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Pancreatic Neoplasms: HELP
Articles by Nadia Slimani
Based on 9 articles published since 2010
(Why 9 articles?)
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Between 2010 and 2020, N. Slimani wrote the following 9 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Article Dietary folate intake and pancreatic cancer risk: Results from the European prospective investigation into cancer and nutrition. 2019

Park, Jin Young / Bueno-de-Mesquita, H Bas / Ferrari, Pietro / Weiderpass, Elisabete / de Batlle, Jordi / Tjønneland, Anne / Kyro, Cecilie / Rebours, Vinciane / Boutron-Ruault, Marie-Christine / Mancini, Francesca Romana / Katzke, Verena / Kühn, Tilman / Boeing, Heiner / Trichopoulou, Antonia / La Vecchia, Carlo / Kritikou, Maria / Masala, Giovanna / Pala, Valeria / Tumino, Rosario / Panico, Salvatore / Peeters, Petra H / Skeie, Guri / Merino, Susana / Duell, Eric J / Rodríguez-Barranco, Miguel / Dorronsoro, Miren / Chirlaque, Maria-Dolores / Ardanaz, Eva / Gylling, Björn / Schneede, Jörn / Ericson, Ulrika / Sternby, Hanna / Khaw, Kay-Tee / Bradbury, Kathryn E / Huybrechts, Inge / Aune, Dagfinn / Vineis, Paolo / Slimani, Nadia. ·International Agency for Research on Cancer, Lyon, France. · National Institute for Public Health and the Environment (RIVM), Bilthoven, The Netherlands. · Department of Gastroenterology and Hepatology, University Medical Centre, Utrecht, The Netherlands. · School of Public Health, Imperial College London, London, United Kingdom. · Department of Community Medicine, Faculty of Health Sciences, University of Tromsø, Tromsø, Norway. · Cancer Registry of Norway, Institute of Population-Based Cancer Research, Oslo, Norway. · Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden. · Genetic Epidemiology Group, Folkhälsan Research Center, Helsinki, Finland. · Group of Translational Research in Respiratory Medicine, IRBLleida, Hospital Universitari Arnau de Vilanova and Santa Maria, Lleida, Spain. · Centro de Investigación Biomédica en Red de Enfermedades Respiratorias (CIBERES), Madrid, Spain. · Danish Cancer Society Research Center, Copenhagen, Denmark. · Pancreatology Unit, Beaujon Hospital, Clichy, France. · INSERM-UMR 1149, University Paris 7, France. · CESP, INSERM U1018, University of Paris-Sud, UVSQ, Université Paris-Saclay, France. · Gustave Roussy, Villejuif, France. · German Cancer Research Center (DKFZ), Division of Cancer Epidemiology, Heidelberg, Germany. · Department of Epidemiology, German Institute of Human Nutrition (DIfE) Potsdam-Rehbrücke, Germany. · Hellenic Health Foundation, Athens, Greece. · Department of Clinical Sciences and Community Health, Università degli Studi di Milano, Milan, Italy. · Cancer Risk Factors and Life-Style Epidemiology Unit, Institute for Cancer Research, Prevention and Clinical Network-ISPRO, Florence, Italy. · Epidemiology and Prevention Unit, IRCCS Foundation National Cancer Institute, Milan, Italy. · Cancer Registry and Histopathology Department, 'Civic-M.P. Arezzo' Hospital, ASP Ragusa, Italy. · Department of Clinical Medicine and Surgery, Federico II University, Naples, Italy. · Department of Epidemiology, Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht. · Public Health Directorate, Asturias, Spain. · Unit of Nutrition and Cancer, Cancer Epidemiology Research Program, Catalan Institute of Oncology-IDIBELL, L'Hospitalet de Llobregat, Barcelona, Spain. · Escuela Andaluza de Salud Pública, Instituto de Investigación Biosanitaria ibs.GRANADA, Hospitales Universitarios de Granada/Universidad de Granada, Granada, Spain. · CIBER de Epidemiología y Salud Pública (CIBERESP), Madrid, Spain. · Dirección de Salud Pública y Adicciones, Gobierno Vasco, Vitoria, Spain. · Instituto de Investigación Sanitaria Biodonostia, San Sebastián, Spain. · Department of Epidemiology, Regional Health Council, IMIB-Arrixaca, Murcia, Spain. · Department of Health and Social Sciences, Universidad de Murcia, Murcia, Spain. · Navarra Public Health Institute, Pamplona, Spain. · IdiSNA, Navarra Institute for Health Research, Pamplona, Spain. · Department of Medical Biosciences, Pathology, Umeå University, Umeå, Sweden. · Department of Clinical Pharmacology, Pharmacology and Clinical Neurosciences, Umeå University, Umeå, Sweden. · Diabetes and Cardiovascular disease, Genetic Epidemiology, Department of Clinical Sciences in Malmö, Lund University, Sweden. · Department of Surgery, Institution of Clinical Sciences Malmö, Lund University, Sweden. · Department of Public Health and Primary Care, University of Cambridge, Cambridge, United Kingdom. · Cancer Epidemiology Unit, Nuffield Department of Population Health, University of Oxford, United Kingdom. · Bjørknes University College, Oslo, Norway. · IIGM Foundation, Turin, Italy. ·Int J Cancer · Pubmed #30178496.

ABSTRACT: Pancreatic cancer (PC) has an exceptionally low survival rate and primary prevention strategies are limited. Folate plays an important role in one-carbon metabolism and has been associated with the risk of several cancers, but not consistently with PC risk. We aimed to investigate the association between dietary folate intake and PC risk, using the standardised folate database across 10 European countries. A total of 477,206 participants were followed up for 11 years, during which 865 incident primary PC cases were recorded. Folate intake was energy-adjusted using the residual method. Hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated using Cox proportional hazards models. In multivariable analyses stratified by age, sex, study centre and adjusted for energy intake, smoking status, BMI, educational level, diabetes status, supplement use and dietary fibre intake, we found no significant association between folate intake and PC risk: the HR of PC risk for those in the highest quartile of folate intake (≥353 μg/day) compared to the lowest (<241 μg/day) was 0.81 (95% CI: 0.51, 1.31; p

2 Article An absolute risk model to identify individuals at elevated risk for pancreatic cancer in the general population. 2013

Klein, Alison P / Lindström, Sara / Mendelsohn, Julie B / Steplowski, Emily / Arslan, Alan A / Bueno-de-Mesquita, H Bas / Fuchs, Charles S / Gallinger, Steven / Gross, Myron / Helzlsouer, Kathy / Holly, Elizabeth A / Jacobs, Eric J / Lacroix, Andrea / Li, Donghui / Mandelson, Margaret T / Olson, Sara H / Petersen, Gloria M / Risch, Harvey A / Stolzenberg-Solomon, Rachael Z / Zheng, Wei / Amundadottir, Laufey / Albanes, Demetrius / Allen, Naomi E / Bamlet, William R / Boutron-Ruault, Marie-Christine / Buring, Julie E / Bracci, Paige M / Canzian, Federico / Clipp, Sandra / Cotterchio, Michelle / Duell, Eric J / Elena, Joanne / Gaziano, J Michael / Giovannucci, Edward L / Goggins, Michael / Hallmans, Göran / Hassan, Manal / Hutchinson, Amy / Hunter, David J / Kooperberg, Charles / Kurtz, Robert C / Liu, Simin / Overvad, Kim / Palli, Domenico / Patel, Alpa V / Rabe, Kari G / Shu, Xiao-Ou / Slimani, Nadia / Tobias, Geoffrey S / Trichopoulos, Dimitrios / Van Den Eeden, Stephen K / Vineis, Paolo / Virtamo, Jarmo / Wactawski-Wende, Jean / Wolpin, Brian M / Yu, Herbert / Yu, Kai / Zeleniuch-Jacquotte, Anne / Chanock, Stephen J / Hoover, Robert N / Hartge, Patricia / Kraft, Peter. ·Department of Oncology, Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore, Maryland, United States of America ; Department of Pathology, Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins School of Medicine, Baltimore, Maryland, United States of America ; Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland, United States of America. ·PLoS One · Pubmed #24058443.

ABSTRACT: PURPOSE: We developed an absolute risk model to identify individuals in the general population at elevated risk of pancreatic cancer. PATIENTS AND METHODS: Using data on 3,349 cases and 3,654 controls from the PanScan Consortium, we developed a relative risk model for men and women of European ancestry based on non-genetic and genetic risk factors for pancreatic cancer. We estimated absolute risks based on these relative risks and population incidence rates. RESULTS: Our risk model included current smoking (multivariable adjusted odds ratio (OR) and 95% confidence interval: 2.20 [1.84-2.62]), heavy alcohol use (>3 drinks/day) (OR: 1.45 [1.19-1.76]), obesity (body mass index >30 kg/m(2)) (OR: 1.26 [1.09-1.45]), diabetes >3 years (nested case-control OR: 1.57 [1.13-2.18], case-control OR: 1.80 [1.40-2.32]), family history of pancreatic cancer (OR: 1.60 [1.20-2.12]), non-O ABO genotype (AO vs. OO genotype) (OR: 1.23 [1.10-1.37]) to (BB vs. OO genotype) (OR 1.58 [0.97-2.59]), rs3790844(chr1q32.1) (OR: 1.29 [1.19-1.40]), rs401681(5p15.33) (OR: 1.18 [1.10-1.26]) and rs9543325(13q22.1) (OR: 1.27 [1.18-1.36]). The areas under the ROC curve for risk models including only non-genetic factors, only genetic factors, and both non-genetic and genetic factors were 58%, 57% and 61%, respectively. We estimate that fewer than 3/1,000 U.S. non-Hispanic whites have more than a 5% predicted lifetime absolute risk. CONCLUSION: Although absolute risk modeling using established risk factors may help to identify a group of individuals at higher than average risk of pancreatic cancer, the immediate clinical utility of our model is limited. However, a risk model can increase awareness of the various risk factors for pancreatic cancer, including modifiable behaviors.

3 Article Dietary intake of acrylamide and pancreatic cancer risk in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. 2013

Obón-Santacana, M / Slimani, N / Lujan-Barroso, L / Travier, N / Hallmans, G / Freisling, H / Ferrari, P / Boutron-Ruault, M C / Racine, A / Clavel, F / Saieva, C / Pala, V / Tumino, R / Mattiello, A / Vineis, P / Argüelles, M / Ardanaz, E / Amiano, P / Navarro, C / Sánchez, M J / Molina Montes, E / Key, T / Khaw, K-T / Wareham, N / Peeters, P H / Trichopoulou, A / Bamia, C / Trichopoulos, D / Boeing, H / Kaaks, R / Katzke, V / Ye, W / Sund, M / Ericson, U / Wirfält, E / Overvad, K / Tjønneland, A / Olsen, A / Skeie, G / Åsli, L A / Weiderpass, E / Riboli, E / Bueno-de-Mesquita, H B / Duell, E J. ·Unit of Nutrition, Environment and Cancer, Cancer Epidemiology Research Program, Catalan Institute of Oncology (ICO-IDIBELL), Barcelona, Spain. ·Ann Oncol · Pubmed #23857962.

ABSTRACT: BACKGROUND: In 1994, acrylamide (AA) was classified as a probable human carcinogen by the International Agency for Research on Cancer. In 2002, AA was discovered at relatively high concentrations in some starchy, plant-based foods cooked at high temperatures. PATIENTS AND METHODS: A prospective analysis was conducted to evaluate the association between the dietary intake of AA and ductal adenocarcinoma of the exocrine pancreatic cancer (PC) risk in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort using Cox regression modeling. EPIC includes >500,000 men and women aged 35-75 at enrollment from 10 European countries. AA intake was estimated for each participant by combining questionnaire-based food consumption data with a harmonized AA database derived from the EU monitoring database of AA levels in foods, and evaluated in quintiles and continuously. RESULTS: After a mean follow-up of 11 years, 865 first incident adenocarcinomas of the exocrine pancreas were observed and included in the present analysis. At baseline, the mean dietary AA intake in EPIC was 26.22 µg/day. No overall association was found between continuous or quintiles of dietary AA intake and PC risk in EPIC (HR:0.95, 95%CI:0.89-1.01 per 10 µg/day). There was no effect measure modification by smoking status, sex, diabetes, alcohol intake or geographic region. However, there was an inverse association (HR: 0.73, 95% CI: 0.61-0.88 per 10 µg/day) between AA intake and PC risk in obese persons as defined using the body mass index (BMI, ≥ 30 kg/m(2)), but not when body fatness was defined using waist and hip circumference or their ratio. CONCLUSIONS: Dietary intake of AA was not associated with an increased risk of PC in the EPIC cohort.

4 Article Diabetes and risk of pancreatic cancer: a pooled analysis from the pancreatic cancer cohort consortium. 2013

Elena, Joanne W / Steplowski, Emily / Yu, Kai / Hartge, Patricia / Tobias, Geoffrey S / Brotzman, Michelle J / Chanock, Stephen J / Stolzenberg-Solomon, Rachael Z / Arslan, Alan A / Bueno-de-Mesquita, H Bas / Helzlsouer, Kathy / Jacobs, Eric J / LaCroix, Andrea / Petersen, Gloria / Zheng, Wei / Albanes, Demetrius / Allen, Naomi E / Amundadottir, Laufey / Bao, Ying / Boeing, Heiner / Boutron-Ruault, Marie-Christine / Buring, Julie E / Gaziano, J Michael / Giovannucci, Edward L / Duell, Eric J / Hallmans, Göran / Howard, Barbara V / Hunter, David J / Hutchinson, Amy / Jacobs, Kevin B / Kooperberg, Charles / Kraft, Peter / Mendelsohn, Julie B / Michaud, Dominique S / Palli, Domenico / Phillips, Lawrence S / Overvad, Kim / Patel, Alpa V / Sansbury, Leah / Shu, Xiao-Ou / Simon, Michael S / Slimani, Nadia / Trichopoulos, Dimitrios / Visvanathan, Kala / Virtamo, Jarmo / Wolpin, Brian M / Zeleniuch-Jacquotte, Anne / Fuchs, Charles S / Hoover, Robert N / Gross, Myron. ·Division of Cancer Control and Population Science, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, MD 20892, USA. elenajw@mail.nih.gov ·Cancer Causes Control · Pubmed #23112111.

ABSTRACT: PURPOSE: Diabetes is a suspected risk factor for pancreatic cancer, but questions remain about whether it is a risk factor or a result of the disease. This study prospectively examined the association between diabetes and the risk of pancreatic adenocarcinoma in pooled data from the NCI pancreatic cancer cohort consortium (PanScan). METHODS: The pooled data included 1,621 pancreatic adenocarcinoma cases and 1,719 matched controls from twelve cohorts using a nested case-control study design. Subjects who were diagnosed with diabetes near the time (<2 years) of pancreatic cancer diagnosis were excluded from all analyses. All analyses were adjusted for age, race, gender, study, alcohol use, smoking, BMI, and family history of pancreatic cancer. RESULTS: Self-reported diabetes was associated with a forty percent increased risk of pancreatic cancer (OR = 1.40, 95 % CI: 1.07, 1.84). The association differed by duration of diabetes; risk was highest for those with a duration of 2-8 years (OR = 1.79, 95 % CI: 1.25, 2.55); there was no association for those with 9+ years of diabetes (OR = 1.02, 95 % CI: 0.68, 1.52). CONCLUSIONS: These findings provide support for a relationship between diabetes and pancreatic cancer risk. The absence of association in those with the longest duration of diabetes may reflect hypoinsulinemia and warrants further investigation.

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

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

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

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

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

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

7 Article Variant ABO blood group alleles, secretor status, and risk of pancreatic cancer: results from the pancreatic cancer cohort consortium. 2010

Wolpin, Brian M / Kraft, Peter / Xu, Mousheng / Steplowski, Emily / Olsson, Martin L / Arslan, Alan A / Bueno-de-Mesquita, H Bas / Gross, Myron / Helzlsouer, Kathy / Jacobs, Eric J / LaCroix, Andrea / Petersen, Gloria / Stolzenberg-Solomon, Rachael Z / Zheng, Wei / Albanes, Demetrius / Allen, Naomi E / Amundadottir, Laufey / Austin, Melissa A / Boutron-Ruault, Marie-Christine / Buring, Julie E / Canzian, Federico / Chanock, Stephen J / Gaziano, J Michael / Giovannucci, Edward L / Hallmans, Göran / Hankinson, Susan E / Hoover, Robert N / Hunter, David J / Hutchinson, Amy / Jacobs, Kevin B / Kooperberg, Charles / Mendelsohn, Julie B / Michaud, Dominique S / Overvad, Kim / Patel, Alpa V / Sanchéz, Maria-José / Sansbury, Leah / Shu, Xiao-Ou / Slimani, Nadia / Tobias, Geoffrey S / Trichopoulos, Dimitrios / Vineis, Paolo / Visvanathan, Kala / Virtamo, Jarmo / Wactawski-Wende, Jean / Watters, Joanne / Yu, Kai / Zeleniuch-Jacquotte, Anne / Hartge, Patricia / Fuchs, Charles S. ·Department of Medical Oncology, Dana-Farber Cancer Institute, 44 Binney Street, Boston, MA 02115, USA. bwolpin@partners.org ·Cancer Epidemiol Biomarkers Prev · Pubmed #20971884.

ABSTRACT: BACKGROUND: Subjects with non-O ABO blood group alleles have increased risk of pancreatic cancer. Glycosyltransferase activity is greater for the A(1) versus A(2) variant, whereas O01 and O02 variants are nonfunctioning. We hypothesized: 1) A(1) allele would confer greater risk than A(2) allele, 2) protective effect of the O allele would be equivalent for O01 and O02 variants, 3) secretor phenotype would modify the association with risk. METHODS: We determined ABO variants and secretor phenotype from single nucleotide polymorphisms in ABO and FUT2 genes in 1,533 cases and 1,582 controls from 12 prospective cohort studies. Adjusted odds ratios (OR) for pancreatic cancer were calculated using logistic regression. RESULTS: An increased risk was observed in participants with A(1) but not A(2) alleles. Compared with subjects with genotype O/O, genotypes A(2)/O, A(2)/A(1), A(1)/O, and A(1)/A(1) had ORs of 0.96 (95% CI, 0.72-1.26), 1.46 (95% CI, 0.98-2.17), 1.48 (95% CI, 1.23-1.78), and 1.71 (95% CI, 1.18-2.47). Risk was similar for O01 and O02 variant O alleles. Compared with O01/O01, the ORs for each additional allele of O02, A(1), and A(2) were 1.00 (95% CI, 0.87-1.14), 1.38 (95% CI, 1.20-1.58), and 0.96 (95% CI, 0.77-1.20); P, O01 versus O02 = 0.94, A(1) versus A(2) = 0.004. Secretor phenotype was not an effect modifier (P-interaction = 0.63). CONCLUSIONS: Among participants in a large prospective cohort consortium, ABO allele subtypes corresponding to increased glycosyltransferase activity were associated with increased pancreatic cancer risk. IMPACT: These data support the hypothesis that ABO glycosyltransferase activity influences pancreatic cancer risk rather than actions of other nearby genes on chromosome 9q34.

8 Article Anthropometric measures, body mass index, and pancreatic cancer: a pooled analysis from the Pancreatic Cancer Cohort Consortium (PanScan). 2010

Arslan, Alan A / Helzlsouer, Kathy J / Kooperberg, Charles / Shu, Xiao-Ou / Steplowski, Emily / Bueno-de-Mesquita, H Bas / Fuchs, Charles S / Gross, Myron D / Jacobs, Eric J / Lacroix, Andrea Z / Petersen, Gloria M / Stolzenberg-Solomon, Rachael Z / Zheng, Wei / Albanes, Demetrius / Amundadottir, Laufey / Bamlet, William R / Barricarte, Aurelio / Bingham, Sheila A / Boeing, Heiner / Boutron-Ruault, Marie-Christine / Buring, Julie E / Chanock, Stephen J / Clipp, Sandra / Gaziano, J Michael / Giovannucci, Edward L / Hankinson, Susan E / Hartge, Patricia / Hoover, Robert N / Hunter, David J / Hutchinson, Amy / Jacobs, Kevin B / Kraft, Peter / Lynch, Shannon M / Manjer, Jonas / Manson, Joann E / McTiernan, Anne / McWilliams, Robert R / Mendelsohn, Julie B / Michaud, Dominique S / Palli, Domenico / Rohan, Thomas E / Slimani, Nadia / Thomas, Gilles / Tjønneland, Anne / Tobias, Geoffrey S / Trichopoulos, Dimitrios / Virtamo, Jarmo / Wolpin, Brian M / Yu, Kai / Zeleniuch-Jacquotte, Anne / Patel, Alpa V / Anonymous3240660. ·Department of Obstetrics and Gynecology, New York University School of Medicine, 550 First Ave, TH-528, New York, NY 10016, USA. alan.arslan@nyumc.org ·Arch Intern Med · Pubmed #20458087.

ABSTRACT: BACKGROUND: Obesity has been proposed as a risk factor for pancreatic cancer. METHODS: Pooled data were analyzed from the National Cancer Institute Pancreatic Cancer Cohort Consortium (PanScan) to study the association between prediagnostic anthropometric measures and risk of pancreatic cancer. PanScan applied a nested case-control study design and included 2170 cases and 2209 control subjects. Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using unconditional logistic regression for cohort-specific quartiles of body mass index (BMI [calculated as weight in kilograms divided by height in meters squared]), weight, height, waist circumference, and waist to hip ratio as well as conventional BMI categories (underweight, <18.5; normal weight, 18.5-24.9; overweight, 25.0-29.9; obese, 30.0-34.9; and severely obese, > or = 35.0). Models were adjusted for potential confounders. RESULTS: In all of the participants, a positive association between increasing BMI and risk of pancreatic cancer was observed (adjusted OR for the highest vs lowest BMI quartile, 1.33; 95% CI, 1.12-1.58; P(trend) < .001). In men, the adjusted OR for pancreatic cancer for the highest vs lowest quartile of BMI was 1.33 (95% CI, 1.04-1.69; P(trend) < .03), and in women it was 1.34 (95% CI, 1.05-1.70; P(trend) = .01). Increased waist to hip ratio was associated with increased risk of pancreatic cancer in women (adjusted OR for the highest vs lowest quartile, 1.87; 95% CI, 1.31-2.69; P(trend) = .003) but less so in men. CONCLUSIONS: These findings provide strong support for a positive association between BMI and pancreatic cancer risk. In addition, centralized fat distribution may increase pancreatic cancer risk, especially in women.

9 Article Pancreatic cancer risk and ABO blood group alleles: results from the pancreatic cancer cohort consortium. 2010

Wolpin, Brian M / Kraft, Peter / Gross, Myron / Helzlsouer, Kathy / Bueno-de-Mesquita, H Bas / Steplowski, Emily / Stolzenberg-Solomon, Rachael Z / Arslan, Alan A / Jacobs, Eric J / Lacroix, Andrea / Petersen, Gloria / Zheng, Wei / Albanes, Demetrius / Allen, Naomi E / Amundadottir, Laufey / Anderson, Garnet / Boutron-Ruault, Marie-Christine / Buring, Julie E / Canzian, Federico / Chanock, Stephen J / Clipp, Sandra / Gaziano, John Michael / Giovannucci, Edward L / Hallmans, Göran / Hankinson, Susan E / Hoover, Robert N / Hunter, David J / Hutchinson, Amy / Jacobs, Kevin / Kooperberg, Charles / Lynch, Shannon M / Mendelsohn, Julie B / Michaud, Dominique S / Overvad, Kim / Patel, Alpa V / Rajkovic, Aleksandar / Sanchéz, Maria-José / Shu, Xiao-Ou / Slimani, Nadia / Thomas, Gilles / Tobias, Geoffrey S / Trichopoulos, Dimitrios / Vineis, Paolo / Virtamo, Jarmo / Wactawski-Wende, Jean / Yu, Kai / Zeleniuch-Jacquotte, Anne / Hartge, Patricia / Fuchs, Charles S. ·Department of Medical Oncology, Dana-Farber Cancer Institute, 44 Binney Street, Boston, MA 02115, USA. bwolpin@partners.org ·Cancer Res · Pubmed #20103627.

ABSTRACT: A recent genome-wide association study (PanScan) identified significant associations at the ABO gene locus with risk of pancreatic cancer, but the influence of specific ABO genotypes remains unknown. We determined ABO genotypes (OO, AO, AA, AB, BO, and BB) in 1,534 cases and 1,583 controls from 12 prospective cohorts in PanScan, grouping participants by genotype-derived serologic blood type (O, A, AB, and B). Adjusted odds ratios (ORs) for pancreatic cancer by ABO alleles were calculated using logistic regression. Compared with blood type O, the ORs for pancreatic cancer in subjects with types A, AB, and B were 1.38 [95% confidence interval (95% CI), 1.18-1.62], 1.47 (95% CI, 1.07-2.02), and 1.53 (95% CI, 1.21-1.92), respectively. The incidence rates for blood types O, A, AB, and B were 28.9, 39.9, 41.8, and 44.5 cases per 100,000 subjects per year. An increase in risk was noted with the addition of each non-O allele. Compared with OO genotype, subjects with AO and AA genotype had ORs of 1.33 (95% CI, 1.13-1.58) and 1.61 (95% CI, 1.22-2.18), whereas subjects with BO and BB genotypes had ORs of 1.45 (95% CI, 1.14-1.85) and 2.42 (1.28-4.57). The population attributable fraction for non-O blood type was 19.5%. In a joint model with smoking, current smokers with non-O blood type had an adjusted OR of 2.68 (95% CI, 2.03-3.54) compared with nonsmokers of blood type O. We concluded that ABO genotypes were significantly associated with pancreatic cancer risk.