing surgery from 2007 to 2012 (n = 73) were followed from diagnosis until death or the end of the study. We applied an anchored multiplex PCR (AMP)-based next-generation sequencing (NGS) method to a panel of 65 selected genes and assessed analytical performance by sequencing a quantitative multiplex DNA reference standard. In clinical PDAC samples, detection of low-level KRAS (Kirsten rat sarcoma viral oncogene homolog) mutations was validated by allele-specific PCR and digital PCR. We compared overall survival of patients according to KRAS mutation status by log-rank test and applied logistic regression to evaluate the association between smoking and tumor variant types. RESULTS: The AMP-based NGS method could detect variants with allele frequencies as low as 1% given sufficient sequencing depth (>1500×). Low-frequency KRAS G12 mutations (allele frequency 1%-5%) were all confirmed by allele-specific PCR and digital PCR. The most prevalent genetic alterations were in KRAS (78% of patients), TP53 (tumor protein p53) (25%), and SMAD4 (SMAD family member 4) (8%). Overall survival in T3-stage PDAC patients differed among KRAS mutation subtypes (P = 0.019). Transversion variants were more common in ever-smokers than in never-smokers (odds ratio 5.7; 95% CI 1.2-27.8). CONCLUSIONS: The AMP-based NGS method is applicable for profiling tumor variants. Using this approach, we demonstrated that in PDAC patients, KRAS mutant subtype G12V is associated with poorer survival, and that transversion variants are more common among smokers.

9 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.

10 Article Pancreatic cancer risk after loss of a child: a register-based study in Sweden during 1991-2009. 2013

Huang, Jiaqi / Valdimarsdóttir, Unnur / Fall, Katja / Ye, Weimin / Fang, Fang. ·Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Box 281, 171 77 Stockholm, Sweden. Jiaqi.huang@ki.se ·Am J Epidemiol · Pubmed #23788670.

ABSTRACT: The potential role of psychological stress in pancreatic cancer has rarely been investigated in epidemiologic studies. During 1991-2009, we conducted a nested case-control study based on Swedish national population and health registers to investigate whether severe psychological stress induced by the death of a child was associated with subsequent risk of pancreatic cancer. The study included 16,522 cases and 82,107 controls who were matched to the cases on sex and year of birth. Conditional logistic regression was used to estimate odds ratios and 95% confidence intervals. Overall, loss of a child was associated with an odds ratio of 1.09 for pancreatic cancer (95% confidence interval (CI): 1.02, 1.17). The risk elevation was mainly seen during the first 5 years after the loss (odds ratio (OR) = 1.27, 95% CI: 1.12, 1.45) and for loss of a child due to suicide (OR = 1.23, 95% CI: 1.03, 1.46). The association was statistically significant among women but not among men, and it appeared stronger for early-onset pancreatic cancer. Persons with a history of psychiatric illness had the greatest risk increase after child loss (OR = 1.43, 95% CI: 1.17, 1.76). Although other explanations are possible, our findings provide some evidence that psychological stress may be associated with pancreatic cancer.

11 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.

12 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.

13 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.

14 Article Meat and fish consumption and risk of pancreatic cancer: results from the European Prospective Investigation into Cancer and Nutrition. 2013

Rohrmann, Sabine / Linseisen, Jakob / Nöthlings, Ute / Overvad, Kim / Egeberg, Rikke / Tjønneland, Anne / Boutron-Ruault, Marie Christine / Clavel-Chapelon, Françoise / Cottet, Vanessa / Pala, Valeria / Tumino, Rosario / Palli, Domenico / Panico, Salvatore / Vineis, Paolo / Boeing, Heiner / Pischon, Tobias / Grote, Verena / Teucher, Birigit / Khaw, Kay-Tee / Wareham, Nicholas J / Crowe, Francesca L / Goufa, Ioulia / Orfanos, Philippos / Trichopoulou, Antonia / Jeurnink, Suzanne M / Siersema, Peter D / Peeters, Petra H M / Brustad, Magritt / Engeset, Dagrun / Skeie, Guri / Duell, Eric J / Amiano, Pilar / Barricarte, Aurelio / Molina-Montes, Esther / Rodríguez, Laudina / Tormo, María-José / Sund, Malin / Ye, Weimin / Lindkvist, Björn / Johansen, Dorthe / Ferrari, Pietro / Jenab, Mazda / Slimani, Nadia / Ward, Heather / Riboli, Elio / Norat, Teresa / Bueno-de-Mesquita, H Bas. ·Division of Cancer Epidemiology and Prevention, Institute of Social and Preventive Medicine, University of Zurich, Zurich, Switzerland. sabine.rohrmann@ifspm.uzh.ch ·Int J Cancer · Pubmed #22610753.

ABSTRACT: Pancreatic cancer is the fourth most common cause of cancer death worldwide with large geographical variation, which implies the contribution of diet and lifestyle in its etiology. We examined the association of meat and fish consumption with risk of pancreatic cancer in the European Prospective Investigation into Cancer and Nutrition (EPIC). A total of 477,202 EPIC participants from 10 European countries recruited between 1992 and 2000 were included in our analysis. Until 2008, 865 nonendocrine pancreatic cancer cases have been observed. Calibrated relative risks (RRs) and 95% confidence intervals (CIs) were computed using multivariable-adjusted Cox hazard regression models. The consumption of red meat (RR per 50 g increase per day = 1.03, 95% CI = 0.93-1.14) and processed meat (RR per 50 g increase per day = 0.93, 95% CI = 0.71-1.23) were not associated with an increased pancreatic cancer risk. Poultry consumption tended to be associated with an increased pancreatic cancer risk (RR per 50 g increase per day = 1.72, 95% CI = 1.04-2.84); however, there was no association with fish consumption (RR per 50 g increase per day = 1.22, 95% CI = 0.92-1.62). Our results do not support the conclusion of the World Cancer Research Fund that red or processed meat consumption may possibly increase the risk of pancreatic cancer. The positive association of poultry consumption with pancreatic cancer might be a chance finding as it contradicts most previous findings.

15 Article Dietary intake of iron, heme-iron and magnesium and pancreatic cancer risk in the European prospective investigation into cancer and nutrition cohort. 2012

Molina-Montes, Esther / Wark, Petra A / Sánchez, María-José / Norat, Teresa / Jakszyn, Paula / Luján-Barroso, Leila / Michaud, Dominique S / Crowe, Francesca / Allen, Naomi / Khaw, Kay-Tee / Wareham, Nicholas / Trichopoulou, Antonia / Adarakis, George / Katarachia, Helen / Skeie, Guri / Henningsen, Maria / Broderstad, Ann Ragnhild / Berrino, Franco / Tumino, Rosario / Palli, Domenico / Mattiello, Amalia / Vineis, Paolo / Amiano, Pilar / Barricarte, Aurelio / Huerta, José-María / Duell, Eric J / Quirós, José-Ramón / Ye, Weimin / Sund, Malin / Lindkvist, Björn / Johansen, Dorthe / Overvad, Kim / Tjønneland, Anne / Roswall, Nina / Li, Kuanrong / Grote, Verena A / Steffen, Annika / Boeing, Heiner / Racine, Antoine / Boutron-Ruault, Marie-Christine / Carbonnel, Franck / Peeters, Petra H M / Siersema, Peter D / Fedirko, Veronika / Jenab, Mazda / Riboli, Elio / Bueno-de-Mesquita, Bas. ·Andalusian School of Public Health. Granada Cancer Registry, Spain. ·Int J Cancer · Pubmed #22438075.

ABSTRACT: Several studies support a protective effect of dietary magnesium against type 2 diabetes, but a harmful effect for iron. As diabetes has been linked to pancreatic cancer, intake of these nutrients may be also associated with this cancer. We examined the association between dietary intake of magnesium, total iron and heme-iron and pancreatic cancer risk in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. In total, 142,203 men and 334,999 women, recruited between 1992 and 2000, were included. After an average follow-up of 11.3 years, 396 men and 469 women developed exocrine pancreatic cancer. Hazard ratios and 95% confidence intervals (CIs) were obtained using Cox regression stratified by age and center, and adjusted for energy intake, smoking status, height, weight, and self-reported diabetes status. Neither intake of magnesium, total iron nor heme-iron was associated with pancreatic cancer risk. In stratified analyses, a borderline inverse association was observed among overweight men (body mass index, ≥ 25 kg/m(2) ) with magnesium (HR(per 100 mg/day increase) = 0.79, 95% CI = 0.63-1.01) although this was less apparent using calibrated intake. In female smokers, a higher intake of heme-iron was associated with a higher pancreatic cancer risk (HR (per 1 mg/day increase) = 1.38, 95% CI = 1.10-1.74). After calibration, this risk increased significantly to 2.5-fold (95% CI = 1.22-5.28). Overall, dietary magnesium, total iron and heme-iron were not associated with pancreatic cancer risk during the follow-up period. Our observation that heme-iron was associated with increased pancreatic cancer risk in female smokers warrants replication in additional study populations.

16 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.

17 Article Plasma cotinine levels and pancreatic cancer in the EPIC cohort study. 2012

Leenders, Max / Chuang, Shu-Chun / Dahm, Christina C / Overvad, Kim / Ueland, Per Magne / Midttun, Oivind / Vollset, Stein Emil / Tjønneland, Anne / Halkjaer, Jytte / Jenab, Mazda / Clavel-Chapelon, Françoise / Boutron-Ruault, Marie-Christine / Kaaks, Rudolf / Canzian, Federico / Boeing, Heiner / Weikert, Cornelia / Trichopoulou, Antonia / Bamia, Christina / Naska, Androniki / Palli, Domenico / Pala, Valeria / Mattiello, Amalia / Tumino, Rosario / Sacerdote, Carlotta / van Duijnhoven, Fränzel J B / Peeters, Petra H M / van Gils, Carla H / Lund, Eiliv / Rodriguez, Laudina / Duell, Eric J / Pérez, María-José Sánchez / Molina-Montes, Esther / Castaño, José María Huerta / Barricarte, Aurelio / Larrañaga, Nerea / Johansen, Dorthe / Lindkvist, Björn / Sund, Malin / Ye, Weimin / Khaw, Kay-Tee / Wareham, Nicholas J / Michaud, Dominique S / Riboli, Elio / Xun, Wei W / Allen, Naomi E / Crowe, Francesca L / Bueno-de-Mesquita, H Bas / Vineis, Paolo. ·School of Public Health, Imperial College London, London, UK. m.leenders-6@umcutrecht.nl ·Int J Cancer · Pubmed #21953524.

ABSTRACT: Smoking is an established risk factor for pancreatic cancer, previously investigated by the means of questionnaires. Using cotinine as a biomarker for tobacco exposure allows more accurate quantitative analyses to be performed. This study on pancreatic cancer, nested within the European Prospective Investigation into Cancer and Nutrition (EPIC cohort), included 146 cases and 146 matched controls. Using liquid chromatography-mass spectrometry, plasma cotinine levels were analyzed on average 8.0 years before cancer onset (5-95% range: 2.8-12.0 years). The relation between plasma cotinine levels and pancreatic cancer was analyzed with conditional logistic regression for different levels of cotinine in a population of never and current smokers. This was also done for the self-reported number of smoked cigarettes per day at baseline. Every increase of 350 nmol/L of plasma cotinine was found to significantly elevate risk of pancreatic cancer [odds ratio (OR): 1.33, 95% confidence interval (CI): 1.11-1.60]. People with a cotinine level over 1187.8 nmol/L, a level comparable to smoking 17 cigarettes per day, have an elevated risk of pancreatic cancer, compared to people with cotinine levels below 55 nmol/L (OR: 3.66, 95% CI: 1.44-9.26). The results for self-reported smoking at baseline also show an increased risk of pancreatic cancer from cigarette smoking based on questionnaire information. People who smoke more than 30 cigarettes per day showed the highest risk compared to never smokers (OR: 4.15, 95% CI: 1.02-16.42). This study is the first to show that plasma cotinine levels are strongly related to pancreatic cancer.

18 Article The association of circulating adiponectin levels with pancreatic cancer risk: a study within the prospective EPIC cohort. 2012

Grote, Verena A / Rohrmann, Sabine / Dossus, Laure / Nieters, Alexandra / Halkjaer, Jytte / Tjønneland, Anne / Overvad, Kim / Stegger, Jakob / Chabbert-Buffet, Nathalie / Boutron-Ruault, Marie-Christine / Clavel-Chapelon, Françoise / Teucher, Birgit / Becker, Susen / Montonen, Jukka / Boeing, Heiner / Trichopoulou, Antonia / Lagiou, Pagona / Trichopoulos, Dimitrios / Palli, Domenico / Sieri, Sabina / Tumino, Rosario / Vineis, Paolo / Mattiello, Amalia / Argüelles, Marcial / Duell, Eric J / Molina-Montes, Esther / Larrañaga, Nerea / Chirlaque, María-Dolores / Gurrea, Aurelio Barricarte / Jeurnink, Suzanne M / Peeters, Petra Hm / Ye, Weimin / Sund, Malin / Lindkvist, Björn / Johansen, Dorthe / Khaw, Kay-Tee / Wareham, Nick / Crowe, Francesca L / Romieu, Isabelle / Rinaldi, Sabina / Jenab, Mazda / Romaguera, Dora / Michaud, Dominique S / Riboli, Elio / Bas Bueno-de-Mesquita, H / Kaaks, Rudolf. ·German Cancer Research Center, Heidelberg, Germany. ·Int J Cancer · Pubmed #21681743.

ABSTRACT: Excess body weight and type 2 diabetes mellitus, risk factors of pancreatic cancer, are characterized by decreased levels of adiponectin. In addition to anti-inflammatory and anti-proliferative actions, adiponectin has an important role in regulating glucose metabolism, i.e., decreasing circulating blood glucose levels. Prospectively, hyperglycemia has been associated with risk of pancreatic cancer. The aim of this study was to investigate the association of pre-diagnostic adiponectin levels with pancreatic cancer risk. We conducted a case-control study nested within European Prospective Investigation into Cancer and Nutrition. Blood samples of 452 pancreatic cancer cases and 452 individually matched controls were analyzed by immunoassays. Multivariate conditional logistic regression was used to estimate odds ratios (OR) and 95% confidence intervals (CI). Overall, adiponectin showed no association with pancreas cancer risk; however, among never smokers, higher circulating levels of adiponectin were associated with a reduction in pancreatic cancer risk (OR = 0.44 [95% CI 0.23-0.82] for highest vs. lowest quartile), whereas among current smokers there was no significant association (OR = 1.59 [95% CI 0.67-3.76] for highest vs. lowest quartile; p-trend = 0.530; p-interaction = 0.309). In our study, lower adiponectin concentrations may be associated with the development of pancreatic cancer among never smokers, whereas the only other prospective study being conducted so far showed a decrease in risk among male smokers. Therefore, further studies are needed to clarify the role of adiponectin in pancreatic cancer development.

19 Article A U-shaped relationship between plasma folate and pancreatic cancer risk in the European Prospective Investigation into Cancer and Nutrition. 2011

Chuang, Shu-Chun / Stolzenberg-Solomon, Rachael / Ueland, Per Magne / Vollset, Stein Emil / Midttun, Øivind / Olsen, Anja / Tjønneland, Anne / Overvad, Kim / Boutron-Ruault, Marie-Christine / Morois, Sophie / Clavel-Chapelon, Françoise / Teucher, Birgit / Kaaks, Rudolf / Weikert, Cornelia / Boeing, Heiner / Trichopoulou, Antonia / Benetou, Vassiliki / Naska, Androniki / Jenab, Mazda / Slimani, Nadia / Romieu, Isabelle / Michaud, Dominique S / Palli, Domenico / Sieri, Sabina / Panico, Salvatore / Sacerdote, Carlotta / Tumino, Rosario / Skeie, Guri / Duell, Eric J / Rodriguez, Laudina / Molina-Montes, Esther / Huerta, José Marı A / Larrañaga, Nerea / Gurrea, Aurelio Barricarte / Johansen, Dorthe / Manjer, Jonas / Ye, Weimin / Sund, Malin / Peeters, Petra H M / Jeurnink, Suzanne / Wareham, Nicholas / Khaw, Kay-Tee / Crowe, Francesca / Riboli, Elio / Bueno-de-Mesquita, Bas / Vineis, Paolo. ·School of Public Health, Imperial College London, London, UK. ·Eur J Cancer · Pubmed #21411310.

ABSTRACT: Folate intake has shown an inverse association with pancreatic cancer; nevertheless, results from plasma measurements were inconsistent. The aim of this study is to examine the association between plasma total homocysteine, methionine, folate, cobalamin, pyridoxal 5'-phosphate, riboflavin, flavin mononucleotide and pancreatic cancer risk in the European Prospective Investigation into Cancer and Nutrition (EPIC). We conducted a nested case-control study in the EPIC cohort, which has an average of 9.6 years of follow-up (1992-2006), using 463 incident pancreatic cancer cases. Controls were matched to each case by center, sex, age (± 1 year), date (± 1 year) and time (± 3 h) at blood collection and fasting status. Conditional logistic regression was used to calculate the odds ratios (OR) and 95% confidence intervals (CI), adjusting for education, smoking status, plasma cotinine concentration, alcohol drinking, body mass index and diabetes status. We observed a U-shaped association between plasma folate and pancreatic cancer risk. The ORs for plasma folate ≤ 5, 5-10, 10-15 (reference), 15-20, and > 20 nmol/L were 1.58 (95% CI=0.72-3.46), 1.39 (0.93-2.08), 1.0 (reference), 0.79 (0.52-1.21), and 1.34 (0.89-2.02), respectively. Methionine was associated with an increased risk in men (per quintile increment: OR=1.17, 95% CI=1.00-1.38) but not in women (OR=0.91, 95% CI=0.78-1.07; p for heterogeneity <0.01). Our results suggest a U-shaped association between plasma folate and pancreatic cancer risk in both men and women. The positive association that we observed between methionine and pancreatic cancer may be sex dependent and may differ by time of follow-up. However, the mechanisms behind the observed associations warrant further investigation.

20 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.