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Pancreatic Neoplasms: HELP
Articles by Eva Negri
Based on 24 articles published since 2010
(Why 24 articles?)
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Between 2010 and 2020, E. Negri wrote the following 24 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 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.

2 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.

3 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.

4 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.

5 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.

6 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.

7 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.

8 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.

9 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.

10 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.

11 Article Pancreatic cancer: overview of descriptive epidemiology. 2012

Bosetti, Cristina / Bertuccio, Paola / Negri, Eva / La Vecchia, Carlo / Zeegers, Maurice P / Boffetta, Paolo. ·Dipartimento di Epidemiologia, Istituto di Ricerche Farmacologiche Mario Negri, Milan, Italy. ·Mol Carcinog · Pubmed #22162227.

ABSTRACT: Pancreatic cancer mortality rates have been increasing in high-income countries between the 1950s and the 1980s, and have leveled off or declined thereafter, particularly in men. To provide a global overview of recent pancreatic cancer mortality, we analyzed official death of the world certification data derived from the World Health Organization for 35 European countries and 19 other countries over the period 1980-2007. In 2007, the highest mortality rates from pancreatic cancer were in the Baltic countries, and some central/eastern and northern European countries (over 9.5/100 000 men and 6/100 000 women), whereas the lowest ones were in Latin America and Hong Kong (below 5/100 000 men and 3/100 000 women). Japan, the USA, Russia and the European Union (EU), as well as the largest countries in the EU, had rates around 7-9/100 000 men and 5-6/100 000 women. In the early 2000s, rates have been approximately stable in many European countries, as in the USA, Japan, and Australia. In Nordic countries and the UK, where declines in rates have been observed between the 1980s and the 1990s, mortality from pancreatic cancer has tended to rise over most recent calendar years. Some persisting rises were still found in men from a few countries of southern and central/eastern Europe (with low rates in the past), as well as in the EU overall, and in women from European and Asian countries. Recent trends were generally more favorable in young adults (30-49 yr), suggesting that overall trends are likely to improve in the near future.

12 Article Cigarette smoking and pancreatic cancer: an analysis from the International Pancreatic Cancer Case-Control Consortium (Panc4). 2012

Bosetti, C / Lucenteforte, E / Silverman, D T / Petersen, G / Bracci, P M / Ji, B T / Negri, E / Li, D / 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 / Bamlet, W R / Holly, E A / Bertuccio, P / Gao, Y T / Hassan, M / Yu, H / Kurtz, R C / Cotterchio, M / Su, J / Maisonneuve, P / Duell, E J / Boffetta, P / La Vecchia, C. ·Department of Epidemiology, Istituto di Ricerche Farmacologiche Mario Negri, Milan, Italy. cristina.bosetti@marionegri.it ·Ann Oncol · Pubmed #22104574.

ABSTRACT: BACKGROUND: To evaluate the dose-response relationship between cigarette smoking and pancreatic cancer and to examine the effects of temporal variables. METHODS: We analyzed data from 12 case-control studies within the International Pancreatic Cancer Case-Control Consortium (PanC4), including 6507 pancreatic cases and 12 890 controls. We estimated summary odds ratios (ORs) by pooling study-specific ORs using random-effects models. RESULTS: Compared with never smokers, the OR was 1.2 (95% confidence interval [CI] 1.0-1.3) for former smokers and 2.2 (95% CI 1.7-2.8) for current cigarette smokers, with a significant increasing trend in risk with increasing number of cigarettes among current smokers (OR=3.4 for ≥35 cigarettes per day, P for trend<0.0001). Risk increased in relation to duration of cigarette smoking up to 40 years of smoking (OR=2.4). No trend in risk was observed for age at starting cigarette smoking, whereas risk decreased with increasing time since cigarette cessation, the OR being 0.98 after 20 years. CONCLUSIONS: This uniquely large pooled analysis confirms that current cigarette smoking is associated with a twofold increased risk of pancreatic cancer and that the risk increases with the number of cigarettes smoked and duration of smoking. Risk of pancreatic cancer reaches the level of never smokers ∼20 years after quitting.

13 Article Proanthocyanidins and other flavonoids in relation to pancreatic cancer: a case-control study in Italy. 2012

Rossi, M / Lugo, A / Lagiou, P / Zucchetto, A / Polesel, J / Serraino, D / Negri, E / Trichopoulos, D / La Vecchia, C. ·Department of Epidemiology, Mario Negri Institute for Pharmacological Research, Milan, Italy. marta.rossi@marionegri.it ·Ann Oncol · Pubmed #22052986.

ABSTRACT: BACKGROUND: Four cohort studies have examined the relation between flavonoids and pancreatic cancer risk providing inconsistent results. PATIENTS AND METHODS: We conducted a case-control study between 1991 and 2008 in Northern Italy. Subjects were 326 cases with incident pancreatic cancer and 652 frequency-matched controls (admitted to the same hospitals as cases for acute non-neoplastic conditions) who answered a reproducible and valid food-frequency questionnaire. We computed odds ratios (ORs) using logistic regression models conditioned on gender, age and study center, and adjusted for education, history of diabetes, tobacco smoking, alcohol drinking and energy intake. RESULTS: Proanthocyanidins with three or more mers were inversely related to pancreatic cancer risk. The ORs were similar in all classes of polymers with three or more mers and in their combination (OR for the highest versus the lowest quintile of intake, 0.41; 95% confidence interval 0.24-0.69), and did not substantially change after adjustment for fruit and vegetable consumption, and for vitamin C and folate intakes. Eating an additional portion of fruits rich in proanthocyanidins every day reduced the risk of pancreatic cancer by 25%. CONCLUSION: Dietary proanthocyanidins-mostly present in apples, pears and pulses-may convey some protection against pancreatic cancer risk.

14 Article Alcohol consumption and pancreatic cancer: a pooled analysis in the International Pancreatic Cancer Case-Control Consortium (PanC4). 2012

Lucenteforte, E / La Vecchia, C / Silverman, D / Petersen, G M / Bracci, P M / Ji, B T / Bosetti, C / Li, D / Gallinger, S / Miller, A B / Bueno-de-Mesquita, H B / Talamini, R / Polesel, J / Ghadirian, P / Baghurst, P A / Zatonski, W / Fontham, E / Bamlet, W R / Holly, E A / Gao, Y T / Negri, E / Hassan, M / Cotterchio, M / Su, J / Maisonneuve, P / Boffetta, P / Duell, E J. ·Department of Epidemiology, Istituto di Ricerche Farmacologiche Mario Negri Milan, Milan, Italy. ·Ann Oncol · Pubmed #21536662.

ABSTRACT: BACKGROUND: Heavy alcohol drinking has been related to pancreatic cancer, but the issue is still unsolved. METHODS: To evaluate the role of alcohol consumption in relation to pancreatic cancer, we conducted a pooled analysis of 10 case-control studies (5585 cases and 11,827 controls) participating in the International Pancreatic Cancer Case-Control Consortium. We computed pooled odds ratios (ORs) by estimating study-specific ORs adjusted for selected covariates and pooling them using random effects models. RESULTS: Compared with abstainers and occasional drinkers (< 1 drink per day), we observed no association for light-to-moderate alcohol consumption (≤ 4 drinks per day) and pancreatic cancer risk; however, associations were above unity for higher consumption levels (OR = 1.6, 95% confidence interval 1.2-2.2 for subjects drinking ≥ 9 drinks per day). Results did not change substantially when we evaluated associations by tobacco smoking status, or when we excluded participants who reported a history of pancreatitis, or participants whose data were based upon proxy responses. Further, no notable differences in pooled risk estimates emerged across strata of sex, age, race, study type, and study area. CONCLUSION: This collaborative-pooled analysis provides additional evidence for a positive association between heavy alcohol consumption and the risk of pancreatic cancer.

15 Article Fiber intake and pancreatic cancer risk: a case-control study. 2012

Bidoli, E / Pelucchi, C / Zucchetto, A / Negri, E / Dal Maso, L / Polesel, J / Boz, G / Montella, M / Franceschi, S / Serraino, D / La Vecchia, C / Talamini, R. ·Unit of Epidemiology and Biostatistics, Centro di Riferimento Oncologico, Aviano, Italy. epidemiology@cro.it ·Ann Oncol · Pubmed #21460379.

ABSTRACT: BACKGROUND: Scanty and inconsistent studies are available on the relation between dietary fiber intake and pancreatic cancer. A case-control study was carried out in northern Italy to further investigate the role of various types of dietary fibers in the etiology of pancreatic cancer. PATIENTS AND METHODS: Cases were 326 patients with incident pancreatic cancer, excluding neuroendocrine tumors, admitted to major teaching and general hospitals during 1991-2008. Controls were 652 patients admitted for acute, nonneoplastic conditions to the same hospital network of cases. Information was elicited using a validated food frequency questionnaire. Odds ratios (ORs) and the corresponding 95% confidence intervals (CIs) were estimated for intake quintiles of different types of fiber after allowance for total energy intake and other potential confounding factors. RESULTS: Total fiber intake was inversely related to risk of pancreatic cancer (OR=0.4 for highest versus lowest quintile of intake; 95% CI 0.2-0.7). An inverse association emerged between pancreatic cancer and both soluble (OR=0.4; 95% CI 0.2-0.7) and total insoluble fiber (OR=0.5; 95% CI 0.3-0.8), particularly cellulose (OR=0.4; 95% CI 0.3-0.7) and lignin (OR=0.5; 95% CI 0.3-0.9). Fruit fiber intake was inversely associated with pancreatic cancer (OR=0.5; 95% CI 0.3-0.8), whereas grain fiber was not (OR=1.2; 95% CI 0.7-2.0). CONCLUSIONS: This study suggests that selected types of fiber and total fiber are inversely related to pancreatic cancer.

16 Article Metabolic syndrome and pancreatic cancer risk: a case-control study in Italy and meta-analysis. 2011

Rosato, Valentina / Tavani, Alessandra / Bosetti, Cristina / Pelucchi, Claudio / Talamini, Renato / Polesel, Jerry / Serraino, Diego / Negri, Eva / La Vecchia, Carlo. ·Department of Epidemiology, Istituto di Ricerche Farmacologiche Mario Negri, Milan, Italy. ·Metabolism · Pubmed #21550085.

ABSTRACT: We assessed the relation between metabolic syndrome (MetS), its components, and pancreatic cancer risk in an Italian case-control study and performed a meta-analysis of epidemiological studies published up to February 2011. The case-control study included 326 patients with incident pancreatic cancer and 652 controls admitted to the same hospitals for acute, non-neoplastic conditions. MetS was defined as having at least 3 conditions among diabetes, drug-treated hypertension, hyperlipidemia, and body mass index at least 25 kg/m(2) at age 30 years. We computed multivariate odds ratios (ORs) and the corresponding 95% confidence intervals (CIs) from logistic regression models adjusted for tobacco smoking, education, and other sociodemographic variables. For the meta-analysis, we calculated summary relative risks (RRs) using random-effects models. The OR of pancreatic cancer in the case-control study was 2.36 (95% CI, 1.43-3.90) for diabetes, 0.77 (95% CI, 0.55-1.08) for hypertension, 1.38 (95% CI, 0.94-2.01) for hypercholesterolemia, and 1.27 (95% CI, 0.91-1.78) for being overweight at age 30 years. The risk was significantly increased for subjects with 3 or more MetS components (OR = 2.13, 95% CI 1.01-4.49) compared with subjects with no component, the estimates being consistent among strata of sex, age, and alcohol consumption. The meta-analysis included 3 cohort studies and our case-control study, and found a summary RR of 1.55 (95% CI, 1.19-2.01) for subjects with MetS. Metabolic syndrome is related to pancreatic cancer risk. Diabetes is the key component related to risk.

17 Article Reproductive and hormonal factors and pancreatic cancer risk in women. 2011

Lucenteforte, Ersilia / Zucchetto, Antonella / Bosetti, Cristina / Talamini, Renato / Negri, Eva / Serraino, Diego / Franceschi, Silvia / Lipworth, Loren / La Vecchia, Carlo. ·Dipartimento di Epidemiologia, Istituto di Ricerche Farmacologiche Mario Negri, Milan, Italy. ersilia.lucenteforte@marionegri.it ·Pancreas · Pubmed #21343831.

ABSTRACT: OBJECTIVES: To investigate the role of menstrual, reproductive, and hormonal factors, as well as benign female conditions, on pancreatic cancer risk. METHODS: We analyzed the combined data from 2 Italian case-control studies including 285 female case patients of pancreatic cancer and 713 female controls. All subjects were interviewed by trained interviewers during their hospital stay using similar structured questionnaires. Odds ratios (ORs) and their corresponding 95% confidence intervals (CIs) were estimated using multiple logistic regression models adjusted for selected covariates. RESULTS: Compared to nulliparae, the OR was 0.76 (95% CI, 0.51-1.12) for parous women and 0.46 (95% CI, 0.26-0.85) for women with 4 or more births, in the absence, however, of a significant trend with increasing number of births. Pancreatic cancer risk was also nonsignificantly reduced among women with age at first birth lower than 25 years (OR, 0.65; 95% CI, 0.42-1.01). Other factors, including age at menarche and menopause, menopausal status, type of menopause, history of spontaneous and induced abortions, use of oral contraceptives and hormone replacement therapy, and history of most female benign conditions were not related to pancreatic cancer risk. CONCLUSIONS: This study provides little support for the hypothesis that menstrual, reproductive, or hormonal factors are related to the development of pancreatic cancer.

18 Article Diabetes mellitus, other medical conditions and pancreatic cancer: a case-control study. 2011

Lipworth, Loren / Zucchetto, Antonella / Bosetti, Cristina / Franceschi, Silvia / Talamini, Renato / Serraino, Diego / McLaughlin, Joseph K / La Vecchia, Carlo / Negri, Eva. ·International Epidemiology Institute, Rockville, MD, USA. ·Diabetes Metab Res Rev · Pubmed #21309046.

ABSTRACT: BACKGROUND: Diabetes and other medical conditions have been related to pancreatic cancer, but time risk quantification is unsettled. METHODS: We combined data from two case-control studies conducted in Italy, including 688 pancreatic cancer cases and 2204 controls. All subjects were interviewed by trained interviewers during their hospital stay. Odds ratios (ORs) and corresponding 95% confidence intervals (CIs) were estimated using multiple logistic regression. RESULTS: Overall, 103 cases (15%) and 125 controls (5.7%) reported a history of diabetes. The OR for pancreatic cancer was more pronounced among those diagnosed with diabetes in the previous 2 years (OR = 5.17; 95% CI = 2.71-9.87) than among those with diabetes diagnosed more than 2 years ago (OR = 2.35; 95% CI = 1.70-3.26). The ORs remained significantly elevated 2-4 years (OR = 3.81; 95% CI = 2.07-7.04) and 5-9 years (OR = 3.75; 95% CI = 2.13-6.59) since diagnosis of diabetes, after which a non-significant 20% increased risk for pancreatic cancer was observed. As compared to non-diabetic non-smokers, the OR was 1.85 among non-diabetic current smokers, 2.17 among diabetic never/former smokers, and rose to 4.67 among diabetic current smokers, indicating a multiplicative effect between these two risk factors. Pancreatic cancer was significantly associated with pancreatitis, primarily among those diagnosed within 2 years (OR = 7.16; 95% CI = 2.25-22.78). In addition, the ORs were elevated for cholelithiasis (3.53; 95% CI = 1.67-7.45) and gastroduodenal ulcer (3.16; 95% CI = 1.14-8.73) only among those diagnosed within the past 2 years. CONCLUSIONS: Diabetes is associated with heightened risk of pancreatic cancer. The association is significant for diabetes diagnosed up to 10 years before pancreatic cancer.

19 Article Dietary acrylamide and pancreatic cancer risk in an Italian case--control study. 2011

Pelucchi, C / Galeone, C / Talamini, R / Negri, E / Polesel, J / Serraino, D / La Vecchia, C. ·Department of Epidemiology, Istituto di Ricerche Farmacologiche Mario Negri, Milan, Italy. claudio.pelucchi@marionegri.it ·Ann Oncol · Pubmed #21285136.

ABSTRACT: BACKGROUND: Information on the relation between acrylamide exposure and risk of pancreatic cancer is scanty and inconsistent. PATIENTS AND METHODS: We investigated the issue in a case-control study conducted from 1991 to 2008 in Northern Italy. Cases were 326 patients with incident pancreatic cancer, admitted to major teaching and general hospitals. Controls were 652 subjects admitted to the same hospitals with acute non-neoplastic conditions. Acrylamide mean content of various food items was derived from international databases and Italian sources. Odds ratios (ORs) and 95% confidence intervals (CIs) of pancreatic cancer were derived using conditional logistic regression adjusted for several covariates, including energy intake. RESULTS: The ORs of pancreatic cancer for subsequent quintiles of acrylamide intake, as compared with the lowest one, were 1.48 (95% CI 0.88-2.50), 1.57 (95% CI 0.91-2.69), 1.70 (95% CI 0.98-2.96) and 1.49 (95% CI 0.83-2.70), with no trend in risk (P value 0.21). The OR for an increase in acrylamide intake of 10 μg/day was 1.01 (95% CI 0.92-1.10). No meaningful difference between ORs was found in strata of smoking habit, alcohol drinking, body mass index and other selected covariates. CONCLUSION: This study found no association between dietary acrylamide and pancreatic cancer in an Italian population.

20 Article Cigar and pipe smoking, smokeless tobacco use and pancreatic cancer: an analysis from the International Pancreatic Cancer Case-Control Consortium (PanC4). 2011

Bertuccio, P / La Vecchia, C / Silverman, D T / Petersen, G M / Bracci, P M / Negri, E / Li, D / 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 T / Bamlet, W R / Holly, E A / Lucenteforte, E / Hassan, M / Yu, H / Kurtz, R C / Cotterchio, M / Su, J / Maisonneuve, P / Duell, E J / Bosetti, C / Boffetta, P. ·Department of Epidemiology, Istituto di Ricerche Farmacologiche Mario Negri, Milan, Italy. ·Ann Oncol · Pubmed #21245160.

ABSTRACT: BACKGROUND: Cigarette smoking is the best-characterized risk factor for pancreatic cancer. However, data are limited for other tobacco smoking products and smokeless tobacco. MATERIALS AND METHODS: We conducted a pooled analysis of cigar and pipe smoking and smokeless tobacco use and risk of pancreatic cancer using data from 11 case-control studies (6056 cases and 11,338 controls) within the International Pancreatic Cancer Case-Control Consortium (PanC4). Pooled odds ratios (OR) and the corresponding 95% confidence intervals (CI) were estimated by unconditional multiple logistic regression models adjusted for study center and selected covariates. RESULTS: Compared with never tobacco users, the OR for cigar-only smokers was 1.6 (95% CI: 1.2-2.3), i.e. comparable to that of cigarette-only smokers (OR 1.5; 95% CI 1.4-1.6). The OR was 1.1 (95% CI 0.69-1.6) for pipe-only smokers. There was some evidence of increasing risk with increasing amount of cigar smoked per day (OR 1.82 for ≥ 10 grams of tobacco), although not with duration. The OR for ever smokeless tobacco users as compared with never tobacco users was 0.98 (95% CI 0.75-1.3). CONCLUSION: This collaborative analysis provides evidence that cigar smoking is associated with an excess risk of pancreatic cancer, while no significant association emerged for pipe smoking and smokeless tobacco use.

21 Article Dietary intake of selected micronutrients and the risk of pancreatic cancer: an Italian case-control study. 2011

Bravi, F / Polesel, J / Bosetti, C / Talamini, R / Negri, E / Dal Maso, L / Serraino, D / La Vecchia, C. ·Department of Epidemiology, Mario Negri Institute for Pharmacological Research, Milan, Italy. francesca.bravi@marionegri.it ·Ann Oncol · Pubmed #20530201.

ABSTRACT: OBJECTIVE: several studies have shown an inverse relation between vegetable and fruit intake and pancreatic cancer, but no specific beneficial component of such foods has been consistently identified. We considered the role of 15 selected vitamins and carotenoids and 6 minerals on pancreatic cancer risk in an Italian case-control study. METHODS: subjects were 326 patients with incident pancreatic cancer and 652 controls, admitted to the same hospitals as cases for acute conditions. Micronutrient computation was based on a validated and reproducible food-frequency questionnaire. We estimated the odds ratios (OR) and confidence intervals (CI) using conditional logistic regression models, adjusted for various confounding factors and for energy intake, according to the residual model. RESULTS: comparing the highest to the lowest quintile of intake, the OR were 0.60 (95% CI 0.36-0.98) for vitamin E, 0.44 (95% CI 0.27-0.73) for vitamin C, 0.56 (95% CI 0.34-0.93) for folate, and 0.57 (95% CI 0.35-0.92) for potassium. No significant inverse associations were observed for α-carotene (OR = 0.69, 95% CI 0.43-1.12), β-carotene (OR = 0.64, 95% CI 0.39-1.06), and β-cryptoxanthin (OR = 0.66, 95% CI 0.39-1.09). No relation was found for other micronutrients considered. CONCLUSION: our findings support a favorable role of vitamins E and C, selected carotenoids, and folate on pancreatic carcinogenesis.

22 Article Aspirin use and pancreatic cancer risk. 2010

Bonifazi, Martina / Gallus, Silvano / Bosetti, Cristina / Polesel, Jerry / Serraino, Diego / Talamini, Renato / Negri, Eva / La Vecchia, Carlo. ·Istituto di Ricerche Farmacologiche Mario Negri, Via Giuseppe La Masa, Milan, Italy. ·Eur J Cancer Prev · Pubmed #20502343.

ABSTRACT: Preclinical findings suggest that aspirin might inhibit pancreatic carcinogenesis, but epidemiological data are scanty and controversial. The role of aspirin use in pancreatic cancer is further analyzed in a multicentric hospital-based case-control study conducted in Italy between 1991 and 2008. Cases were 308 patients with incident pancreatic cancer and controls were 477 patients admitted to the same hospitals as cases for acute conditions, not related to risk factors for pancreatic cancer. A total of 22 cases (7%) and 37 controls (8%) reported regular aspirin use, with a corresponding adjusted odds ratio (OR) of 0.87 [95% confidence interval (CI): 0.47-1.61]. A slight protection, although not significant, was observed for duration of use > or =5 years (OR=0.53; 95% CI: 0.21-1.33) and for time since first use > or =10 years (OR=0.69; 95% CI: 0.25-1.93). The risk of pancreatic cancer was significantly below unity for current users of > or =5 years (OR=0.23; 95% CI: 0.06-0.90), but the risk was based on three cases and 16 controls only. We observed no association between regular aspirin use and pancreatic cancer risk, although our results suggested a possible protective effect for long-term current users.

23 Article Dietary glycemic index and glycemic load and risk of pancreatic cancer: a case-control study. 2010

Rossi, Marta / Lipworth, Loren / Polesel, Jerry / Negri, Eva / Bosetti, Cristina / Talamini, Renato / McLaughlin, Joseph K / La Vecchia, Carlo. ·Istituto di Ricerche Farmacologiche Mario Negri, Milan, Italy. ·Ann Epidemiol · Pubmed #20470973.

ABSTRACT: PURPOSE: Carbohydrates and dietary glycemic index (GI) influence the secretion of insulin and insulin-related growth factors and may play a role in the development of diabetes and obesity, both of which have been related to pancreatic cancer risk. METHODS: We examined the association between dietary GI and glycemic load (GL) and pancreatic cancer by conducting a hospital-based case-control study in Italy in 1991-2008 of 326 cases of pancreatic cancer and 652 control patients. Dietary data were obtained with the use of a validated food-frequency questionnaire. Odds ratios (ORs) and corresponding 95% confidence intervals (95% CIs) were computed with the use of multiple logistic regression. RESULTS: GI was positively associated with pancreatic cancer, with ORs of 1.56 (95% CI, 1.06-2.30) and 1.78 (95% CI, 1.20-2.62) for the second and third tertiles, respectively, compared with the lowest. No significant association was observed between GL and pancreatic cancer. Consumption of sugar, candy, honey, and jam was positively associated with pancreatic cancer, whereas consumption of fruit was inversely associated. CONCLUSIONS: In conclusion, the positive association with high GI, in the absence of an association with dietary GL, fruit, or total carbohydrates, likely reflects the positive association between sweets or refined carbohydrates and pancreatic cancer in this study population.

24 Article Dietary habits and risk of pancreatic cancer: an Italian case-control study. 2010

Polesel, Jerry / Talamini, Renato / Negri, Eva / Bosetti, Cristina / Boz, Giovanni / Lucenteforte, Ersilia / Franceschi, Silvia / Serraino, Diego / La Vecchia, Carlo. ·Unità di Epidemiologia e Biostatistica, Centro di Riferimento Oncologico, IRCCS, Via Franco Gallini, 2, 33081 Aviano, Pordenone, Italy. polesel@cro.it ·Cancer Causes Control · Pubmed #20091114.

ABSTRACT: OBJECTIVE: To investigate the association between dietary habits and pancreatic cancer. METHODS: Between 1991 and 2008, we conducted a hospital-based case-control study in northern Italy. CASES: 326 patients (median age 63 years) with incident pancreatic cancer admitted to general hospitals in the areas of Milan and Pordenone, northern Italy. CONTROLS: 652 patients (median age 63 years) with acute non-neoplastic conditions admitted to the same hospital network of cases. Diet was assessed using a validated food frequency questionnaire. Conditional logistic regression was used to estimate odds ratios (OR) and the corresponding 95% confidence intervals (CI). RESULTS: Frequent meat consumption was associated to a twofold increased risk of pancreatic cancer (95% CI: 1.18-3.36); the risk was significant for meat cooked by boiling/stewing or broiling/roasting. Added table sugar (OR = 2.23; 95% CI: 1.34-3.71) and potatoes (OR = 1.79; 95% CI: 1.12-2.86) were related to pancreatic cancer. An inverse association emerged for non-citrus fruits (OR = 0.41; 95% CI: 0.24-0.69), cooked vegetables (OR = 0.57; 95% CI: 0.36-0.92), and, possibly, for pulses (OR = 0.59; 95% CI: 0.35-1.00). CONCLUSIONS: The present study supports an inverse association between fruits and vegetables and pancreatic cancer risk, and it confirms a direct relation with meat. The increased risk for table sugar suggests that insulin resistance may play a role in pancreatic carcinogenesis.