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Pancreatic Neoplasms: HELP
Articles by Jonas Manjer
Based on 9 articles published since 2010
(Why 9 articles?)
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Between 2010 and 2020, Jonas Manjer wrote the following 9 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Article CA19-9 and apolipoprotein-A2 isoforms as detection markers for pancreatic cancer: a prospective evaluation. 2019

Honda, Kazufumi / Katzke, Verena A / Hüsing, Anika / Okaya, Shinobu / Shoji, Hirokazu / Onidani, Kaoru / Olsen, Anja / Tjønneland, Anne / Overvad, Kim / Weiderpass, Elisabete / Vineis, Paolo / Muller, David / Tsilidis, Kostas / Palli, Domenico / Pala, Valeria / Tumino, Rosario / Naccarati, Alessio / Panico, Salvatore / Aleksandrova, Krasimira / Boeing, Heiner / Bueno-de-Mesquita, H Bas / Peeters, Petra H / Trichopoulou, Antonia / Lagiou, Pagona / Khaw, Kay-Tee / Wareham, Nick / Travis, Ruth C / Merino, Susana / Duell, Eric J / Rodríguez-Barranco, Miguel / Chirlaque, María Dolores / Barricarte, Aurelio / Rebours, Vinciane / Boutron-Ruault, Marie-Chiristine / Romana Mancini, Francesca / Brennan, Paul / Scelo, Ghislaine / Manjer, Jonas / Sund, Malin / Öhlund, Daniel / Canzian, Federico / Kaaks, Rudolf. ·Department of Biomarker for Early Detection of Cancer, National Cancer Center Research Institute, Tokyo, Japan. · Japan Agency for Medical Research and Development (AMED) CREST, Tokyo, Japan. · Division of Cancer Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany. · Gastrointestinal Medical Oncology Division, National Cancer Center Hospital, Tokyo, Japan. · Diet, Genes and Environment, Danish Cancer Society Research Center, Copenhagen, Denmark. · Department of Public Health, Section for Epidemiology, Aarhus University, Aarhus, Denmark. · Department of Community Medicine, Faculty of Health Sciences, University of Tromsø, The Arctic University of Norway, Tromsø, Norway. · Department of Research, 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. · Department of Epidemiology and Biostatistics, The School of Public Health, Imperial College London, London, United Kingdom. · Department of Hygiene and Epidemiology, School of Medicine, University of Ioannina, Ioannina, Greece. · Cancer Risk Factors and Life-Style Epidemiology Unit, Cancer Research and Prevention Institute - ISPO, Florence, Italy. · Epidemiology and Prevention Unit, Fondazione IRCCS Istituto Nazionale dei Tumori, Milano, Italy. · Cancer Registry and Histopathology Unit, "Civic - M.P. Arezzo" Hospital, Ragusa, Italy. · Department of Molecular and Genetic Epidemiology, IIGM - Italian Institute for Genomic Medicine, Torino, Italy. · Dipartimento di Medicina Clinica e Chirurgia, Federico II University, Naples, Italy. · Department of Epidemiology, German Institute of Human Nutrition, Potsdam-Rehbruecke (DIfE), Nuthetal, Germany. · Department of Determinants of Chronic Diseases (DCD), National Institute for Public Health and the Environment (RIVM), Bilthoven, The Netherlands. · Department of Gastroenterology and Hepatology, University Medical Centre, Utrecht, The Netherlands. · Department of Social and Preventive Medicine, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia. · Department of Epidemiology, Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, The Netherlands. · MRC-PHE Centre for Environment and Health, Department of Epidemiology and Biostatistics, School of Public Health, Imperial College, London, United Kingdom. · Unit of Nutritional Epidemiology and Nutrition in Public Health, Department of Hygiene, Epidemiology and Medical Statistics, National and Kapodistrian University of Athens, School of Medicine, WHO Collaborating Center for Nutrition and Health. · Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts. · Cancer Epidemiology Unit, University of Cambridge, Cambridge, United Kingdom. · MRC Epidemiology Unit, University of Cambridge, Cambridge, United Kingdom. · Cancer Epidemiology Unit, Nuffield Department of Population Health, University of Oxford, Oxford, United Kingdom. · Public Health Directorate, Asturias, Spain, Acknowledgment of funds: Regional Government of Asturias. · PanC4 Consortium, Unit of Nutrition and Cancer, Cancer Epidemiology Research Program, Catalan Institute of Oncology (ICO-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 Epidemiology and Public Health CIBERESP, Madrid, Spain. · Department of Epidemiology, Murcia Regional Health Council, CIBER Epidemiología y Salud Pública (CIBERESP), Spain, Ronda de Levante, Murcia, Spain. · Navarra Public Health Institute, Pamplona, Spain. · IdiSNA, Navarra Institute for Health Research, Pamplona, Spain. · Pancreatology Unit, Beaujon Hospital, Clichy, France. · INSERM - UMR 1149, University Paris 7, Paris, France. · CESP, INSERM U1018, Univ. Paris-Sud, UVSQ, Université Paris-Saclay, Villejuif, France. · Lifestyle, Genes and Health: Integrative Trans-Generational Epidemiology, Gustave Roussy, Villejuif, France. · Section of Genetics, International Agency for Research on Cancer (IARC), World Health Organization, Lyon, France. · Department of Surgery, Skåne University Hospital, Lund University, Lund, Sweden. · Department of Surgical and Preoperative Sciences, Umeå University, Umeå, Sweden. · Department of Radiation Sciences and Wallenberg Centre for Molecular Medicine, Umeå University, Umeå, Sweden. · Genomic Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany. ·Int J Cancer · Pubmed #30259989.

ABSTRACT: Recently, we identified unique processing patterns of apolipoprotein A2 (ApoA2) in patients with pancreatic cancer. Our study provides a first prospective evaluation of an ApoA2 isoform ("ApoA2-ATQ/AT"), alone and in combination with carbohydrate antigen 19-9 (CA19-9), as an early detection biomarker for pancreatic cancer. We performed ELISA measurements of CA19-9 and ApoA2-ATQ/AT in 156 patients with pancreatic cancer and 217 matched controls within the European EPIC cohort, using plasma samples collected up to 60 months prior to diagnosis. The detection discrimination statistics were calculated for risk scores by strata of lag-time. For CA19-9, in univariate marker analyses, C-statistics to distinguish future pancreatic cancer patients from cancer-free individuals were 0.80 for plasma taken ≤6 months before diagnosis, and 0.71 for >6-18 months; for ApoA2-ATQ/AT, C-statistics were 0.62, and 0.65, respectively. Joint models based on ApoA2-ATQ/AT plus CA19-9 significantly improved discrimination within >6-18 months (C = 0.74 vs. 0.71 for CA19-9 alone, p = 0.022) and ≤ 18 months (C = 0.75 vs. 0.74, p = 0.022). At 98% specificity, and for lag times of ≤6, >6-18 or ≤ 18 months, sensitivities were 57%, 36% and 43% for CA19-9 combined with ApoA2-ATQ/AT, respectively, vs. 50%, 29% and 36% for CA19-9 alone. Compared to CA19-9 alone, the combination of CA19-9 and ApoA2-ATQ/AT may improve detection of pancreatic cancer up to 18 months prior to diagnosis under usual care, and may provide a useful first measure for pancreatic cancer detection prior to imaging.

2 Article Circulating concentrations of vitamin D in relation to pancreatic cancer risk in European populations. 2018

van Duijnhoven, Fränzel J B / Jenab, Mazda / Hveem, Kristian / Siersema, Peter D / Fedirko, Veronika / Duell, Eric J / Kampman, Ellen / Halfweeg, Anouk / van Kranen, Henk J / van den Ouweland, Jody M W / Weiderpass, Elisabete / Murphy, Neil / Langhammer, Arnulf / Ness-Jensen, Eivind / Olsen, Anja / Tjønneland, Anne / Overvad, Kim / Cadeau, Claire / Kvaskoff, Marina / Boutron-Ruault, Marie-Christine / Katzke, Verena A / Kühn, Tilman / Boeing, Heiner / Trichopoulou, Antonia / Kotanidou, Anastasia / Kritikou, Maria / Palli, Domenico / Agnoli, Claudia / Tumino, Rosario / Panico, Salvatore / Matullo, Giuseppe / Peeters, Petra / Brustad, Magritt / Olsen, Karina Standahl / Lasheras, Cristina / Obón-Santacana, Mireia / Sánchez, María-José / Dorronsoro, Miren / Chirlaque, Maria-Dolores / Barricarte, Aurelio / Manjer, Jonas / Almquist, Martin / Renström, Frida / Ye, Weimin / Wareham, Nick / Khaw, Kay-Tee / Bradbury, Kathryn E / Freisling, Heinz / Aune, Dagfinn / Norat, Teresa / Riboli, Elio / Bueno-de-Mesquita, H B As. ·National Institute for Public Health and the Environment (RIVM), Bilthoven, The Netherlands. · Division of Human Nutrition, Wageningen University & Research, Wageningen, The Netherlands. · International Agency for Research on Cancer (IARC-WHO), Lyon, France. · HUNT Research Centre, Department of Public Health and General Practice, Norwegian University of Science and Technology, Levanger, Norway. · Department of Gastroenterology and Hepatology, University Medical Center Utrecht, The Netherlands. · Department of Gastroenterology and Hepatology, Radboud University Medical Center, Nijmegen, The Netherlands. · Department of Epidemiology, Rollins School of Public Health, Winship Cancer Institute, Emory University, Atlanta, GA. · Unit of Nutrition and Cancer, Cancer Epidemiology Research Program, Catalan Institute of Oncology (ICO-IDIBELL), L'Hospitalet de Llobregat, Barcelona, Spain. · Department of Clinical Chemistry, Canisius Wilhelmina Hospital, Nijmegen, The Netherlands. · Department of Community Medicine, Faculty of Health Sciences, University of Tromsø, The Arctic University of Norway, Tromsø, Norway. · Cancer Registry of Norway, Institute for Population-based Cancer Research, Oslo, Norway. · Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden. · Genetic Epidemiology Group, Folkhälsan Research Center, Helsinki, Finland. · Danish Cancer Society Research Center, Copenhagen, Denmark. · Section for Epidemiology, Department of Public Health, Aarhus University, Aarhus C, Denmark. · Université Paris-Saclay, Université Paris-Sud, UVSQ, CESP, INSERM, Villejuif, France. · Gustave Roussy, Villejuif, F-94805, France. · Division of Cancer Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany. · Department of Epidemiology, German Institute for Human Nutrition Potsdam-Rehbrücke, Nuthetal, Germany. · Hellenic Health Foundation, Athens, Greece. · WHO Collaborating Center for Nutrition and Health, Unit of Nutritional Epidemiology and Nutrition in Public Health, Dept. of Hygiene, Epidemiology and Medical Statistics, University of Athens Medical School, Greece. · Department of Critical Care Medicine and Pulmonary Services, University of Athens Medical School, Evangelismos Hospital, Athens, Greece. · Molecular and Nutritional Epidemiology Unit, Cancer Research and Prevention Institute-ISPO, Florence, Italy. · Epidemiology and Prevention Unit, Fondazione IRCCS Istituto Nazionale dei Tumori, Milano, Italy. · Cancer Registry and Histopathology Unit, "Civic - M.P.Arezzo" Hospital, ASP Ragusa, (Italy). · Dipartimento di medicina clinica e chirurgia, Federico II university, Naples, Italy. · Department of Medical Sciences, University of Torino, Torino, Italy. · Italian Institute for Genomic Medicine (IIGM/HuGeF), Torino, Italy. · Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Utrecht, The Netherlands. · Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, United Kingdom. · Oviedo University, Asturias, 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), Spain. · Public Health Direction and Biodonostia-Ciberesp, Basque Regional Health Department, San Sebastian, 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. · Navarra Institute for Health Research (IdiSNA) Pamplona, Spain. · Department of Surgery, Lund University, Skåne University Hospital Malmö, Malmö, Sweden. · Department of Surgery, Endocrine-Sarcoma unit, Skane University Hospital, Lund, Sweden. · Genetic and Molecular Epidemiology Unit, Department of Clinical Sciences, Lund University, Malmö, Sweden. · Department of Biobank Research, Umeå University, Umeå, Sweden. · The Medical Biobank at Umeå University, Umeå, Sweden. · MRC Epidemiology Unit, University of Cambridge, Cambridge, United Kingdom. · University of Cambridge, Cambridge, United Kingdom. · Cancer Epidemiology Unit, Nuffield Department of Population Health, University of Oxford, Oxford, United Kingdom. · Department of Social and Preventive Medicine, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia. ·Int J Cancer · Pubmed #29114875.

ABSTRACT: Evidence from in vivo, in vitro and ecological studies are suggestive of a protective effect of vitamin D against pancreatic cancer (PC). However, this has not been confirmed by analytical epidemiological studies. We aimed to examine the association between pre-diagnostic circulating vitamin D concentrations and PC incidence in European populations. We conducted a pooled nested case-control study within the European Prospective Investigation into Cancer and Nutrition (EPIC) and the Nord-Trøndelag Health Study's second survey (HUNT2) cohorts. In total, 738 primary incident PC cases (EPIC n = 626; HUNT2 n = 112; median follow-up = 6.9 years) were matched to 738 controls. Vitamin D [25(OH)D

3 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.

4 Article Exposure to environmental tobacco smoke in childhood and incidence of cancer in adulthood in never smokers in the European Prospective Investigation into Cancer and Nutrition. 2011

Chuang, Shu-Chun / Gallo, Valentina / Michaud, Dominique / Overvad, Kim / Tjønneland, Anne / Clavel-Chapelon, Francoise / Romieu, Isabelle / Straif, Kurt / Palli, Domenico / Pala, Valeria / Tumino, Rosario / Sacerdote, Carlotta / Panico, Salvatore / Peeters, Petra H / Lund, Eiliv / Gram, Inger Torhild / Manjer, Jonas / Borgquist, Signe / Riboli, Elio / Vineis, Paolo. ·School of Public Health, Imperial College London, St Mary's Campus, Norfolk Place, W2 1PG, London, UK. s-c.chuang@imperial.ac.uk ·Cancer Causes Control · Pubmed #21279734.

ABSTRACT: The association between childhood environmental tobacco smoke (ETS) exposure and adult cancer risk is controversial; we examined this relationship in never smokers within the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. Over an average of 10 years, 8,372 cases of cancer were diagnosed in 112,430 never smokers in EPIC. Childhood ETS was self-reported by participants at baseline, along with other lifestyle factors. Hazard ratios (HR) for ETS exposure in childhood and their 95% confidence intervals (CI) were estimated by Cox proportional hazards models stratified by age, sex, and study center and adjusted for education, alcohol drinking, body mass index, physical activity, non-alcoholic energy intake, fruit and vegetable intake, and adulthood ETS exposure. Models were further adjusted for reproductive factors for female cancers, for meat intake for digestive system cancers, and for diabetes status for pancreatic cancer. No association was observed between childhood ETS exposure and overall cancer risks (HR = 0.97, 95% CI = 0.92-1.02), and for selected sites. The only exception was pancreatic cancer, as previously reported by Vrieling et al., among those who had been exposed daily in childhood (overall HR = 2.09, 95% CI = 1.14-3.84). In conclusion, childhood ETS exposure might not be a major risk factor for common cancers in adulthood.

5 Article No association between educational level and pancreatic cancer incidence in the European Prospective Investigation into Cancer and Nutrition. 2010

van Boeckel, Petra G A / Boshuizen, Hendriek C / Siersema, Peter D / Vrieling, Alina / Kunst, Anton E / Ye, Weimin / Sund, Malin / Michaud, Dominique S / Gallo, Valentina / Spencer, Elizabeth A / Trichopoulou, Antonia / Benetou, Vasiliki / Orfanos, Philippos / Cirera, Lluis / Duell, Eric J / Rohrmann, Sabine / Hemann, Silke / Masala, Giovanni / Manjer, Jonas / Mattiello, Amalia / Lindkvist, Bjorn / Sánchez, María-José / Pala, Valeria / Peeters, Petra H M / Braaten, Tonje / Tjonneland, Anne / Dalton, Susanne Oksbjerg / Larranaga, Nerea / Dorronsoro, Miren / Overvad, Kim / Illner, Anne-Kathrin / Ardanaz, Eva / Marron, M / Straif, K / Riboli, E / Bueno-de-Mesquita, B. ·National Institute for Public Health and the Environment (RIVM), Bilthoven, The Netherlands. p.g.a.vanboeckel@umcutrecht.nl ·Cancer Epidemiol · Pubmed #20829145.

ABSTRACT: INTRODUCTION: Until now, studies examining the relationship between socioeconomic status and pancreatic cancer incidence have been inconclusive. AIM: To prospectively investigate to what extent pancreatic cancer incidence varies according to educational level within the European Prospective Investigation into Cancer and Nutrition (EPIC) study. METHODS: In the EPIC study, socioeconomic status at baseline was measured using the highest level of education attained. Hazard ratios by educational level and a summary index, the relative indices of inequality (RII), were estimated using Cox regression models stratified by age, gender, and center and adjusted for known risk factors. In addition, we conducted separate analyses by age, gender and geographical region. RESULTS: Within the source population of 407, 944 individuals at baseline, 490 first incident primary pancreatic adenocarcinoma cases were identified in 9 European countries. The crude difference in risk of pancreatic cancer according to level of education was small and not statistically significant (RII=1.14, 95% CI 0.80-1.62). Adjustment for known risk factors reduced the inequality estimates to only a small extent. In addition, no statistically significant associations were observed for age groups (adjusted RII(≤ 60 years)=0.85, 95% CI 0.44-1.64, adjusted RII(>60 years)=1.18, 95% CI 0.73-1.90), gender (adjusted RII(male)=1.20, 95% CI 0.68-2.10, adjusted RII(female)=0.96, 95% CI 0.56-1.62) or geographical region (adjusted RII(Northern Europe)=1.14, 95% CI 0.81-1.61, adjusted RII(Middle Europe)=1.72, 95% CI 0.93-3.19, adjusted RII(Southern Europe)=0.75, 95% CI 0.32-1.80). CONCLUSION: Despite large educational inequalities in many risk factors within the EPIC study, we found no evidence for an association between educational level and the risk of developing pancreatic cancer in this European cohort.

6 Article Metabolic factors and the risk of pancreatic cancer: a prospective analysis of almost 580,000 men and women in the Metabolic Syndrome and Cancer Project. 2010

Johansen, Dorthe / Stocks, Tanja / Jonsson, Håkan / Lindkvist, Björn / Björge, Tone / Concin, Hans / Almquist, Martin / Häggström, Christel / Engeland, Anders / Ulmer, Hanno / Hallmans, Göran / Selmer, Randi / Nagel, Gabriele / Tretli, Steinar / Stattin, Pär / Manjer, Jonas. ·Department of Surgery, Lund University, Malmö, Sweden. dorthe.johansen@med.lu.se ·Cancer Epidemiol Biomarkers Prev · Pubmed #20826833.

ABSTRACT: BACKGROUND: The aim of this study was to investigate the association between factors in metabolic syndrome (MetS; single and combined) and the risk of pancreatic cancer. METHODS: The Metabolic Syndrome and Cancer Project is a pooled cohort containing data on body mass index, blood pressure, and blood levels of glucose, cholesterol, and triglycerides. During follow-up, 862 individuals were diagnosed with pancreatic cancer. Cox proportional hazards analysis was used to calculate relative risks (RR) with 95% confidence intervals using the above-mentioned factors categorized into quintiles and transformed into z-scores. All z-scores were summarized and a second z-transformation creating a composite z-score for MetS was done. All risk estimates were calibrated to correct for a regression dilution bias. RESULTS: The trend over quintiles was positively associated with the risk of pancreatic cancer for mid-blood pressure (mid-BP) and glucose in men and for body mass index, mid-BP, and glucose in women. The z-score for the adjusted mid-BP (RR, 1.10; 1.01-1.20) and the calibrated z-score for glucose (RR, 1.37; 1.14-1.34) were positively associated with pancreatic cancer in men. In women, a positive association was found for calibrated z-scores for mid-BP (RR, 1.34; 1.08-1.66), for the calibrated z-score for glucose (RR, 1.98; 1.41-2.76), and for the composite z-score for MetS (RR, 1.58; 1.34-1.87). CONCLUSION: Our study adds further evidence to a possible link between abnormal glucose metabolism and risk of pancreatic cancer. IMPACT: To our knowledge, this is the first study on MetS and pancreatic cancer using prediagnostic measurements of the examined factors.

7 Article Pre-diagnostic levels of anionic trypsinogen, cationic trypsinogen, and pancreatic secretory trypsin inhibitor in relation to pancreatic cancer risk. 2010

Johansen, Dorthe / Manjer, Jonas / Regner, Sara / Lindkvist, Björn. ·Department of Surgery, Malmö University Hospital, Lund University, Malmö, Sweden. dorthe.johansen@med.lu.se ·Pancreatology · Pubmed #20484960.

ABSTRACT: BACKGROUND/AIMS: Experimental studies have suggested that trypsinogen may enhance tumor progression and that the ratio between anionic trypsinogen and cationic trypsinogen (HAT/HCT) and between the sum of trypsinogens and pancreatic secretory trypsin inhibitor (PSTI) ((HAT + HCT)/PSTI) are disturbed in patients with pancreatic cancer. The aim of this study was to investigate if pre-diagnostic levels of these parameters are associated with subsequent pancreatic cancer risk. METHODS: A total of 33,346 subjects participated in a health screening programme in Malmö, Sweden. Pancreatic cancer cases (n = 84) were matched to three controls each. HAT, HCT and PSTI were analyzed in pre-diagnostic serum samples. Odds ratios for pancreatic cancer were calculated using logistic regression and were then stratified for other risk factors. RESULTS: In the main analysis, a statistically significant association between the ratio between HAT/HCT and pancreatic cancer was observed for all, for the crude OR and for the ORs adjusted for sex, BMI or Helicobacter pylori. When stratified for sex, statistically significant associations were found for females in the crude OR and for the ORs adjusted for time to analysis, BMI, alcohol consumption or H. pylori. There was a positive association between the ratio of HAT/HCT to pancreatic cancer in the intermediate/high alcohol consumption group and subjects with a BMI <25. The sum of trypsinogens showed a similar pattern, but was only of borderline significance in the intermediate/high alcohol consumption group. CONCLUSION: Our hypothesis predicted an increased risk for pancreatic cancer related to an imbalance between trypsin activity and trypsin inhibition capacity. The findings concerning the ratio of HAT/HCT are in line with this. The results related to analyses stratified for other risk factors should be considered as mainly explorative.

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 Alcohol intake and pancreatic cancer: a pooled analysis from the pancreatic cancer cohort consortium (PanScan). 2010

Michaud, Dominique S / Vrieling, Alina / Jiao, Li / Mendelsohn, Julie B / Steplowski, Emily / Lynch, Shannon M / Wactawski-Wende, Jean / Arslan, Alan A / Bas Bueno-de-Mesquita, H / Fuchs, Charles S / Gross, Myron / Helzlsouer, Kathy / Jacobs, Eric J / Lacroix, Andrea / Petersen, Gloria / Zheng, Wei / Allen, Naomi / Ammundadottir, Laufey / Bergmann, Manuela M / Boffetta, Paolo / Buring, Julie E / Canzian, Federico / Chanock, Stephen J / Clavel-Chapelon, Françoise / Clipp, Sandra / Freiberg, Matthew S / Michael Gaziano, J / Giovannucci, Edward L / Hankinson, Susan / Hartge, Patricia / Hoover, Robert N / Allan Hubbell, F / Hunter, David J / Hutchinson, Amy / Jacobs, Kevin / Kooperberg, Charles / Kraft, Peter / Manjer, Jonas / Navarro, Carmen / Peeters, Petra H M / Shu, Xiao-Ou / Stevens, Victoria / Thomas, Gilles / Tjønneland, Anne / Tobias, Geoffrey S / Trichopoulos, Dimitrios / Tumino, Rosario / Vineis, Paolo / Virtamo, Jarmo / Wallace, Robert / Wolpin, Brian M / Yu, Kai / Zeleniuch-Jacquotte, Anne / Stolzenberg-Solomon, Rachael Z. ·Division of Epidemiology, Public Health and Primary Care, Imperial College London, London, UK. d.michaud@imperial.ac.uk ·Cancer Causes Control · Pubmed #20373013.

ABSTRACT: The literature has consistently reported no association between low to moderate alcohol consumption and pancreatic cancer; however, a few studies have shown that high levels of intake may increase risk. Most single studies have limited power to detect associations even in the highest alcohol intake categories or to examine associations by alcohol type. We analyzed these associations using 1,530 pancreatic cancer cases and 1,530 controls from the Pancreatic Cancer Cohort Consortium (PanScan) nested case-control study. Odds ratios (OR) and 95% confidence intervals (95% CI) were calculated using unconditional logistic regression, adjusting for potential confounders. We observed no significant overall association between total alcohol (ethanol) intake and pancreatic cancer risk (OR = 1.38, 95% CI = 0.86-2.23, for 60 or more g/day vs. >0 to <5 g/day). A statistically significant increase in risk was observed among men consuming 45 or more grams of alcohol from liquor per day (OR = 2.23, 95% CI = 1.02-4.87, compared to 0 g/day of alcohol from liquor, P-trend = 0.12), but not among women (OR = 1.35, 95% CI = 0.63-2.87, for 30 or more g/day of alcohol from liquor, compared to none). No associations were noted for wine or beer intake. Overall, no significant increase in risk was observed, but a small effect among heavy drinkers cannot be ruled out.