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Pancreatic Neoplasms: HELP
Articles by Parviz Ghadirian
Based on 9 articles published since 2010
(Why 9 articles?)
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Between 2010 and 2020, P. Ghadirian wrote the following 9 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 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.

2 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.

3 Article The incidence of pancreatic cancer in BRCA1 and BRCA2 mutation carriers. 2012

Iqbal, J / Ragone, A / Lubinski, J / Lynch, H T / Moller, P / Ghadirian, P / Foulkes, W D / Armel, S / Eisen, A / Neuhausen, S L / Senter, L / Singer, C F / Ainsworth, P / Kim-Sing, C / Tung, N / Friedman, E / Llacuachaqui, M / Ping, S / Narod, S A / Anonymous4680740. ·Women's College Research Institute, Familial Breast Cancer Research, 790 Bay Street, Toronto, Ontario, Canada M5G 1N8. ·Br J Cancer · Pubmed #23099806.

ABSTRACT: BACKGROUND: Germline mutations in BRCA1 and BRCA2 predispose to pancreatic cancer. We estimated the incidence of pancreatic cancer in a cohort of female carriers of BRCA1 and BRCA2 mutation. We also estimated survival rates in pancreatic cancer cases from families with a BRCA mutation. METHODS: We followed 5149 women with a mutation for new cases of pancreatic cancer. The standardised incidence ratios (SIR) for pancreatic cancer were calculated based on age group and country of residence. We also reviewed the pedigrees of 8140 pedigrees with a BRCA1 or a BRCA2 mutation for those with a case of pancreatic cancer. We recorded the year of diagnosis and the year of death for 351 identified cases. RESULTS: Eight incident pancreatic cancer cases were identified among all mutation carriers. The SIR for BRCA1 carriers was 2.55 (95% CI=1.03-5.31, P=0.04) and for BRCA2 carriers was 2.13 (95% CI=0.36-7.03, P=0.3). The 5-year survival rate was 5% for cases from a BRCA1 family and 4% for cases from a BRCA2 family. CONCLUSION: The risk of pancreatic cancer is approximately doubled in female BRCA carriers. The poor survival in familial pancreatic cancer underscores the need for novel anti-tumoural strategies.

4 Article Pancreatitis and pancreatic cancer risk: a pooled analysis in the International Pancreatic Cancer Case-Control Consortium (PanC4). 2012

Duell, E J / Lucenteforte, E / Olson, S H / Bracci, P M / Li, D / Risch, H A / Silverman, D T / Ji, B T / Gallinger, S / Holly, E A / Fontham, E H / Maisonneuve, P / Bueno-de-Mesquita, H B / Ghadirian, P / Kurtz, R C / Ludwig, E / Yu, H / Lowenfels, A B / Seminara, D / Petersen, G M / La Vecchia, C / Boffetta, P. ·Unit of Nutrition, Environment and Cancer, Cancer Epidemiology Research Program, Catalan Institute of Oncology (ICO-IDIBELL), Barcelona, Spain. eduell@iconcologia.net ·Ann Oncol · Pubmed #22767586.

ABSTRACT: BACKGROUND: Pancreatitis is a known risk factor for pancreatic cancer; however, an unknown fraction of the disease is thought to be a consequence of tumor-related duct obstruction. PATIENTS AND METHODS: A pooled analysis of a history of pancreatitis and risk of pancreatic cancer was carried out considering the time interval between diagnoses and potential modification by covariates. Adjusted pooled odds ratios (ORs) and 95% confidence intervals (CIs) were estimated from 10 case-control studies (5048 cases of ductal pancreatic adenocarcinoma and 10,947 controls) taking part in the International Pancreatic Cancer Case-Control Consortium (PanC4). RESULTS: The association between pancreatitis and pancreatic cancer was nearly three-fold at intervals of >2 years between diagnoses (OR: 2.71, 95% CI: 1.96-3.74) and much stronger at intervals of ≤2 years (OR: 13.56, 95% CI: 8.72-21.90) probably reflecting a combination of reverse causation and antecedent misdiagnosis of pancreas cancer as pancreatitis. The younger (<65 years) pancreatic cancer cases showed stronger associations with previous (>2 years) pancreatitis (OR: 3.91, 95% CI: 2.53-6.04) than the older (≥65 years) cases (OR: 1.68, 95% CI: 1.02-2.76; P value for interaction: 0.006). CONCLUSIONS: Despite a moderately strong association between pancreatitis (diagnosed before >2 years) and pancreatic cancer, the population attributable fraction was estimated at 1.34% (95% CI: 0.612-2.07%), suggesting that a relatively small proportion of pancreatic cancer might be avoided if pancreatitis could be prevented.

5 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.

6 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.

7 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.

8 Article Past medical history and pancreatic cancer risk: Results from a multicenter case-control study. 2010

Maisonneuve, Patrick / Lowenfels, Albert B / Bueno-de-Mesquita, H Bas / Ghadirian, Parviz / Baghurst, Peter A / Zatonski, Witold A / Miller, Anthony B / Duell, Eric J / Boffetta, Paolo / Boyle, Peter. ·European Institute of Oncology, Milan, Italy. ·Ann Epidemiol · Pubmed #20123159.

ABSTRACT: PURPOSE: To investigate risk factors that may be linked to pancreatic cancer. METHODS: We designed a multicenter population-based case-control (823 cases, 1679 control patients) study with data collection by using a common protocol and questionnaire. Participating centers were located in Australia, Canada, the Netherlands, and Poland. RESULTS: After adjustment for confounding factors, a positive history of pancreatitis was associated with pancreatic cancer (odds ratio [OR], 4.68; 95% confidence interval [95% CI], 2.23-9.84). The risk was especially high in heavy smokers (OR, 15.4; 95% CI, 3.18-74.9). Patients with diabetes had an increased risk of developing pancreatic cancer (OR, 2.16; 95% CI, 1.60-2.91). The risk was highest in the first year after the development of diabetes (OR, 6.68; 95% CI, 3.56-12.6) and decreased over time. A history of allergy was associated with a reduced risk of pancreas cancer (OR, 0.64; 95% CI, 0.50-0.82). CONCLUSIONS: Patients with newly diagnosed diabetes and patients with pancreatitis, particularly in heavy smokers, have an increased risk for developing pancreatic cancer. In addition to being risk factors, these conditions could be early manifestations of underlying pancreatic cancer. A history of allergy decreases the risk of pancreatic cancer.

9 Article Consumption of food groups and the risk of pancreatic cancer: a case-control study. 2010

Ghadirian, Parviz / Nkondjock, André. ·Epidemiology Research Unit, Research Centre, Centre Hospitalier de l'Université de Montréal (CRCHUM)-Hôtel-Dieu, Faculty of Medicine, Université de Montréal, 3850 St. Urbain St., Montreal, H2W 1T7, QC, Canada. parviz.ghadirian@umontreal.ca ·J Gastrointest Cancer · Pubmed #20101477.

ABSTRACT: PURPOSE: The purpose of this study is to investigate whether the consumption of specific food groups predicts the risk of pancreatic cancer, a case-control study of nutrition and pancreatic cancer among French-Canadians was carried out in Montreal, Quebec, Canada. METHODS: A total of 179 pancreatic cancer cases (97 males and 82 females) and 239 population-based control subjects were interviewed. Dietary intake was evaluated via a validated food frequency questionnaire that gathers information on over 200 different food items and beverages. Odd ratios (ORs) and 95% confidence intervals (CIs) were computed by unconditional logistic regression. RESULTS: After adjustment for age, smoking, diabetes status, proxy interview, gender and total energy intake, a reduced risk of pancreatic cancer was related to vegetables and vegetable products [OR = 0.47; 95%CI: (0.21-1.06) p-trend = 0.024], while an increased risk was associated with the consumption of lamb, veal and game [OR = 2.24; 95%CI: (1.11-4.52) p-trend = 0.026], when the upper and lower quartiles of intake were compared. Changes in dietary intake over the last decade revealed an elevated risk with augmented consumption of soups, sauces and gravies [OR = 2.32; 95%CI: (1.20-4.49) p-trend=0.03], beef products [OR = 2.07; 95%CI: (0.95-4.51) p-trend=0.05] as well as fish and shellfish [OR = 1.48; 95%CI: (0.78-2.80) p-trend=0.05]. CONCLUSIONS: These findings suggest that a diet rich in vegetables and vegetable products may decrease the risk of pancreatic cancer.