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Pancreatic Neoplasms: HELP
Articles by Carlo La Vecchia
Based on 45 articles published since 2010
(Why 45 articles?)
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Between 2010 and 2020, C. La Vecchia wrote the following 45 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
Pages: 1 · 2
1 Review Genomics in Primary and Secondary Prevention of Pancreatic Cancer. 2017

Malats, Núria / Molina-Montes, Esther / La Vecchia, Carlo. ·Genetic and Molecular Epidemiology Group, Spanish National Cancer Research Center (CNIO), and CIBERONC, Madrid, Spain. ·Public Health Genomics · Pubmed #28689205.

ABSTRACT: BACKGROUND: Pancreatic cancer (PC) is one of the deadliest cancers worldwide for which little clinical progress has been made in the last decades. Furthermore, increased trends of PC mortality rates have been reported in Westernised countries. PC is usually diagnosed in advanced stages, precluding patients of an effective treatment. Identifying high-risk populations and early detection markers is the first and crucial step to impact on these figures and change the PC horizon. AIMS/OBJECTIVES: To discuss the published body of evidence on host and tumor genomics promising markers for primary and/or secondary personalised PC prevention, as well as the future perspectives in the field. METHODS: A review of the literature was performed to identify germline and tumor DNA and RNA markers that showed potential usefulness in defining the high-risk population, diagnosing the disease early, and identifying new carcinogens associated with PC. RESULTS: Only high-penetrance inherited mutations are used, at present, to define the high-risk PC population. Although there are some promising genomics markers to be used as early detection tests, none has been validated adequately to be integrated into the clinics routine. CONCLUSIONS: Despite of important efforts made in the recent time, little progress has been made to better characterise high-risk PC populations and to identify genomics-based markers for its early diagnosis. PC rates continue to rise, and this disease is becoming a real public health problem in the Westernised world. International and multidisciplinary strategies to identify new markers and properly validate the promising ones are urgently needed to implement cost-efficient primary and secondary prevention interventions in PC.

2 Review Pancreatic cancer. 2016

Kleeff, Jorg / Korc, Murray / Apte, Minoti / La Vecchia, Carlo / Johnson, Colin D / Biankin, Andrew V / Neale, Rachel E / Tempero, Margaret / Tuveson, David A / Hruban, Ralph H / Neoptolemos, John P. ·NIHR Pancreas Biomedical Research Unit, Department of Molecular and Clinical Cancer Medicine, University of Liverpool, Royal Liverpool and Broadgreen University Hospitals NHS Trust, Duncan Building, Daulby Street, Liverpool L69 3GA, UK. · Department of General, Visceral and Pediatric Surgery, University Hospital Düsseldorf, Heinrich Heine University, Düsseldorf, Germany. · Departments of Medicine, and Biochemistry and Molecular Biology, Indiana University School of Medicine, the Melvin and Bren Simon Cancer Center, and the Pancreatic Cancer Signature Center, Indianapolis, Indiana, USA. · SWS Clinical School, University of New South Wales, and Ingham Institute for Applied Medical Research, Sydney, New South Wales, Australia. · Department of Clinical Sciences and Community Health, University of Milan, Milan, Italy. · University Surgical Unit, University Hospital Southampton, Southampton, UK. · Institute of Cancer Sciences, Wolfson Wohl Cancer Research Centre, University of Glasgow, Garscube Estate, Bearsden, Glasgow, Scotland, UK. · QIMR Berghofer Medical Research Institute, Brisbane, Queensland, Australia. · UCSF Pancreas Center, University of California San Francisco - Mission Bay Campus/Mission Hall, San Francisco, California, USA. · Cold Spring Harbor Laboratory, Cold Spring Harbor, New York, New York, USA. · The Sol Goldman Pancreatic Cancer Research Center, Departments of Pathology and Oncology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. ·Nat Rev Dis Primers · Pubmed #27158978.

ABSTRACT: Pancreatic cancer is a major cause of cancer-associated mortality, with a dismal overall prognosis that has remained virtually unchanged for many decades. Currently, prevention or early diagnosis at a curable stage is exceedingly difficult; patients rarely exhibit symptoms and tumours do not display sensitive and specific markers to aid detection. Pancreatic cancers also have few prevalent genetic mutations; the most commonly mutated genes are KRAS, CDKN2A (encoding p16), TP53 and SMAD4 - none of which are currently druggable. Indeed, therapeutic options are limited and progress in drug development is impeded because most pancreatic cancers are complex at the genomic, epigenetic and metabolic levels, with multiple activated pathways and crosstalk evident. Furthermore, the multilayered interplay between neoplastic and stromal cells in the tumour microenvironment challenges medical treatment. Fewer than 20% of patients have surgically resectable disease; however, neoadjuvant therapies might shift tumours towards resectability. Although newer drug combinations and multimodal regimens in this setting, as well as the adjuvant setting, appreciably extend survival, ∼80% of patients will relapse after surgery and ultimately die of their disease. Thus, consideration of quality of life and overall survival is important. In this Primer, we summarize the current understanding of the salient pathophysiological, molecular, translational and clinical aspects of this disease. In addition, we present an outline of potential future directions for pancreatic cancer research and patient management.

3 Article Exploring the link between diabetes and pancreatic cancer. 2019

Pizzato, Margherita / Turati, Federica / Rosato, Valentina / La Vecchia, Carlo. ·Department of Clinical Sciences and Community Health, Università degli Studi di Milano , Milan , Italy. · Unit of Medical Statistics and Biometry, Fondazione IRCCS Istituto Nazionale dei Tumori di Milano , Milano , Italy. ·Expert Rev Anticancer Ther · Pubmed #31287962.

ABSTRACT:

4 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

5 Article Pancreatic cancer risk is modulated by inflammatory potential of diet and ABO genotype: a consortia-based evaluation and replication study. 2018

Antwi, Samuel O / Bamlet, William R / Pedersen, Katrina S / Chaffee, Kari G / Risch, Harvey A / Shivappa, Nitin / Steck, Susan E / Anderson, Kristin E / Bracci, Paige M / Polesel, Jerry / Serraino, Diego / La Vecchia, Carlo / Bosetti, Cristina / Li, Donghui / Oberg, Ann L / Arslan, Alan A / Albanes, Demetrius / Duell, Eric J / Huybrechts, Inge / Amundadottir, Laufey T / Hoover, Robert / Mannisto, Satu / Chanock, Stephen J / Zheng, Wei / Shu, Xiao-Ou / Stepien, Magdalena / Canzian, Federico / Bueno-de-Mesquita, Bas / Quirós, José Ramon / Zeleniuch-Jacquotte, Anne / Bruinsma, Fiona / Milne, Roger L / Giles, Graham G / Hébert, James R / Stolzenberg-Solomon, Rachael Z / Petersen, Gloria M. ·Division of Epidemiology, Department of Health Sciences Research, Mayo Clinic, Rochester, MN, USA. · Division of Biomedical Statistics and Informatics, Department of Health Sciences Research, Mayo Clinic, Rochester, MN, USA. · Division of Oncology, Washington University, St. Louis, MO, USA. · Department of Chronic Disease Epidemiology, Yale School of Public Health, New Haven, CT, USA. · Cancer Prevention and Control Program, USA. · Department of Epidemiology and Biostatistics, Arnold School of Public Health, University of South Carolina, Columbia, SC, USA. · Division of Epidemiology and Community Health, School of Public Health, University of Minnesota, Minneapolis, MN, USA. · Department of Epidemiology and Biostatistics, University of California, San Francisco, San Francisco, CA, USA. · Unit of Epidemiology and Biostatistics, Centro di Riferimento Oncologico, Aviano (PN), Italy. · Department of Clinical Sciences and Community Health, University of Milan, Milan, Italy. · Department of Oncology, IRCCS-Istituto di Ricerche Farmacologiche Mario Negri, Milan, Italy. · Department of Gastrointestinal Medical Oncology, The University of Texas M. D. Anderson Cancer Center, Houston, TX, USA. · Department of Environmental Medicine, New York University School of Medicine, New York, NY, USA. · Department of Population Health, New York University School of Medicine, New York, NY, USA. · Department of Obstetrics and Gynecology, New York University School of Medicine, New York, NY, USA. · Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, MD, USA. · Unit of Nutrition and Cancer, Bellvitge Biomedical Research Institute-IDIBELL, Catalan Institute of Oncology-ICO. L'Hospitalet de Llobregat, Barcelona, Spain. · International Agency for Research on Cancer, World Health Organization, France. · Department of Public Health Solutions, National Institute for Health and Welfare Helsinki, Finland. · Division of Epidemiology, Department of Medicine, Vanderbilt Epidemiology Center, and Vanderbilt-Ingram Cancer Center, Vanderbilt University, Nashville, TN, USA. · Genomic Epidemiology Group, German Cancer Research Center (DKFZ), Heidelberg, Germany. · Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, St Mary's Campus, Norfolk Place, London, UK. · Department of Social and Preventive Medicine, Faculty of Medicine, University of Malaya, Pantai Valley, Kuala Lumpur, Malaysia. · Public Health Directorate, Asturias, Spain. · Perlmutter Cancer Center, New York University School of Medicine, New York, NY, USA. · Cancer Epidemiology and Intelligence Division, Cancer Council Victoria, and Centre for Epidemiology and Biostatistics, Melbourne School of Global and Population Health, The University of Melbourne, Melbourne, Australia. ·Carcinogenesis · Pubmed #29800239.

ABSTRACT: Diets with high inflammatory potential are suspected to increase risk for pancreatic cancer (PC). Using pooled analyses, we examined whether this association applies to populations from different geographic regions and population subgroups with varying risks for PC, including variation in ABO blood type. Data from six case-control studies (cases, n = 2414; controls, n = 4528) in the Pancreatic Cancer Case-Control Consortium (PanC4) were analyzed, followed by replication in five nested case-control studies (cases, n = 1268; controls, n = 4215) from the Pancreatic Cancer Cohort Consortium (PanScan). Two polymorphisms in the ABO locus (rs505922 and rs8176746) were used to infer participants' blood types. Dietary questionnaire-derived nutrient/food intake was used to compute energy-adjusted dietary inflammatory index (E-DII®) scores to assess inflammatory potential of diet. Pooled odds ratios (ORs) and 95% confidence intervals (CIs) were calculated using multivariable-adjusted logistic regression. Higher E-DII scores, reflecting greater inflammatory potential of diet, were associated with increased PC risk in PanC4 [ORQ5 versus Q1=2.20, 95% confidence interval (CI) = 1.85-2.61, Ptrend < 0.0001; ORcontinuous = 1.20, 95% CI = 1.17-1.24], and PanScan (ORQ5 versus Q1 = 1.23, 95% CI = 0.92-1.66, Ptrend = 0.008; ORcontinuous = 1.09, 95% CI = 1.02-1.15). As expected, genotype-derived non-O blood type was associated with increased PC risk in both the PanC4 and PanScan studies. Stratified analyses of associations between E-DII quintiles and PC by genotype-derived ABO blood type did not show interaction by blood type (Pinteraction = 0.10 in PanC4 and Pinteraction=0.13 in PanScan). The results show that consuming a pro-inflammatory diet and carrying non-O blood type are each individually, but not interactively, associated with increased PC risk.

6 Article The Association of Recently Diagnosed Diabetes and Long-term Diabetes With Survival in Pancreatic Cancer Patients: A Pooled Analysis. 2018

Jeon, Christie Y / Li, Donghui / Cleary, Sean / Stolzenberg-Solomon, Rachael / Bosetti, Cristina / La Vecchia, Carlo / Porta, Miquel / Toriola, Adetunji T / Hung, Rayjean J / Kurtz, Robert C / Olson, Sara H. · ·Pancreas · Pubmed #29401167.

ABSTRACT: OBJECTIVES: It is unclear whether long-standing diabetes or new-onset pancreatogenic diabetes contributes to poor prognosis in patients with pancreatic ductal adenocarcinoma (PDAC). METHODS: We investigated the influence of diabetes diagnosed shortly before PDAC and long-term diabetes on overall survival in 2792 PDAC patients who had participated in 3 PDAC case-control studies in the Pancreatic Cancer Case-Control Consortium. There were 300 patients with long-term diabetes of more than 3 years' duration (11%) and 418 patients with recently diagnosed diabetes of 3-year duration or less (15%). We performed Cox regression to determine the association of long-term diabetes and recently diagnosed diabetes with overall survival, adjusting for study site, age, sex, race, stage of disease, surgery, chemotherapy, smoking history, and body mass index at diagnosis. RESULTS: In the overall population, neither long-term diabetes (hazard ratio [HR], 1.10; 95% confidence interval [CI], 0.97-1.26) nor recently diagnosed diabetes (HR, 1.06; 95% CI, 0.94-1.18) was associated with shorter survival. When stratified by stage of disease, long-term diabetes was associated with 42% increase in rate of death in persons with resectable PDAC (HR, 1.42; 95% CI, 1.13-1.78), whereas it was not associated with survival in PDAC patients with more advanced disease. CONCLUSION: Long-term diabetes was associated with increased rate of death in patients with resectable PDAC.

7 Article A systems approach identifies time-dependent associations of multimorbidities with pancreatic cancer risk. 2017

Gomez-Rubio, P / Rosato, V / Márquez, M / Bosetti, C / Molina-Montes, E / Rava, M / Piñero, J / Michalski, C W / Farré, A / Molero, X / Löhr, M / Ilzarbe, L / Perea, J / Greenhalf, W / O'Rorke, M / Tardón, A / Gress, T / Barberá, V M / Crnogorac-Jurcevic, T / Muñoz-Bellvís, L / Domínguez-Muñoz, E / Gutiérrez-Sacristán, A / Balsells, J / Costello, E / Guillén-Ponce, C / Huang, J / Iglesias, M / Kleeff, J / Kong, B / Mora, J / Murray, L / O'Driscoll, D / Peláez, P / Poves, I / Lawlor, R T / Carrato, A / Hidalgo, M / Scarpa, A / Sharp, L / Furlong, L I / Real, F X / La Vecchia, C / Malats, N / Anonymous3520902. ·Genetic and Molecular Epidemiology Group, Spanish National Cancer Research Center (CNIO), Madrid, and CIBERONC, Spain. · Branch of Medical Statistics, Biometry and Epidemiology "G.A. Maccacaro," Department of Clinical Sciences and Community Health, University of Milan, Milan. · Unit of Medical Statistics, Biometry and Bioinformatics, National Cancer Institute, IRCCS Foundation, Milan. · Department of Epidemiology, Mario Negri Institute for Pharmacological Research-IRCCS, Milan, Italy. · Research Programme on Biomedical Informatics (GRIB), Hospital del Mar Research Institute (IMIM), Pompeu Fabra Univeristy (UPF), Barcelona, Spain. · Department of Surgery, Technical University of Munich, Munich. · Department of Surgery, University of Heidelberg, Heidelberg, Germany. · Department of Gastroenterology, Santa Creu i Sant Pau Hospital, Barcelona. · Exocrine Pancreas Research Unit and Vall d'Hebron Research Institute (VHIR), Vall d'Hebron University Hospital, Barcelona. · Department of Medicine, Universitat Autònoma de Barcelona, Barcelona. · Network of Biomedical Research Centres (CIBER), Hepatic and Digestive Diseases and Epidemiology and Public Health, Madrid, Spain. · Gastrocentrum, Karolinska Institutet and University Hospital, Stockholm, Sweden. · Department of Gastroenterology, Parc de Salut Mar University Hospital, Barcelona. · Department of Surgery, 12 de Octubre University Hospital, Madrid, Spain. · Department of Molecular and Clinical Cancer Medicine, The Royal Liverpool University Hospital, Liverpool. · Centre for Public Health, Queen's University Belfast, Belfast, UK. · Department of Medicine, University Institute of Oncology of Asturias, Oviedo, Spain. · Department of Gastroenterology, University Hospital of Giessen and Marburg, Marburg, Germany. · Molecular Genetics Laboratory, General University Hospital of Elche, Elche, Spain. · Centre for Molecular Oncology, Barts Cancer Institute, Queen Mary University of London, John Vane Science Centre, London, UK. · General and Digestive Surgery Department, Salamanca University Hospital, Salamanca. · Department of Gastroenterology, Clinical University Hospital of Santiago de Compostela, Santiago de Compostela. · Department of Oncology, Ramón y Cajal Hospital, Madrid, and CIBERONC, Spain. · Research Programme, National Cancer Registry Ireland. · ARC-Net Centre for Applied Research on Cancer and Department of Pathology and Diagnostics, University and Hospital trust of Verona, Verona, Italy. · Clara Campal Integrated Oncological Centre, Sanchinarro Hospital, Madrid, Spain. · Institute of Health & Society, Newcastle University, UK. · Epithelial Carcinogenesis Group, Spanish National Cancer Research Centre (CNIO), Madrid, and CIBERONC. · Department of Experimental and Health Sciences, Pompeu Fabra University, Barcelona, Spain. ·Ann Oncol · Pubmed #28383714.

ABSTRACT: Background: Pancreatic ductal adenocarcinoma (PDAC) is usually diagnosed in late adulthood; therefore, many patients suffer or have suffered from other diseases. Identifying disease patterns associated with PDAC risk may enable a better characterization of high-risk patients. Methods: Multimorbidity patterns (MPs) were assessed from 17 self-reported conditions using hierarchical clustering, principal component, and factor analyses in 1705 PDAC cases and 1084 controls from a European population. Their association with PDAC was evaluated using adjusted logistic regression models. Time since diagnosis of morbidities to PDAC diagnosis/recruitment was stratified into recent (<3 years) and long term (≥3 years). The MPs and PDAC genetic networks were explored with DisGeNET bioinformatics-tool which focuses on gene-diseases associations available in curated databases. Results: Three MPs were observed: gastric (heartburn, acid regurgitation, Helicobacter pylori infection, and ulcer), metabolic syndrome (obesity, type-2 diabetes, hypercholesterolemia, and hypertension), and atopic (nasal allergies, skin allergies, and asthma). Strong associations with PDAC were observed for ≥2 recently diagnosed gastric conditions [odds ratio (OR), 6.13; 95% confidence interval CI 3.01-12.5)] and for ≥3 recently diagnosed metabolic syndrome conditions (OR, 1.61; 95% CI 1.11-2.35). Atopic conditions were negatively associated with PDAC (high adherence score OR for tertile III, 0.45; 95% CI, 0.36-0.55). Combining type-2 diabetes with gastric MP resulted in higher PDAC risk for recent (OR, 7.89; 95% CI 3.9-16.1) and long-term diagnosed conditions (OR, 1.86; 95% CI 1.29-2.67). A common genetic basis between MPs and PDAC was observed in the bioinformatics analysis. Conclusions: Specific multimorbidities aggregate and associate with PDAC in a time-dependent manner. A better characterization of a high-risk population for PDAC may help in the early diagnosis of this cancer. The common genetic basis between MP and PDAC points to a mechanistic link between these conditions.

8 Article Dietary acrylamide and the risk of pancreatic cancer in the International Pancreatic Cancer Case-Control Consortium (PanC4). 2017

Pelucchi, C / Rosato, V / Bracci, P M / Li, D / Neale, R E / Lucenteforte, E / Serraino, D / Anderson, K E / Fontham, E / Holly, E A / Hassan, M M / Polesel, J / Bosetti, C / Strayer, L / Su, J / Boffetta, P / Duell, E J / La Vecchia, C. ·Department of Clinical Sciences and Community Health, University of Milan, Milan. · Unit of Medical Statistics, Biometry and Bioinformatics, Fondazione IRCCS Istituto Nazionale dei Tumori, Milan, Italy. · Department of Epidemiology and Biostatistics, School of Medicine, University of California, San Francisco, San Francisco. · Department of Gastrointestinal Medical Oncology, M.D. Anderson Cancer Center, University of Texas, Houston, USA. · Population Health Department, QIMR Berghofer Medical Research Institute, Brisbane, Australia. · Department of Neurosciences, Psychology, Drug Research and Children's Health, University of Florence, Florence. · Unit of Cancer Epidemiology, CRO Aviano National Cancer Institute, Aviano (PN), Italy. · School of Public Health, University of Minnesota, Minneapolis. · Department of Epidemiology, Louisiana State University Health Sciences Center School of Public Health, New Orleans, USA. · Department of Epidemiology, IRCCS Istituto di Ricerche Farmacologiche Mario Negri, Milan, Italy. · Department of Epidemiology, University of Arkansas for Medical Sciences, Little Rock. · The Tisch Cancer Institute, Mount Sinai School of Medicine, New York, USA. · Unit of Nutrition and Cancer, Cancer Epidemiology Research Program, Catalan Institute of Oncology (ICO), Bellvitge Biomedical Research Institute (IDIBELL), Barcelona, Spain. ·Ann Oncol · Pubmed #27836886.

ABSTRACT: Background: Occupational exposure to acrylamide was associated with excess mortality from pancreatic cancer, though in the absence of dose-risk relationship. Few epidemiological studies have examined the association between acrylamide from diet and pancreatic cancer risk. Patients and methods: We considered this issue in a combined set of 1975 cases of pancreatic cancer and 4239 controls enrolled in six studies of the Pancreatic Cancer Case-Control Consortium (PanC4). We calculated pooled odds ratios (ORs) and their 95% confidence intervals (CI) by estimating study-specific ORs through multivariate unconditional logistic regression models and pooling the obtained estimates using random-effects models. Results: Compared with the lowest level of estimated dietary acrylamide intake, the pooled ORs were 0.97 (95% CI, 0.79-1.19) for the second, 0.91 (95% CI, 0.71-1.16) for the third, and 0.92 (95% CI, 0.66-1.28) for the fourth (highest) quartile of intake. For an increase of 10 µg/day of acrylamide intake, the pooled OR was 0.96 (95% CI, 0.87-1.06), with heterogeneity between estimates (I2 = 67%). Results were similar across various subgroups, and were confirmed when using a one-stage modelling approach. Conclusions: This PanC4 pooled-analysis found no association between dietary acrylamide and pancreatic cancer.

9 Article Global Trends in Pancreatic Cancer Mortality From 1980 Through 2013 and Predictions for 2017. 2016

Lucas, Aimee L / Malvezzi, Matteo / Carioli, Greta / Negri, Eva / La Vecchia, Carlo / Boffetta, Paolo / Bosetti, Cristina. ·Henry D. Janowitz Division of Gastroenterology, Samuel Bronfman Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York. Electronic address: aimee.lucas@mssm.edu. · Department of Clinical Sciences and Community Health, Università degli Studi di Milano, Milan, Italy; Department of Epidemiology, IRCCS-Istituto di Ricerche Farmacologiche "Mario Negri", Milan, Italy. · Department of Clinical Sciences and Community Health, Università degli Studi di Milano, Milan, Italy. · Department of Epidemiology, IRCCS-Istituto di Ricerche Farmacologiche "Mario Negri", Milan, Italy. · Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York, New York. ·Clin Gastroenterol Hepatol · Pubmed #27266982.

ABSTRACT: BACKGROUND & AIMS: Pancreatic cancer is a leading cause of cancer mortality, and its mortality has not decreased in recent years. We sought to determine global trends in pancreatic cancer mortality. METHODS: We derived data on deaths from pancreatic cancer from the World Health Organization database for 59 countries from 1980 through 2013. Age-standardized mortalities were computed for persons of all ages and for persons 35-64 years old; for selected countries, they were computed for persons 25-49 years old. Joinpoint regression models were used to identify significant changes in mortality. For selected larger countries, we predicted number of deaths and mortality for 2017. RESULTS: Between 1980 and 2013, overall pancreatic cancer mortality in men increased in the European Union (EU) as well as in Southern and Eastern Europe, Brazil, Japan, and Republic of Korea. Overall pancreatic cancer mortality decreased in most Northern European countries, Australia, Canada, Mexico, and the United States (US). In women, mortality increased in the EU, Brazil, US, Japan, and Republic of Korea but decreased in Canada and Mexico. In 2012, Eastern Europe and Japan had the highest pancreatic cancer mortality for both sexes. In men 25-49 years old, mortality decreased in the EU, US, Japan, and most large European countries. On the basis of our data, we predict overall pancreatic cancer mortality in 2017 to level off in men in the EU and US but increase in Japan. In women, mortality will continue to increase in most countries except the US; the greatest increase is predicted to occur in Japan. CONCLUSIONS: Mortality from pancreatic cancer has not decreased as it has for other cancers in recent years. A notable exception is a decrease in mortality in men 25-49 years old, which could indicate a reversal in the current increasing global trends.

10 Article Dietary total antioxidant capacity and pancreatic cancer risk: an Italian case-control study. 2016

Lucas, Aimee L / Bosetti, Cristina / Boffetta, Paolo / Negri, Eva / Tavani, Alessandra / Serafini, Mauro / Polesel, Jerry / Serraino, Diego / La Vecchia, Carlo / Rossi, Marta. ·Samuel Bronfman Department of Medicine, Henry D. Janowitz Division of Gastroenterology, Icahn School of Medicine at Mount Sinai, New York 10029, USA. · Department of Epidemiology, IRCCS-Istituto di Ricerche Farmacologiche 'Mario Negri', Milan 20156, Italy. · Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York 10029, USA. · Functional Foods and Metabolic Stress Prevention Laboratory, Center for Food and Nutrition, Research Center on Agriculture and Economics, Rome 00178, Italy. · Unit of Epidemiology and Biostatistics, CRO Aviano National Cancer Institute, Aviano (PN) 33081, Italy. · Department of Clinical Sciences and Community Health, Università degli Studi di Milano, Milan 20133, Italy. ·Br J Cancer · Pubmed #27172251.

ABSTRACT: BACKGROUND: Pancreatic cancer is one of the leading causes of cancer mortality. Diet may be associated with pancreatic cancer, but it is unknown whether specific dietary components contribute to its risk. The potential differential role of dietary antioxidants warrants further investigation. METHODS: We analysed data from a case-control study of 326 pancreatic cancer cases and 652 controls conducted between 1991 and 2008 in Northern Italy. Subjects' usual diet was assessed through a validated and reproducible food frequency questionnaire. Using this information and an Italian food composition database, we calculated three indices of dietary total antioxidant capacity (TAC): Trolox equivalent antioxidant capacity (TEAC), total radical-trapping antioxidant parameter (TRAP) and ferric-reducing antioxidant power (FRAP). We estimated the odds ratios (ORs) and 95% confidence intervals (CIs) for pancreatic cancer using multiple logistic regression models conditioned on study centre, sex and age, and adjusted for major known pancreatic cancer risk factors. RESULTS: Significant inverse associations were found for the highest tertile of TAC compared with the lowest tertile for both TEAC and FRAP. The ORs were 0.61 (95% CI 0.39-0.94, P-value for trend 0.03) and 0.63 (95% CI 0.41-0.99, P-value for trend 0.05), respectively. Total radical-trapping antioxidant parameter was inversely, but not significantly, associated with pancreatic cancer risk, with an OR of 0.78 (95% CI 0.49-1.24, P-value for trend 0.27). CONCLUSIONS: Diet high in TAC, as measured by TEAC and FRAP, is inversely associated with pancreatic cancer risk.

11 Article Menstrual and Reproductive Factors, Hormone Use, and Risk of Pancreatic Cancer: Analysis From the International Pancreatic Cancer Case-Control Consortium (PanC4). 2016

Lujan-Barroso, Leila / Zhang, Wei / Olson, Sara H / Gao, Yu-Tang / Yu, Herbert / Baghurst, Peter A / Bracci, Paige M / Bueno-de-Mesquita, H Bas / Foretová, Lenka / Gallinger, Steven / Holcatova, Ivana / Janout, Vladimír / Ji, Bu-Tian / Kurtz, Robert C / La Vecchia, Carlo / Lagiou, Pagona / Li, Donghui / Miller, Anthony B / Serraino, Diego / Zatonski, Witold / Risch, Harvey A / Duell, Eric J. ·From the *Unit of Nutrition and Cancer, Cancer Epidemiology Research Program, Catalan Institute of Oncology (ICO), Bellvitge Biomedical Research Institute (IDIBELL), Barcelona, Spain; †Department of Epidemiology, Shanghai Cancer Institute and Jiao Tong University, Shanghai, China; ‡Department of Epidemiology and Biostatistics, Memorial Sloan Kettering Cancer Center, New York, NY; §Epidemiology Program, University of Hawaii Cancer Center, Honolulu, HI; ∥Public Health, Women's and Children's Hospital, Adelaide, SA, Australia; ¶University of California, San Francisco, San Francisco, CA; #National Institute for Public Health and the Environment (RIVM), Bilthoven; **Department of Gastroenterology and Hepatology, University Medical Center Utrecht, Utrecht, The Netherlands; ††Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, London, UK; ‡‡Department of Social and Preventive Medicine, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia; §§Department of Cancer Epidemiology and Genetics, Masaryk Memorial Cancer Institute, Institute and MF MU, Brno, Czech Republic; ∥∥University Health Network, Department of Surgery, University of Toronto, Toronto, Canada; ¶¶Institute of Hygiene and Epidemiology, 1st Faculty of Medicine, Charles University in Prague, Prague; ##Department of Preventive Medicine, Faculty of Medicine, Palacky University, Olomouc, Czech Republic; ***National Cancer Institute, Bethesda, MD; †††Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY; ‡‡‡Department of Clinical Sciences and Community Health, Università degli Studi di Milano, Milan, Italy; §§§Department of Hygiene, Epidemiology and Medical Statistics, School of Medicine, University of Athens, Greece; ∥∥∥Department of Epidemiology, Harvard School of Public Health, Boston, MA; ¶¶¶M.D. Anderson Cancer Center, University of Texas, Houston, TX; ###Dalla Lana School of Public Health, University of Toronto, Toronto, Canada; ****Unit of Epidemiology and Biostatistics, CRO Aviano, National Cancer Institute, IRCCS, Aviano, Italy; ††††Cancer Center and Institute of Oncology, Warsaw, Poland; and ‡‡‡‡Department of Chronic Disease Epidemiology, Yale School of Public Health, New Haven, CT. ·Pancreas · Pubmed #27088489.

ABSTRACT: OBJECTIVES: We aimed to evaluate the relation between menstrual and reproductive factors, exogenous hormones, and risk of pancreatic cancer (PC). METHODS: Eleven case-control studies within the International Pancreatic Cancer Case-control Consortium took part in the present study, including in total 2838 case and 4748 control women. Pooled estimates of odds ratios (ORs) and their 95% confidence intervals (CIs) were calculated using a 2-step logistic regression model and adjusting for relevant covariates. RESULTS: An inverse OR was observed in women who reported having had hysterectomy (ORyesvs.no, 0.78; 95% CI, 0.67-0.91), remaining significant in postmenopausal women and never-smoking women, adjusted for potential PC confounders. A mutually adjusted model with the joint effect for hormone replacement therapy (HRT) and hysterectomy showed significant inverse associations with PC in women who reported having had hysterectomy with HRT use (OR, 0.64; 95% CI, 0.48-0.84). CONCLUSIONS: Our large pooled analysis suggests that women who have had a hysterectomy may have reduced risk of PC. However, we cannot rule out that the reduced risk could be due to factors or indications for having had a hysterectomy. Further investigation of risk according to HRT use and reason for hysterectomy may be necessary.

12 Article Risk Factors for Early-Onset and Very-Early-Onset Pancreatic Adenocarcinoma: A Pancreatic Cancer Case-Control Consortium (PanC4) Analysis. 2016

McWilliams, Robert R / Maisonneuve, Patrick / Bamlet, William R / Petersen, Gloria M / Li, Donghui / Risch, Harvey A / Yu, Herbert / Fontham, Elizabeth T H / Luckett, Brian / Bosetti, Cristina / Negri, Eva / La Vecchia, Carlo / Talamini, Renato / Bueno de Mesquita, H Bas / Bracci, Paige / Gallinger, Steven / Neale, Rachel E / Lowenfels, Albert B. ·From the *Department of Oncology, Mayo Clinic, Rochester, MN; †Division of Epidemiology and Biostatistics, European Institute of Oncology, Milan, Italy; ‡Division of Biostatistics, Mayo Clinic; §Department of Health Sciences Research, Mayo Clinic, Rochester, MN; ∥Department of Gastrointestinal Medical Oncology, UT MD Anderson Cancer Center, Houston, TX; ¶Department of Chronic Disease Epidemiology, Yale School of Public Health, New Haven, CT; #Cancer Epidemiology Program, University of Hawaii Cancer Center, Honolulu, HI; **Louisiana State University School of Public Health, New Orleans, LA; ††Tulane School of Public Health, New Orleans, LA; ‡‡Department of Epidemiology, IRCCS-Istituto di Ricerche Farmacologiche "Mario Negri," and §§Department of Clinical Sciences and Community Health, Università degli Studi di Milano, Milan, Italy; ∥∥S.O.C. Epidemiologia e Biostatistica, Centro di Riferimento Oncologico, IRCCS, Aviano (PN), Italy; ¶¶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 Epidemiology and Biostatistics, University of California San Francisco, San Francisco, CA; ***Division of General Surgery, University of Toronto, Toronto, Ontario, Canada; †††Cancer and Population Studies Group, QIMR Berghofer Medical Research Institute, Brisbane, Australia; and ‡‡‡Department of Surgery, Department of Family Medicine, New York Medical College, Valhalla, NY. ·Pancreas · Pubmed #26646264.

ABSTRACT: OBJECTIVES: While pancreatic cancer (PC) most often affects older adults, to date, there has been no comprehensive assessment of risk factors among PC patients younger than 60 years. METHODS: We defined early-onset PC (EOPC) and very-early-onset PC (VEOPC) as diagnosis of PC in patients younger than 60 and 45 years, respectively. We pooled data from 8 case-control studies, including 1954 patients with EOPC and 3278 age- and sex-matched control subjects. Logistic regression analysis was performed to identify associations with EOPC and VEOPC. RESULTS: Family history of PC, diabetes mellitus, smoking, obesity, and pancreatitis were associated with EOPC. Alcohol use equal to or greater than 26 g daily also was associated with increased risk of EOPC (odds ratio, 1.49; 95% confidence interval, 1.21-1.84), and there appeared to be a dose- and age-dependent effect of alcohol on risk. The point estimate for risk of VEOPC was an odds ratio of 2.18 (95% confidence interval, 1.17-4.09). CONCLUSIONS: The established risk factors for PC, including smoking, diabetes, family history of PC, and obesity, also apply to EOPC. Alcohol intake appeared to have an age-dependent effect; the strongest association was with VEOPC.

13 Article Adherence to World Cancer Research Fund/American Institute for Cancer Research recommendations and pancreatic cancer risk. 2016

Lucas, Aimee L / Bravi, Francesca / Boffetta, Paolo / Polesel, Jerry / Serraino, Diego / La Vecchia, Carlo / Bosetti, Cristina. ·Henry D. Janowitz Division of Gastroenterology, Icahn School of Medicine at Mount Sinai, NY, USA. Electronic address: aimee.lucas@mssm.edu. · Department of Epidemiology, IRCCS-Istituto di Ricerche Farmacologiche "Mario Negri"-IRCCS, Milan, Italy. · Tisch Cancer Institute and Institute of Translational Epidemiology, Icahn School of Medicine at Mount Sinai, NY, USA. · Unit of Epidemiology and Biostatistics, CRO Aviano National Cancer Institute, Aviano (PN), Italy. · Department of Clinical Sciences and Community Health, Università degli Studi di Milano, Milan, Italy. ·Cancer Epidemiol · Pubmed #26605429.

ABSTRACT: BACKGROUND: Pancreatic cancer is a leading cause of cancer death. A role of dietary factors in pancreatic carcinogenesis has been suggested. The World Cancer Research Fund (WCRF) and the American Institute for Cancer Research (AICR) published 8 recommendations for cancer prevention. We evaluated the effect of adherence to the WCRF/AICR recommendations on pancreatic cancer risk. METHODS: We operationalized 7 of the 8 WCRF/AICR recommendations to generate a WCRF/AICR score. We examined the association of WCRF/AICR score with pancreatic cancer in data from an Italian case-control study of 326 incident cases and 652 controls. RESULTS: Adherence to WCRF/AICR recommendations was associated with a significantly decreased risk of pancreatic cancer. Using a WCRF/AICR score <3.5 as a reference, the adjusted odds ratio (OR) for a score 3.5-<4 was 0.80 (95% CI 0.49, 1.28), for a score 4-<5 0.54 (95% CI 0.35, 0.82), and for score 5 or more 0.41 (95% CI 0.24, 0.68; p-value for trend 0.0002). The OR for a continuous increment of one unit of the WCRF/AICR score was 0.72 (95% CI 0.60, 0.87). CONCLUSION: Adherence to the WCRF/AICR recommendations may reduce pancreatic cancer risk.

14 Article Vitamin D and pancreatic cancer: a pooled analysis from the Pancreatic Cancer Case-Control Consortium. 2015

Waterhouse, M / Risch, H A / Bosetti, C / Anderson, K E / Petersen, G M / Bamlet, W R / Cotterchio, M / Cleary, S P / Ibiebele, T I / La Vecchia, C / Skinner, H G / Strayer, L / Bracci, P M / Maisonneuve, P / Bueno-de-Mesquita, H B / Zaton Ski, W / Lu, L / Yu, H / Janik-Koncewicz, K / Polesel, J / Serraino, D / Neale, R E / Anonymous2000830. ·Division of Population Health, QIMR Berghofer Medical Research Institute, Herston Centre for Research Excellence in Sun and Health, Queensland University of Technology, Kelvin Grove, Australia. · Department of Chronic Disease Epidemiology, Yale School of Public Health, New Haven, USA. · Department of Epidemiology, IRCCS-Istituto di Ricerche Farmacologiche 'Mario Negri', Milan, Italy. · Division of Epidemiology and Community Health, University of Minnesota, Minneapolis. · Department of Health Sciences Research, Mayo Clinic, Rochester, USA. · Prevention and Cancer Control, Cancer Care Ontario, Toronto Dalla Lana School of Public Health, University of Toronto, Toronto. · Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto Department of Surgery, University of Toronto, Toronto, Canada. · Division of Population Health, QIMR Berghofer Medical Research Institute, Herston. · Department of Clinical Sciences and Community Health, Università degli Studi di Milano, Milan, Italy. · Truven Health Analytics, Durham. · Department of Epidemiology and Biostatistics, University of California San Francisco, San Francisco, USA. · Division of Epidemiology and Biostatistics, European Institute of Oncology, Milan, Italy. · National Institute for Public Health and the Environment, Bilthoven Department of Gastroenterology and Hepatology, University Medical Centre Utrecht, Utrecht, The Netherlands Department of Epidemiology and Biostatistics, The School of Public Health, Imperial College London, London, UK. · Department of Epidemiology, The Maria Skłodowska-Curie Memorial Cancer Center and Institute of Oncology, Warsaw, Poland. · Epidemiology Program, University of Hawaii Cancer Center, Honolulu, USA. · Division of Population Health, QIMR Berghofer Medical Research Institute, Herston Centre for Research Excellence in Sun and Health, Queensland University of Technology, Kelvin Grove, Australia rachel.neale@qimrberghofer.edu.au. ·Ann Oncol · Pubmed #25977560.

ABSTRACT: BACKGROUND: The potential role of vitamin D in the aetiology of pancreatic cancer is unclear, with recent studies suggesting both positive and negative associations. PATIENTS AND METHODS: We used data from nine case-control studies from the International Pancreatic Cancer Case-Control Consortium (PanC4) to examine associations between pancreatic cancer risk and dietary vitamin D intake. Study-specific odds ratios (ORs) were estimated using multivariable logistic regression, and ORs were then pooled using a random-effects model. From a subset of four studies, we also calculated pooled estimates of association for supplementary and total vitamin D intake. RESULTS: Risk of pancreatic cancer increased with dietary intake of vitamin D [per 100 international units (IU)/day: OR = 1.13, 95% confidence interval (CI) 1.07-1.19, P = 7.4 × 10(-6), P-heterogeneity = 0.52; ≥230 versus <110 IU/day: OR = 1.31, 95% CI 1.10-1.55, P = 2.4 × 10(-3), P-heterogeneity = 0.81], with the association possibly stronger in people with low retinol/vitamin A intake. CONCLUSION: Increased risk of pancreatic cancer was observed with higher levels of dietary vitamin D intake. Additional studies are required to determine whether or not our finding has a causal basis.

15 Article Dietary inflammatory index and risk of pancreatic cancer in an Italian case-control study. 2015

Shivappa, Nitin / Bosetti, Cristina / Zucchetto, Antonella / Serraino, Diego / La Vecchia, Carlo / Hébert, James R. ·Cancer Prevention and Control Program, University of South Carolina,915 Greene Street, Suite 241,Columbia,SC29208,USA. · Department of Epidemiology,IRCCS - Istituto di Ricerche Farmacologiche "Mario Negri",Milan,Italy. · S.O.C. di Epidemiologia e Biostatistica, Centro di Riferimento Oncologico,Aviano (PN),Italy. · Department of Clinical Sciences and Community Health,Università degli Studi di Milano,Milan,Italy. ·Br J Nutr · Pubmed #25515552.

ABSTRACT: Previous studies have shown that various dietary components may be implicated in the aetiology of pancreatic cancer. However, the possible relationship between diet-related inflammation and the risk of pancreatic cancer has not yet been investigated. We examined the ability of a newly developed literature-derived dietary inflammatory index (DII) to predict the risk of pancreatic cancer in a case-control study conducted in Italy between 1991 and 2008. This included 326 incident cases and 652 controls admitted to the major teaching and general hospitals for non-neoplastic diseases, frequency-matched to cases by study centre, sex and age. The DII was computed based on dietary intake assessed using a validated and reproducible seventy-eight-item FFQ. Logistic regression models were used to estimate multivariable OR adjusted for age, sex, study centre, education, BMI, smoking status, alcohol drinking and history of diabetes. Energy adjustment was performed using the residual method. Subjects with higher DII scores (i.e., representing a more pro-inflammatory diet) had a higher risk of pancreatic cancer, with the DII being used as both a continuous variable (ORcontinuous 1.24, 95% CI 1.11, 1.38) and a categorical variable (i.e., compared with the subjects in the lowest quintile of the DII, those in the second, third, fourth and fifth quintiles had, respectively, OR(quintile2 v. 1) 1.70, 95% CI 1.02, 2.80; OR(quintile3 v. 1) 1.91, 95% CI 1.16, 3.16; OR(quintile4 v. 1) 1.98, 95% CI 1.20, 3.27; OR(quintile5 v. 1) 2.48, 95% CI 1.50, 4.10; P trend= 0.0015). These data suggest that a pro-inflammatory diet increases the risk of pancreatic cancer.

16 Article Population attributable risk for pancreatic cancer in Northern Italy. 2015

Rosato, Valentina / Polesel, Jerry / Bosetti, Cristina / Serraino, Diego / Negri, Eva / La Vecchia, Carlo. ·From the *Department of Epidemiology, IRCCS-Istituto di Ricerche Farmacologiche Mario Negri, Milan, †Unit of Epidemiology and Biostatistics, IRCCS-CRO Aviano National Cancer Institute, Aviano (PN); and ‡Department of Clinical Sciences and Community Health, Università degli Studi di Milano, Milan, Italy. ·Pancreas · Pubmed #25479588.

ABSTRACT: OBJECTIVE: To provide data on the impact of known risk factors on pancreatic cancer burden, we estimated the population attributable risks (PARs) in the Italian population. METHODS: Data were derived from a case-control study conducted in Northern Italy between 1991 and 2008, including 326 case patients with incident pancreatic cancer and 652 hospital control subjects. RESULTS: We found that 13.6% (95% confidence interval [CI], 6.3-20.8) of pancreatic cancers were attributable to tobacco smoking, 13.0% (95% CI, 2.7-23.2) were attributable to heavy alcohol drinking, 9.7% (95% CI, 5.3-14.1) were attributable to diabetes, 11.9% (95% CI, -8.0 to 31.8) were attributable to a low adherence to Mediterranean diet, and 0.6% (95% CI, -1.8 to 2.9) were attributable to a family history of pancreatic cancer. The PARs for tobacco smoking increased up to 25.7% when we considered it jointly with alcohol, up to 21.7% with diabetes, and up to 24.8% with low Mediterranean diet adherence. For all the risk factors considered, the PARs were higher in men than in women, the differences being particularly evident for heavy alcohol consumption and for a low Mediterranean diet adherence. CONCLUSIONS: These results suggest that an appreciable proportion of pancreatic cancers could be avoided in this Italian population by intervention on a few selected modifiable lifestyle factors.

17 Article Diabetes, antidiabetic medications, and pancreatic cancer risk: an analysis from the International Pancreatic Cancer Case-Control Consortium. 2014

Bosetti, C / Rosato, V / Li, D / Silverman, D / Petersen, G M / Bracci, P M / Neale, R E / Muscat, J / Anderson, K / Gallinger, S / Olson, S H / Miller, A B / Bas Bueno-de-Mesquita, H / Scelo, G / Janout, V / Holcatova, I / Lagiou, P / Serraino, D / Lucenteforte, E / Fabianova, E / Ghadirian, P / Baghurst, P A / Zatonski, W / Foretova, L / Fontham, E / Bamlet, W R / Holly, E A / Negri, E / Hassan, M / Prizment, A / Cotterchio, M / Cleary, S / Kurtz, R C / Maisonneuve, P / Trichopoulos, D / Polesel, J / Duell, E J / Boffetta, P / La Vecchia, C. ·Department of Epidemiology, IRCCS - Istituto di Ricerche Farmacologiche 'Mario Negri', Milan, Italy cristina.bosetti@marionegri.it. · Department of Epidemiology, IRCCS - Istituto di Ricerche Farmacologiche 'Mario Negri', Milan, Italy. · M.D. Anderson Cancer Center, University of Texas, Houston. · Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda. · Department of Health Sciences Research, Medicine and Medical Genetics, Mayo Clinic, Rochester. · Department of Epidemiology and Biostatistics, University of California San Francisco, San Francisco, USA. · Queensland Institute of Medical Research, Brisbane, Australia. · Department of Public Health Sciences, Penn State University, Penn State. · Division of Epidemiology and Community Health, University of Minnesota, Minneapolis, USA. · University Health Network, Department of Surgery, University of Toronto, Toronto, Canada. · Department of Epidemiology and Biostatistics, Memorial Sloan Kettering Cancer Center, New York, USA. · Dalla Lana School of Public Health, University of Toronto, Toronto, Canada. · National Institute for Public Health and the Environment (RIVM), Bilthoven Department of Gastroenterology and Hepatology, University Medical Center Utrecht (UMCU), Utrecht, The Netherlands Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, London, UK. · International Agency for Research on Cancer (IARC), Lyon, France. · Department of Preventive Medicine, Faculty of Medicine, Palacky University, Olomouc. · Institute of Hygiene and Epidemiology, 1st Faculty of Medicine, Charles University in Prague, Prague, Czech Republic. · Department of Epidemiology, Harvard School of Public Health, Boston, USA Department of Hygiene, Epidemiology and Medical Statistics, School of Medicine, University of Athens, Athens, Greece. · Unit of Epidemiology and Biostatistics, CRO Aviano National Cancer Institute, IRCCS, Aviano. · Department of Preclinical and Clinical Pharmacology Mario Aiazzi Mancini, Università degli Studi di Firenze, Florence, Italy. · Regional Authority of Public Health in Banská Bystrica, Banská Bystrica, Slovakia. · Department of Epidemiology, IRCCS - Istituto di Ricerche Farmacologiche 'Mario Negri', Milan, Italy M.D. Anderson Cancer Center, University of Texas, Houston Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda Department of Health Sciences Research, Medicine and Medical Genetics, Mayo Clinic, Rochester Department of Epidemiology and Biostatistics, University of California San Francisco, San Francisco, USA Queensland Institute of Medical Research, Brisbane, Australia Department of Public Health Sciences, Penn State University, Penn State Division of Epidemiology and Community Health, University of Minnesota, Minneapolis, USA University Health Network, Department of Surgery, University of Toronto, Toronto, Canada Department of Epidemiology and Biostatistics, Memorial Sloan Kettering Cancer Center, New York, USA Dalla Lana School of Public Health, University of Toronto, Toronto, Canada National Institute for Public Health and the Environment (RIVM), Bilthoven Department of Gastroenterology and Hepatology, University Medical Center Utrecht (UMCU), Utrecht, The Netherlands Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, London, UK International Agency for Research on Cancer (IARC), Lyon, France Department of Preventive Medicine, Faculty of Medicine, Palacky University, Olomouc Institute of Hygiene and Epidemiology, 1st Faculty of Medicine, Charles University in Prague, Prague, Czech Republic Department of Epidemiology, Harvard School of Public Health, Boston, USA Department of Hygiene, Epidemiology and Medical Statistics, School of Medicine, University of Athens, Athens, Greece Unit of Epidemiology and Biostatistics, CRO Aviano National Cancer Institute, IRCCS, Aviano Department of Preclinical and Clinical Pharmacology Mario Aiazzi Mancini, Università degli Studi di Firenze, Florence, Italy Regional Authority of Public Health in Banská Bystrica, Banská Bystrica, Slovakia Public Health, Women · Public Health, Women's and Children's Hospital, Adelaide, SA, Australia. · Cancer Center and Institute of Oncology, Warsaw, Poland. · Department of Cancer Epidemiology and Genetics, Masaryk Memorial Cancer Institute, Institute and MF MU, Brno, Czech Republic. · Louisiana State University School of Public Health, New Orleans, USA. · Dalla Lana School of Public Health, University of Toronto, Toronto, Canada Cancer Care Ontario, Toronto, Canada. · Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, USA. · Division of Epidemiology and Biostatistics, European Institute of Oncology, Milan, Italy. · Department of Epidemiology, Harvard School of Public Health, Boston, USA. · Unit of Nutrition, Environment and Cancer, Catalan Institute of Oncology (ICO-IDIBELL), L'Hospitalet de Llobregat, Barcelona, Spain. · The Tisch Cancer Institute and Institute for Translational Epidemiology, Icahn School of Medicine at Mount Sinai, New York, USA. · Department of Clinical Sciences and Community Health, Università degli Studi di Milano, Milan, Italy. ·Ann Oncol · Pubmed #25057164.

ABSTRACT: BACKGROUND: Type 2 diabetes mellitus has been associated with an excess risk of pancreatic cancer, but the magnitude of the risk and the time-risk relationship are unclear, and there is limited information on the role of antidiabetic medications. PATIENTS AND METHODS: We analyzed individual-level data from 15 case-control studies within the Pancreatic Cancer Case-Control Consortium, including 8305 cases and 13 987 controls. Pooled odds ratios (ORs) were estimated from multiple logistic regression models, adjusted for relevant covariates. RESULTS: Overall, 1155 (15%) cases and 1087 (8%) controls reported a diagnosis of diabetes 2 or more years before cancer diagnosis (or interview, for controls), corresponding to an OR of 1.90 (95% confidence interval, CI, 1.72-2.09). Consistent risk estimates were observed across strata of selected covariates, including body mass index and tobacco smoking. Pancreatic cancer risk decreased with duration of diabetes, but a significant excess risk was still evident 20 or more years after diabetes diagnosis (OR 1.30, 95% CI 1.03-1.63). Among diabetics, long duration of oral antidiabetic use was associated with a decreased pancreatic cancer risk (OR 0.31, 95% CI 0.14-0.69, for ≥15 years). Conversely, insulin use was associated with a pancreatic cancer risk in the short term (OR 5.60, 95% CI 3.75-8.35, for <5 years), but not for longer duration of use (OR 0.95, 95% CI 0.53-1.70, for ≥15 years). CONCLUSION: This study provides the most definitive quantification to date of an excess risk of pancreatic cancer among diabetics. It also shows that a 30% excess risk persists for more than two decades after diabetes diagnosis, thus supporting a causal role of diabetes in pancreatic cancer. Oral antidiabetics may decrease the risk of pancreatic cancer, whereas insulin showed an inconsistent duration-risk relationship.

18 Article Mortality from lymphohematopoietic neoplasms and other causes in a cohort of laminated plastic workers exposed to formaldehyde. 2014

Pira, Enrico / Romano, Canzio / Verga, Federica / La Vecchia, Carlo. ·Section of Occupational Medicine, Department of Public Health and Pediatrics, University of Turin, Via Zuretti 29, 10126, Turin, Italy. ·Cancer Causes Control · Pubmed #25053406.

ABSTRACT: PURPOSE: A possible relationship between exposure to formaldehyde and leukemia-particularly myeloid leukemia-as well as of lymphoid neoplasms has been debated and is still controversial. We thus examined the issue using data from a cohort of workers of a laminated plastic factory sited in Piedmont, northern Italy. METHODS: The study cohort included 2,750 subjects (2,227 men and 523 women) who worked in the factory between 1947 and 2011, for at least 180 days. Follow-up ended in May 2011, for a total of 70,933 person-years of observation. We computed standardized mortality ratios (SMR) and 95% confidence intervals (CI) using national and (whenever available) Piedmont Region death rates. RESULTS: Overall, there were 417 deaths versus 493.4 expected ones (SMR = 84.5, 95% CI 76.6-93.0). The SMRs were 79.8 (95% CI 67.5-93.6) for total cancer mortality, 148.5 (95% CI 68.0-282.2) for oral cavity and pharynx (three deaths were registered, but not confirmed, as nasopharyngeal cancer), 48.3 (95% CI 13.1-123.7) for pancreas, 66.1 (95% CI 13.6-193.0) for larynx, and 96.7 (95% CI 72.0-127.2) for lung cancer. The SMR of all lymphohematopoietic malignancies was 68.6 (95% CI 31.4-130.3; nine observed deaths). This tended to increase with duration of exposure and to decrease with period at first exposure, always remaining below 100. There were four deaths from lymphoma (SMR = 74.1, 95% CI 20.1-189.6) and five deaths from leukemia (SMR = 92.4, 95% CI 29.9-215.3). CONCLUSIONS: We found no meaningful excess mortality from any lymphohematopoietic nor other neoplasms, except possibly for nasopharyngeal cancer.

19 Article European cancer mortality predictions for the year 2014. 2014

Malvezzi, M / Bertuccio, P / Levi, F / La Vecchia, C / Negri, E. ·Department of Epidemiology, IRCCS-Istituto di Ricerche Farmacologiche 'Mario Negri', Milan Department of Clinical Sciences and Community Health, Universitá Degli Studi di Milano, Milan, Italy. · Department of Epidemiology, IRCCS-Istituto di Ricerche Farmacologiche 'Mario Negri', Milan. · Cancer Epidemiology Unit, Institute of Social and Preventive Medicine (IUMSP), Lausanne University Hospital, Lausanne, Switzerland. · Department of Clinical Sciences and Community Health, Universitá Degli Studi di Milano, Milan, Italy carlo.lavecchia@unimi.it. ·Ann Oncol · Pubmed #24759568.

ABSTRACT: BACKGROUND: From most recent available data, we projected cancer mortality statistics for 2014, for the European Union (EU) and its six more populous countries. Specific attention was given to pancreatic cancer, the only major neoplasm showing unfavorable trends in both sexes. PATIENTS AND METHODS: Population and death certification data from stomach, colorectum, pancreas, lung, breast, uterus, prostate, leukemias and total cancers were obtained from the World Health Organisation database and Eurostat. Figures were derived for the EU, France, Germany, Italy, Poland, Spain and the UK. Projected 2014 numbers of deaths by age group were obtained by linear regression on estimated numbers of deaths over the most recent time period identified by a joinpoint regression model. RESULTS: In the EU in 2014, 1,323,600 deaths from cancer are predicted (742,500 men and 581,100 women), corresponding to standardized death rates of 138.1/100,000 men and 84.7/100,000 women, falling by 7% and 5%, respectively, since 2009. In men, predicted rates for the three major cancers (lung, colorectum and prostate cancer) are lower than in 2009, falling by 8%, 4% and 10%, respectively. In women, breast and colorectal cancers had favorable trends (-9% and -7%), but female lung cancer rates are predicted to rise 8%. Pancreatic cancer is the only neoplasm with a negative outlook in both sexes. Only in the young (25-49 years), EU trends become more favorable in men, while women keep registering slight predicted rises. CONCLUSIONS: Cancer mortality predictions for 2014 confirm the overall favorable cancer mortality trend in the EU, translating to an overall 26% fall in men since its peak in 1988, and 20% in women, and the avoidance of over 250,000 deaths in 2014 compared with the peak rate. Notable exceptions are female lung cancer and pancreatic cancer in both sexes.

20 Article Smoking and body mass index and survival in pancreatic cancer patients. 2014

Pelucchi, Claudio / Galeone, Carlotta / Polesel, Jerry / Manzari, Marco / Zucchetto, Antonella / Talamini, Renato / Franceschi, Silvia / Negri, Eva / La Vecchia, Carlo. ·From the *Dipartimento di Epidemiologia, IRCCS-Istituto di Ricerche Farmacologiche Mario Negri; †Dipartimento di Scienze Cliniche e di Comunità, Università degli Studi di Milano, Milan; ‡S.O.C. di Epidemiologia e Biostatistica, IRCCS-Centro di Riferimento Oncologico, Aviano (PN); §Dipartimento di Traumatologia, Ortopedia e Medicina del Lavoro, Università degli Studi di Torino, Turin, Italy; and ∥International Agency for Research on Cancer, Lyon, France. ·Pancreas · Pubmed #24177141.

ABSTRACT: OBJECTIVE: The objective of this study was to provide further information on the role of personal characteristics and lifestyle factors, including obesity, diabetes, and tobacco smoking, on survival from pancreatic cancer. METHODS: We obtained follow-up data of pancreatic cancer patients enrolled in 2 Italian case-control studies. Information on characteristics and habits up to the time of diagnosis was collected by trained interviewers. Vital status was ascertained through population registers and record linkage with health system databases. Hazard ratios (HRs) of all-cause mortality and 95% confidence intervals (CIs) were estimated using Cox proportional hazards models. RESULTS: Follow-up information was retrieved for 648 cancer patients. Compared with subjects with body mass index of less than 25 kg/m, the HRs were 1.14 (95% CI, 0.94-1.39) for overweight (ie, 25-29.9 kg/m) and 1.32 (95% CI, 0.98-1.79) for obese (ie, ≥30 kg/m) patients (trend P = 0.046). The HRs were 1.37 (95% CI, 1.14-1.65) for ever, 1.30 (95% CI, 1.03-1.65) for ex-smokers, and 1.42 (95% CI, 1.16-1.73) for current versus never smokers. Increasing amount and duration of smoking were associated with reduced survival after pancreatic cancer. No association emerged with diabetes, alcohol consumption, and diet. CONCLUSIONS: Smoking and overweight before diagnosis may play a role in the prognosis of pancreatic cancer, besides its etiology.

21 Article EU Pancreas: an integrated European platform for pancreas cancer research--from basic science to clinical and public health interventions for a rare disease. 2013

Milne, R / La Vecchia, C / Van Steen, K / Hahn, S / Buchholz, M / Costello, E / Esposito, I / Hoheisel, J D / Lange, B / Lopez-Bigas, N / Michalski, C W / Real, F X / Brand, A / Malats, N. ·Genetic and Molecular Epidemiology Group, Spanish National Cancer Research Centre (CNIO), Madrid, Spain. ·Public Health Genomics · Pubmed #24503591.

ABSTRACT: BACKGROUND: Large-scale international collaboration is essential to decipher relevant information in the context of omics-scale interrogations in cancer research. This is even more important for rare and fatal diseases like pancreas cancer (PC). METHODS: The COST Action BM1204 is a unique platform to facilitate the collaboration of a broad range of European and international PC multidisciplinary research groups in order to: (1) integrate knowledge and experience in a multidisciplinary way 'from cell to society', (2) promote the application of uniform study tools and protocols, (3) foster their optimal use by early-stage researchers, (4) enhance the mobility and training of researchers, and (5) disseminate the results produced to the broader society. RESULTS: This Action will develop novel interdisciplinary tools for collaborative research to improve our understanding of PC and its prevention, diagnosis and treatment. It also aims to answer questions related to the etiology, early detection, evidence-based and personalized treatment, and health management for PC. Furthermore, the Action will contribute to new insights into PC personalized medicine and beyond as well as to the understanding of complex and rare diseases taking PC as a best practice example. The Action aims at attracting young scholars across a range of disciplines in collaboration with more experienced researchers and enhancing active European participation in the international scenario of PC research. CONCLUSION: The ultimate aim is to foster PC research in Europe and to coordinate this effort with other international initiatives to reduce disease mortality.

22 Article Ulcer, gastric surgery and pancreatic cancer risk: an analysis from the International Pancreatic Cancer Case-Control Consortium (PanC4). 2013

Bosetti, C / Lucenteforte, E / Bracci, P M / Negri, E / Neale, R E / Risch, H A / Olson, S H / Gallinger, S / Miller, A B / Bueno-de-Mesquita, H B / Talamini, R / Polesel, J / Ghadirian, P / Baghurst, P A / Zatonski, W / Fontham, E / Holly, E A / Gao, Y T / Yu, H / Kurtz, R C / Cotterchio, M / Maisonneuve, P / Zeegers, M P / Duell, E J / Boffetta, P / La Vecchia, C. ·Department of Epidemiology, IRCCS, Istituto di Ricerche Farmacologiche 'Mario Negri', Milan. ·Ann Oncol · Pubmed #23970016.

ABSTRACT: BACKGROUND: Peptic ulcer and its treatments have been associated to pancreatic cancer risk, although the evidence is inconsistent. METHODS: We pooled 10 case-control studies within the Pancreatic Cancer Case-control Consortium (PanC4), including 4717 pancreatic cancer cases and 9374 controls, and estimated summary odds ratios (OR) using multivariable logistic regression models. RESULTS: The OR for pancreatic cancer was 1.10 [95% confidence interval (CI) 0.98-1.23] for history of ulcer (OR = 1.08 for gastric and 0.97 for duodenal ulcer). The association was stronger for a diagnosis within 2 years before cancer diagnosis (OR = 2.43 for peptic, 1.75 for gastric, and 1.98 for duodenal ulcer). The OR was 1.53 (95% CI 1.15-2.03) for history of gastrectomy; however, the excess risk was limited to a gastrectomy within 2 years before cancer diagnosis (OR = 6.18, 95% CI 1.82-20.96), while no significant increased risk was observed for longer time since gastrectomy. No associations were observed for pharmacological treatments for ulcer, such as antacids, H2-receptor antagonists, or proton-pump inhibitors. CONCLUSIONS: This uniquely large collaborative study does not support the hypothesis that peptic ulcer and its treatment materially affect pancreatic cancer risk. The increased risk for short-term history of ulcer and gastrectomy suggests that any such association is due to increased cancer surveillance.

23 Article The role of Mediterranean diet on the risk of pancreatic cancer. 2013

Bosetti, C / Turati, F / Dal Pont, A / Ferraroni, M / Polesel, J / Negri, E / Serraino, D / Talamini, R / La Vecchia, C / Zeegers, M P. ·Department of Epidemiology, IRCCS-Istituto di Ricerche Farmacologiche Mario Negri, Milan, Italy. cristina.bosetti@marionegri.it ·Br J Cancer · Pubmed #23928660.

ABSTRACT: BACKGROUND: The Mediterranean diet has been shown to have a beneficial role on various neoplasms, but data are scanty on pancreatic cancer. METHODS: We analysed data from two case-control studies conducted in Italy between 1983 and 2008, including 362 and 326 pancreatic cancer cases and 1552 and 652 hospital-controls, respectively. A Mediterranean Diet Score (MDS) summarising major characteristics of the Mediterranean diet was used in the two studies separately and overall. Two further scores of adherence to the Mediterranean diet were applied in the second study only, the Mediterranean Dietary Pattern Adherence Index (MDP) and the Mediterranean Adequacy Index (MAI). RESULTS: Odds ratios (ORs) for increasing levels of the scores (i.e., increasing adherence) were estimated using multiple logistic regression models. Odds ratio for a MDS score ≥6 compared with <3 was 0.57 (95% confidence interval (CI) 0.34-0.95) in the first study, 0.51 (95% CI 0.29-0.92) in the second study, and 0.48 (95% CI 0.35-0.67) overall. A trend of decreasing risk was observed also for the MDP and MAI the ORs for the highest vs the lowest quintile being 0.44 (95% CI 0.27-0.73) for MDP and 0.68 (95% CI 0.42-1.11) for the MAI. The results were consistent across strata of age, sex, education, body mass index, alcohol drinking, tobacco smoking, and diabetes. CONCLUSION: Our study provides evidence that a priori-defined scores measuring adherence to the Mediterranean diet are favourably associated with pancreatic cancer risk.

24 Article Allergies and risk of pancreatic cancer: a pooled analysis from the Pancreatic Cancer Case-Control Consortium. 2013

Olson, Sara H / Hsu, Meier / Satagopan, Jaya M / Maisonneuve, Patrick / Silverman, Debra T / Lucenteforte, Ersilia / Anderson, Kristin E / Borgida, Ayelet / Bracci, Paige M / Bueno-de-Mesquita, H Bas / Cotterchio, Michelle / Dai, Qi / Duell, Eric J / Fontham, Elizabeth H / Gallinger, Steven / Holly, Elizabeth A / Ji, Bu-Tian / Kurtz, Robert C / La Vecchia, Carlo / Lowenfels, Albert B / Luckett, Brian / Ludwig, Emmy / Petersen, Gloria M / Polesel, Jerry / Seminara, Daniela / Strayer, Lori / Talamini, Renato / Anonymous6300762. ·Department of Epidemiology and Biostatistics, 307 East 63rd Street, New York, NY 10065, USA. olsons@mskcc.org ·Am J Epidemiol · Pubmed #23820785.

ABSTRACT: In order to quantify the risk of pancreatic cancer associated with history of any allergy and specific allergies, to investigate differences in the association with risk according to age, gender, smoking status, or body mass index, and to study the influence of age at onset, we pooled data from 10 case-control studies. In total, there were 3,567 cases and 9,145 controls. Study-specific odds ratios and 95% confidence intervals were calculated by using unconditional logistic regression adjusted for age, gender, smoking status, and body mass index. Between-study heterogeneity was assessed by using the Cochran Q statistic. Study-specific odds ratios were pooled by using a random-effects model. The odds ratio for any allergy was 0.79 (95% confidence interval (CI): 0.62, 1.00) with heterogeneity among studies (P < 0.001). Heterogeneity was attributable to one study; with that study excluded, the pooled odds ratio was 0.73 (95% CI: 0.64, 0.84) (Pheterogeneity = 0.23). Hay fever (odds ratio = 0.74, 95% CI: 0.56, 0.96) and allergy to animals (odds ratio = 0.62, 95% CI: 0.41, 0.94) were related to lower risk, while there was no statistically significant association with other allergies or asthma. There were no major differences among subgroups defined by age, gender, smoking status, or body mass index. Older age at onset of allergies was slightly more protective than earlier age.

25 Article Nutrient-based dietary patterns and pancreatic cancer risk. 2013

Bosetti, Cristina / Bravi, Francesca / Turati, Federica / Edefonti, Valeria / Polesel, Jerry / Decarli, Adriano / Negri, Eva / Talamini, Renato / Franceschi, Silvia / La Vecchia, Carlo / Zeegers, Maurice P. ·Dipartimento di Epidemiologia, Istituto di Ricerche Farmacologiche Mario Negri Milan, Italy. cristina.bosetti@marionegri.it ·Ann Epidemiol · Pubmed #23332711.

ABSTRACT: PURPOSE: Few data are available on the role of combinations of foods and/or nutrients on pancreatic cancer risk. To add further information on dietary patterns potentially associated to pancreatic cancer, we applied an exploratory principal component factor analysis on 28 major nutrients derived from an Italian case-control study. METHODS: Cases were 326 incident pancreatic cancer cases and controls 652 frequency-matched controls admitted to hospital for non-neoplastic diseases. Dietary information was collected through a validated and reproducible food frequency questionnaire. Multiple logistic regression models adjusted for sociodemographic variables and major recognized risk factors for pancreatic cancer were used to estimate the odds ratios (OR) of pancreatic cancer for each dietary pattern. RESULTS: We identified four dietary patterns-named "animal products," "unsaturated fats," "vitamins and fiber," and "starch rich," that explain 75% of the total variance in nutrient intake in this population. After allowing for all the four patterns, positive associations were found for the animal products and the starch rich patterns, the OR for the highest versus the lowest quartiles being 2.03 (95% confidence interval [CI], 1.29-3.19) and 1.69 (95% CI, 1.02-2.79), respectively; an inverse association emerged for the vitamins and fiber pattern (OR, 0.55; 95% CI, 0.35-0.86), whereas no association was observed for the unsaturated fats pattern (OR, 1.13; 95% CI, 0.71-1.78). CONCLUSIONS: A diet characterized by a high consumption of meat and other animal products, as well as of (refined) cereals and sugars, is positively associated with pancreatic cancer risk, whereas a diet rich in fruit and vegetables is inversely associated.

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