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Pancreatic Neoplasms: HELP
Articles by Diego Serraino
Based on 20 articles published since 2010
(Why 20 articles?)
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Between 2010 and 2020, D. Serraino wrote the following 20 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 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.

2 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.

3 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.

4 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.

5 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.

6 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.

7 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.

8 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.

9 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.

10 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.

11 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.

12 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.

13 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.

14 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.

15 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.

16 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.

17 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.

18 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.

19 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.

20 Minor Physical activity and pancreatic cancer risk. 2011

Pelucchi, Claudio / Zucchetto, Antonella / Tavani, Alessandra / Dal Maso, Luigino / Serraino, Diego / La Vecchia, Carlo. · ·Int J Cancer · Pubmed #20617512.

ABSTRACT: -- No abstract --