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Pancreatic Neoplasms: HELP
Articles by Suzanne M. Jeurnink
Based on 10 articles published since 2010
(Why 10 articles?)
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Between 2010 and 2020, S. Jeurnink wrote the following 10 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Article Methodological issues in a prospective study on plasma concentrations of persistent organic pollutants and pancreatic cancer risk within the EPIC cohort. 2019

Gasull, Magda / Pumarega, José / Kiviranta, Hannu / Rantakokko, Panu / Raaschou-Nielsen, Ole / Bergdahl, Ingvar A / Sandanger, Torkjel Manning / Goñi, Fernando / Cirera, Lluís / Donat-Vargas, Carolina / Alguacil, Juan / Iglesias, Mar / Tjønneland, Anne / Overvad, Kim / Mancini, Francesca Romana / Boutron-Ruault, Marie-Christine / Severi, Gianluca / Johnson, Theron / Kühn, Tilman / Trichopoulou, Antonia / Karakatsani, Anna / Peppa, Eleni / Palli, Domenico / Pala, Valeria / Tumino, Rosario / Naccarati, Alessio / Panico, Salvatore / Verschuren, Monique / Vermeulen, Roel / Rylander, Charlotta / Nøst, Therese Haugdahl / Rodríguez-Barranco, Miguel / Molinuevo, Amaia / Chirlaque, María-Dolores / Ardanaz, Eva / Sund, Malin / Key, Tim / Ye, Weimin / Jenab, Mazda / Michaud, Dominique / Matullo, Giuseppe / Canzian, Federico / Kaaks, Rudolf / Nieters, Alexandra / Nöthlings, Ute / Jeurnink, Suzanne / Chajes, Veronique / Matejcic, Marco / Gunter, Marc / Aune, Dagfinn / Riboli, Elio / Agudo, Antoni / Gonzalez, Carlos Alberto / Weiderpass, Elisabete / Bueno-de-Mesquita, Bas / Duell, Eric J / Vineis, Paolo / Porta, Miquel. ·Hospital del Mar Institute of Medical Research (IMIM), Barcelona, Catalonia, Spain; Universitat Autònoma de Barcelona, Barcelona, Catalonia, Spain; CIBER de Epidemiología y Salud Pública (CIBERESP), Madrid, Spain. · Hospital del Mar Institute of Medical Research (IMIM), Barcelona, Catalonia, Spain; CIBER de Epidemiología y Salud Pública (CIBERESP), Madrid, Spain. · National Institute for Health and Welfare, Department of Health Security, Kuopio, Finland. · Danish Cancer Society Research Center, Copenhagen, Denmark. · Department of Biobank Research, Umeå University, Umeå, Sweden; Occupational and Environmental Medicine, Department of Public Health and Clinical Medicine, Umeå University, Umeå, Sweden. · Department of Community Medicine, UiT-The Arctic University of Norway, Tromsø, Norway. · CIBER de Epidemiología y Salud Pública (CIBERESP), Madrid, Spain; Biodonostia Health Research Institute; Public Health Laboratory in Gipuzkoa, Basque Government, San Sebastian, Spain. · CIBER de Epidemiología y Salud Pública (CIBERESP), Madrid, Spain; Department of Epidemiology, Murcia Regional Health Council, IMIB - Arrixaca, Murcia, Spain. · Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden. · CIBER de Epidemiología y Salud Pública (CIBERESP), Madrid, Spain; Universidad de Huelva, Huelva, Spain. · Department of Pathology, Hospital del Mar (PSMar), Barcelona, Spain. · Section for Epidemiology, Department of Public Health, Aarhus University, Aarhus, Denmark. · CESP, Faculté de Médecine - Univ. Paris-Sud, Faculté de Médecine - UVSQ, INSERM, Université Paris-Saclay, Villejuif, France; Gustave Roussy, Villejuif, France. · Division of Cancer Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany. · Hospital del Mar Institute of Medical Research (IMIM), Barcelona, Catalonia, Spain. · Hellenic Health Foundation, Athens, Greece. · Hellenic Health Foundation, Athens, Greece; 2nd Pulmonary Medicine Department, School of Medicine, National and Kapodistrian University of Athens, "ATTIKON" University Hospital, Haidari, Greece. · Cancer Risk Factors and Life-Style Epidemiology Unit, Institute for Cancer Research, Prevention and Clinical Network - ISPRO, Florence, Italy. · Epidemiology and Prevention Unit, Fondazione IRCCS Istituto Nazionale dei Tumori, Milan, Italy. · Cancer Registry and Histopathology Department, "Civic - M.P. Arezzo" Hospital, ASP Ragusa, Italy. · Molecular and Genetic Epidemiology Unit, Italian Institute for Genomic Medicine (IIGM), Turin, Italy. · Dipartimento di Medicina Clinica e Chirurgia, Federico II University, Naples, Italy. · Centre for Nutrition, Prevention and Health Services, National Institute for Public Health and the Environment (RIVM), Bilthoven, the Netherlands. · Institute for Risk Assessment Sciences (IRAS), Utrecht University, Utrecht, The Netherlands. · CIBER de Epidemiología y Salud Pública (CIBERESP), Madrid, Spain; Escuela Andaluza de Salud Pública. Instituto de Investigación Biosanitaria, Granada, Hospitales Universitarios de Granada/Universidad de Granada, Granada, Spain. · CIBER de Epidemiología y Salud Pública (CIBERESP), Madrid, Spain; Department of Epidemiology, Murcia Regional Health Council, IMIB - Arrixaca, Murcia, Spain; Department of Health and Social Sciences, University of Murcia, Murcia, Spain. · CIBER de Epidemiología y Salud Pública (CIBERESP), Madrid, Spain; Navarra Public Health Institute, Pamplona, Spain; IdiSNA, Navarra Institute for Health Research, Pamplona, Spain. · Department of Surgical and Perioperative Sciences, Umeå University, Umeå, Sweden. · Cancer Epidemiology Unit, Nuffield Department of Population Health, University of Oxford, Oxford, United Kingdom. · Department of Biobank Research, Umeå University, Umeå, Sweden; Department of Medical Epidemiology and Biostatistics Karolinska Institutet, Stockholm, Sweden. · Nutrition and Metabolism Section, International Agency for Research on Cancer (IARC), Lyon, France. · Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, London, United Kingdom. · Department Medical Sciences, University of Torino, Italian Institute for Genomic Medicine -IIGM/HuGeF, Torino, Italy. · Genomic Epidemiology Group, German Cancer Research Center (DKFZ), Heidelberg, Germany. · Center for Chronic Immunodeficiency, Molecular Epidemiology, University Medical Center Freiburg, Freiburg, Germany. · Department of Nutrition and Food Sciences, University of Bonn, Bonn, Germany. · Department of Gastroenterology and Hepatology, University Medical Center Utrecht, Utrecht, the Netherlands; National Institute for Public Health and the Environment (RIVM), Bilthoven, the Netherlands. · Unit of Nutrition and Cancer, Catalan Institute of Oncology (ICO-Idibell), Barcelona, Spain. · Department of Community Medicine, UiT-The Arctic University of Norway, Tromsø, Norway; Department of Medical Epidemiology and Biostatistics Karolinska Institutet, Stockholm, Sweden; Cancer Registry of Norway, Institute of Population-Based Cancer Research, Oslo, Norway; Genetic Epidemiology Group, Folkhälsan Research Center, Faculty of Medicine, University of Helsinki, Helsinki, Finland. · Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, London, United Kingdom; National Institute for Public Health and the Environment (RIVM), Bilthoven, the Netherlands; Department of Social & Preventive Medicine, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia. · Molecular and Genetic Epidemiology Unit, Italian Institute for Genomic Medicine (IIGM), Turin, Italy; Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, London, United Kingdom. · Hospital del Mar Institute of Medical Research (IMIM), Barcelona, Catalonia, Spain; Universitat Autònoma de Barcelona, Barcelona, Catalonia, Spain; CIBER de Epidemiología y Salud Pública (CIBERESP), Madrid, Spain. Electronic address: mporta@imim.es. ·Environ Res · Pubmed #30529143.

ABSTRACT: BACKGROUND: The use of biomarkers of environmental exposure to explore new risk factors for pancreatic cancer presents clinical, logistic, and methodological challenges that are also relevant in research on other complex diseases. OBJECTIVES: First, to summarize the main design features of a prospective case-control study -nested within the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort- on plasma concentrations of persistent organic pollutants (POPs) and pancreatic cancer risk. And second, to assess the main methodological challenges posed by associations among characteristics and habits of study participants, fasting status, time from blood draw to cancer diagnosis, disease progression bias, basis of cancer diagnosis, and plasma concentrations of lipids and POPs. Results from etiologic analyses on POPs and pancreatic cancer risk, and other analyses, will be reported in future articles. METHODS: Study subjects were 1533 participants (513 cases and 1020 controls matched by study centre, sex, age at blood collection, date and time of blood collection, and fasting status) enrolled between 1992 and 2000. Plasma concentrations of 22 POPs were measured by gas chromatography - triple quadrupole mass spectrometry (GC-MS/MS). To estimate the magnitude of the associations we calculated multivariate-adjusted odds ratios by unconditional logistic regression, and adjusted geometric means by General Linear Regression Models. RESULTS: There were differences among countries in subjects' characteristics (as age, gender, smoking, lipid and POP concentrations), and in study characteristics (as time from blood collection to index date, year of last follow-up, length of follow-up, basis of cancer diagnosis, and fasting status). Adjusting for centre and time of blood collection, no factors were significantly associated with fasting status. Plasma concentrations of lipids were related to age, body mass index, fasting, country, and smoking. We detected and quantified 16 of the 22 POPs in more than 90% of individuals. All 22 POPs were detected in some participants, and the smallest number of POPs detected in one person was 15 (median, 19) with few differences by country. The highest concentrations were found for p,p'-DDE, PCBs 153 and 180 (median concentration: 3371, 1023, and 810 pg/mL, respectively). We assessed the possible occurrence of disease progression bias (DPB) in eight situations defined by lipid and POP measurements, on one hand, and by four factors: interval from blood draw to index date, tumour subsite, tumour stage, and grade of differentiation, on the other. In seven of the eight situations results supported the absence of DPB. CONCLUSIONS: The coexistence of differences across study centres in some design features and participant characteristics is of relevance to other multicentre studies. Relationships among subjects' characteristics and among such characteristics and design features may play important roles in the forthcoming analyses on the association between plasma concentrations of POPs and pancreatic cancer risk.

2 Article Plasma carotenoids, vitamin C, retinol and tocopherols levels and pancreatic cancer risk within the European Prospective Investigation into Cancer and Nutrition: a nested case-control study: plasma micronutrients and pancreatic cancer risk. 2015

Jeurnink, Suzanne M / Ros, Martine M / Leenders, Max / van Duijnhoven, Franzel J B / Siersema, Peter D / Jansen, Eugene H J M / van Gils, Carla H / Bakker, Marije F / Overvad, Kim / Roswall, Nina / Tjønneland, Anne / Boutron-Ruault, Marie-Christine / Racine, Antoine / Cadeau, Claire / Grote, Verena / Kaaks, Rudolf / Aleksandrova, Krasimira / Boeing, Heiner / Trichopoulou, Antonia / Benetou, Vasiliki / Valanou, Elisavet / Palli, Domenico / Krogh, Vittorio / Vineis, Paolo / Tumino, Rosario / Mattiello, Amalia / Weiderpass, Elisabete / Skeie, Guri / Castaño, José María Huerta / Duell, Eric J / Barricarte, Aurelio / Molina-Montes, Esther / Argüelles, Marcial / Dorronsoro, Mire / Johansen, Dorthe / Lindkvist, Björn / Sund, Malin / Crowe, Francesca L / Khaw, Kay-Tee / Jenab, Mazda / Fedirko, Veronika / Riboli, E / Bueno-de-Mesquita, H B. ·Department of Gastroenterology and Hepatology, University Medical Center Utrecht, the Netherlands; National Institute for Public Health and the Environment (RIVM), Bilthoven, the Netherlands. ·Int J Cancer · Pubmed #25175624.

ABSTRACT: Evidence of a protective effect of several antioxidants and other nutrients on pancreatic cancer risk is inconsistent. The aim of this study was to investigate the association for prediagnostic plasma levels of carotenoids, vitamin C, retinol and tocopherols with risk of pancreatic cancer in a case-control study nested within the European Prospective Investigation into Cancer and Nutrition (EPIC). 446 incident exocrine pancreatic cancer cases were matched to 446 controls by age at blood collection, study center, sex, date and time of blood collection, fasting status and hormone use. Plasma carotenoids (α- and β-carotene, lycopene, β-cryptoxanthin, canthaxanthin, zeaxanthin and lutein), α- and γ-tocopherol and retinol were measured by reverse phase high-performance liquid chromatography and plasma vitamin C by a colorimetric assay. Incidence rate ratios (IRRs) with 95% confidence intervals (95%CIs) for pancreatic cancer risk were estimated using a conditional logistic regression analysis, adjusted for smoking status, smoking duration and intensity, waist circumference, cotinine levels and diabetes status. Inverse associations with pancreatic cancer risk were found for plasma β-carotene (IRR highest vs. lowest quartile 0.52, 95%CI 0.31-0.88, p for trend = 0.02), zeaxanthin (IRR highest vs. lowest quartile 0.53, 95%CI 0.30-0.94, p for trend = 0.06) and α-tocopherol (IRR highest vs. lowest quartile 0.62, 95%CI 0.39-0.99, p for trend = 0.08. For α- and β-carotene, lutein, sum of carotenoids and γ-tocopherol, heterogeneity between geographical regions was observed. In conclusion, our results show that higher plasma concentrations of β-carotene, zeaxanthin and α-tocopherol may be inversely associated with risk of pancreatic cancer, but further studies are warranted.

3 Article Intake of coffee, decaffeinated coffee, or tea does not affect risk for pancreatic cancer: results from the European Prospective Investigation into Nutrition and Cancer Study. 2013

Bhoo-Pathy, Nirmala / Uiterwaal, Cuno S P M / Dik, Vincent K / Jeurnink, Suzanne M / Bech, Bodil H / Overvad, Kim / Halkjær, Jytte / Tjønneland, Anne / Boutron-Ruault, Marie-Christine / Fagherazzi, Guy / Racine, Antoine / Katzke, Verena A / Li, Kuanrong / Boeing, Heiner / Floegel, Anna / Androulidaki, Anna / Bamia, Christina / Trichopoulou, Antonia / Masala, Giovanna / Panico, Salvatore / Crosignani, Paolo / Tumino, Rosario / Vineis, Paolo / Peeters, Petra H M / Gavrilyuk, Oxana / Skeie, Guri / Weiderpass, Elisabete / Duell, Eric J / Arguelles, Marcial / Molina-Montes, Esther / Navarro, Carmen / Ardanaz, Eva / Dorronsoro, Miren / Lindkvist, Björn / Wallström, Peter / Sund, Malin / Ye, Weimin / Khaw, Kay-Tee / Wareham, Nick / Key, Timothy J / Travis, Ruth C / Duarte-Salles, Talita / Freisling, Heinz / Licaj, Idlir / Gallo, Valentina / Michaud, Dominique S / Riboli, Elio / Bueno-De-Mesquita, H Bas. ·Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Utrecht, The Netherlands; Department of Social and Preventive Medicine, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia; National Clinical Research Centre, Kuala Lumpur Hospital, Kuala Lumpur, Malaysia. ·Clin Gastroenterol Hepatol · Pubmed #23756220.

ABSTRACT: BACKGROUND & AIMS: Few modifiable risk factors have been implicated in the etiology of pancreatic cancer. There is little evidence for the effects of caffeinated coffee, decaffeinated coffee, or tea intake on risk of pancreatic cancer. We investigated the association of total coffee, caffeinated coffee, decaffeinated coffee, and tea consumption with risk of pancreatic cancer. METHODS: This study was conducted within the European Prospective Investigation into Nutrition and Cancer cohort, comprising male and female participants from 10 European countries. Between 1992 and 2000, there were 477,312 participants without cancer who completed a dietary questionnaire and were followed up to determine pancreatic cancer incidence. Coffee and tea intake was calibrated with a 24-hour dietary recall. Adjusted hazard ratios (HRs) were computed using multivariable Cox regression. RESULTS: During a mean follow-up period of 11.6 y, 865 first incidences of pancreatic cancers were reported. When divided into fourths, neither total intake of coffee (HR, 1.03; 95% confidence interval [CI], 0.83-1.27; high vs low intake), decaffeinated coffee (HR, 1.12; 95% CI, 0.76-1.63; high vs low intake), nor tea were associated with risk of pancreatic cancer (HR, 1.22, 95% CI, 0.95-1.56; high vs low intake). Moderately low intake of caffeinated coffee was associated with an increased risk of pancreatic cancer (HR, 1.33; 95% CI, 1.02-1.74), compared with low intake. However, no graded dose response was observed, and the association attenuated after restriction to histologically confirmed pancreatic cancers. CONCLUSIONS: Based on an analysis of data from the European Prospective Investigation into Nutrition and Cancer cohort, total coffee, decaffeinated coffee, and tea consumption are not related to the risk of pancreatic cancer.

4 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.

5 Article Concentrations of IGF-I and IGFBP-3 and pancreatic cancer risk in the European Prospective Investigation into Cancer and Nutrition. 2012

Rohrmann, S / Grote, V A / Becker, S / Rinaldi, S / Tjønneland, A / Roswall, N / Grønbæk, H / Overvad, K / Boutron-Ruault, M C / Clavel-Chapelon, F / Racine, A / Teucher, B / Boeing, H / Drogan, D / Dilis, V / Lagiou, P / Trichopoulou, A / Palli, D / Tagliabue, G / Tumino, R / Vineis, P / Mattiello, A / Rodríguez, L / Duell, E J / Molina-Montes, E / Dorronsoro, M / Huerta, J-M / Ardanaz, E / Jeurnink, S / Peeters, P H M / Lindkvist, B / Johansen, D / Sund, M / Ye, W / Khaw, K-T / Wareham, N J / Allen, N E / Crowe, F L / Fedirko, V / Jenab, M / Michaud, D S / Norat, T / Riboli, E / Bueno-de-Mesquita, H B / Kaaks, R. ·Division of Cancer Epidemiology and Prevention, Institute of Social and Preventive Medicine, University of Zurich, Hirschengraben 84, Zürich 8001, Switzerland. sabine.rohrmann@ifspm.uzh.ch ·Br J Cancer · Pubmed #22315049.

ABSTRACT: BACKGROUND: Insulin-like growth factors (IGFs) and their binding proteins (BPs) regulate cell differentiation, proliferation and apoptosis, and may have a role in the aetiology of various cancers. Information on their role in pancreatic cancer is limited and was examined here in a case-control study nested within the European Prospective Investigation into Cancer and Nutrition. METHODS: Serum concentrations of IGF-I and IGFBP-3 were measured using enzyme-linked immunosorbent assays in 422 cases and 422 controls matched on age, sex, study centre, recruitment date, and time since last meal. Conditional logistic regression was used to compute odds ratios (OR) and 95% confidence intervals (CI) adjusted for confounding variables. RESULTS: Neither circulating levels of IGF-I (OR=1.21, 95% CI 0.75-1.93 for top vs bottom quartile, P-trend 0.301), IGFBP-3 (OR=1.00, 95% CI 0.66-1.51, P-trend 0.79), nor the molar IGF-I/IGFBP-3 ratio, an indicator of free IGF-I level (OR=1.22, 95% CI 0.75-1.97, P-trend 0.27), were statistically significantly associated with the risk of pancreatic cancer. In a cross-classification, however, a high concentration of IGF-I with concurrently low levels of IGFBP-3 was related to an increased risk of pancreatic cancer (OR=1.72, 95% CI 1.05-2.83; P-interaction=0.154). CONCLUSION: On the basis of these results, circulating levels of components of the IGF axis do not appear to be the risk factors for pancreatic cancer. However, on the basis of the results of a subanalysis, it cannot be excluded that a relatively large amount of IGF-1 together with very low levels of IGFBP-3 might still be associated with an increase in pancreatic cancer risk.

6 Article The associations of advanced glycation end products and its soluble receptor with pancreatic cancer risk: a case-control study within the prospective EPIC Cohort. 2012

Grote, Verena A / Nieters, Alexandra / Kaaks, Rudolf / Tjønneland, Anne / Roswall, Nina / Overvad, Kim / Nielsen, Michael R Skjelbo / Clavel-Chapelon, Françoise / Boutron-Ruault, Marie Christine / Racine, Antoine / Teucher, Birgit / Lukanova, Annekatrin / Boeing, Heiner / Drogan, Dagmar / Trichopoulou, Antonia / Trichopoulos, Dimitrios / Lagiou, Pagona / Palli, Domenico / Sieri, Sabina / Tumino, Rosario / Vineis, Paolo / Mattiello, Amalia / Argüelles Suárez, Marcial Vicente / Duell, Eric J / Sánchez, María-José / Dorronsoro, Miren / Huerta Castaño, José María / Barricarte, Aurelio / Jeurnink, Suzanne M / Peeters, Petra H M / Sund, Malin / Ye, Weimin / Regner, Sara / Lindkvist, Björn / Khaw, Kay-Tee / Wareham, Nick / Allen, Naomi E / Crowe, Francesca L / Fedirko, Veronika / Jenab, Mazda / Romaguera, Dora / Siddiq, Afshan / Bueno-de-Mesquita, H Bas / Rohrmann, Sabine. ·Division of Cancer Epidemiology c020, German Cancer Research Center (DKFZ), Im Neuenheimer Feld 581, Heidelberg, Germany. ·Cancer Epidemiol Biomarkers Prev · Pubmed #22301828.

ABSTRACT: BACKGROUND: Advanced glycation end products (AGE) and their receptors (RAGE) have been implicated in cancer development through their proinflammatory capabilities. However, prospective data on their association with cancer of specific sites, including pancreatic cancer, are limited. METHODS: Prediagnostic blood levels of the AGE product Nε-(carboxymethyl)lysine (CML) and the endogenous secreted receptor for AGE (esRAGE) were measured using ELISA in 454 patients with exocrine pancreatic cancer and individually matched controls within the European Prospective Investigation into Cancer and Nutrition (EPIC). Pancreatic cancer risk was estimated by calculating ORs with corresponding 95% confidence intervals (CI). RESULTS: Elevated CML levels tended to be associated with a reduction in pancreatic cancer risk [OR = 0.57 (95% CI, 0.32-1.01) comparing highest with lowest quintile), whereas no association was observed for esRAGE (OR = 0.98; 95% CI, 0.62-1.54). Adjustments for body mass index and smoking attenuated the inverse associations of CML with pancreatic cancer risk (OR = 0.78; 95% CI, 0.41-1.49). There was an inverse association between esRAGE and risk of pancreatic cancer for cases that were diagnosed within the first 2 years of follow-up [OR = 0.46 (95% CI, 0.22-0.96) for a doubling in concentration], whereas there was no association among those with a longer follow-up (OR = 1.11; 95% CI, 0.88-1.39; P(interaction) = 0.002). CONCLUSIONS AND IMPACT: Our results do not provide evidence for an association of higher CML or lower esRAGE levels with risk of pancreatic cancer. The role of AGE/RAGE in pancreatic cancer would benefit from further investigations.

7 Article The association of circulating adiponectin levels with pancreatic cancer risk: a study within the prospective EPIC cohort. 2012

Grote, Verena A / Rohrmann, Sabine / Dossus, Laure / Nieters, Alexandra / Halkjaer, Jytte / Tjønneland, Anne / Overvad, Kim / Stegger, Jakob / Chabbert-Buffet, Nathalie / Boutron-Ruault, Marie-Christine / Clavel-Chapelon, Françoise / Teucher, Birgit / Becker, Susen / Montonen, Jukka / Boeing, Heiner / Trichopoulou, Antonia / Lagiou, Pagona / Trichopoulos, Dimitrios / Palli, Domenico / Sieri, Sabina / Tumino, Rosario / Vineis, Paolo / Mattiello, Amalia / Argüelles, Marcial / Duell, Eric J / Molina-Montes, Esther / Larrañaga, Nerea / Chirlaque, María-Dolores / Gurrea, Aurelio Barricarte / Jeurnink, Suzanne M / Peeters, Petra Hm / Ye, Weimin / Sund, Malin / Lindkvist, Björn / Johansen, Dorthe / Khaw, Kay-Tee / Wareham, Nick / Crowe, Francesca L / Romieu, Isabelle / Rinaldi, Sabina / Jenab, Mazda / Romaguera, Dora / Michaud, Dominique S / Riboli, Elio / Bas Bueno-de-Mesquita, H / Kaaks, Rudolf. ·German Cancer Research Center, Heidelberg, Germany. ·Int J Cancer · Pubmed #21681743.

ABSTRACT: Excess body weight and type 2 diabetes mellitus, risk factors of pancreatic cancer, are characterized by decreased levels of adiponectin. In addition to anti-inflammatory and anti-proliferative actions, adiponectin has an important role in regulating glucose metabolism, i.e., decreasing circulating blood glucose levels. Prospectively, hyperglycemia has been associated with risk of pancreatic cancer. The aim of this study was to investigate the association of pre-diagnostic adiponectin levels with pancreatic cancer risk. We conducted a case-control study nested within European Prospective Investigation into Cancer and Nutrition. Blood samples of 452 pancreatic cancer cases and 452 individually matched controls were analyzed by immunoassays. Multivariate conditional logistic regression was used to estimate odds ratios (OR) and 95% confidence intervals (CI). Overall, adiponectin showed no association with pancreas cancer risk; however, among never smokers, higher circulating levels of adiponectin were associated with a reduction in pancreatic cancer risk (OR = 0.44 [95% CI 0.23-0.82] for highest vs. lowest quartile), whereas among current smokers there was no significant association (OR = 1.59 [95% CI 0.67-3.76] for highest vs. lowest quartile; p-trend = 0.530; p-interaction = 0.309). In our study, lower adiponectin concentrations may be associated with the development of pancreatic cancer among never smokers, whereas the only other prospective study being conducted so far showed a decrease in risk among male smokers. Therefore, further studies are needed to clarify the role of adiponectin in pancreatic cancer development.

8 Article Diabetes mellitus, glycated haemoglobin and C-peptide levels in relation to pancreatic cancer risk: a study within the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. 2011

Grote, V A / Rohrmann, S / Nieters, A / Dossus, L / Tjønneland, A / Halkjær, J / Overvad, K / Fagherazzi, G / Boutron-Ruault, M C / Morois, S / Teucher, B / Becker, S / Sluik, D / Boeing, H / Trichopoulou, A / Lagiou, P / Trichopoulos, D / Palli, D / Pala, V / Tumino, R / Vineis, P / Panico, S / Rodríguez, L / Duell, E J / Molina-Montes, E / Dorronsoro, M / Huerta, J M / Ardanaz, E / Jeurnink, S M / Beulens, J W J / Peeters, P H M / Sund, M / Ye, W / Lindkvist, B / Johansen, D / Khaw, K T / Wareham, N / Allen, N / Crowe, F / Jenab, M / Romieu, I / Michaud, D S / Riboli, E / Romaguera, D / Bueno-de-Mesquita, H B / Kaaks, R. ·Division of Cancer Epidemiology c020, German Cancer Research Center (DKFZ), Im Neuenheimer Feld 581, 69120 Heidelberg, Germany. ·Diabetologia · Pubmed #21953276.

ABSTRACT: AIMS/HYPOTHESIS: There has been long-standing debate about whether diabetes is a causal risk factor for pancreatic cancer or a consequence of tumour development. Prospective epidemiological studies have shown variable relationships between pancreatic cancer risk and blood markers of glucose and insulin metabolism, overall and as a function of lag times between marker measurements (blood donation) and date of tumour diagnosis. METHODS: Pre-diagnostic levels of HbA(1c) and C-peptide were measured for 466 participants with pancreatic cancer and 466 individually matched controls within the European Prospective Investigation into Cancer and Nutrition. Conditional logistic regression models were used to estimate ORs for pancreatic cancer. RESULTS: Pancreatic cancer risk gradually increased with increasing pre-diagnostic HbA(1c) levels up to an OR of 2.42 (95% CI 1.33, 4.39 highest [≥ 6.5%, 48 mmol/mol] vs lowest [≤ 5.4%, 36 mmol/mol] category), even for individuals with HbA(1c) levels within the non-diabetic range. C-peptide levels showed no significant relationship with pancreatic cancer risk, irrespective of fasting status. Analyses showed no clear trends towards increasing hyperglycaemia (as marked by HbA(1c) levels) or reduced pancreatic beta cell responsiveness (as marked by C-peptide levels) with decreasing time intervals from blood donation to cancer diagnosis. CONCLUSIONS/INTERPRETATION: Our data on HbA(1c) show that individuals who develop exocrine pancreatic cancer tend to have moderate increases in HbA(1c) levels, relatively independently of obesity and insulin resistance-the classic and major risk factors for type 2 diabetes. While there is no strong difference by lag time, more data are needed on this in order to reach a firm conclusion.

9 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.

10 Article Predictors of survival in patients with malignant gastric outlet obstruction: a patient-oriented decision approach for palliative treatment. 2011

Jeurnink, Suzanne M / Steyerberg, Ewout W / Vleggaar, Frank P / van Eijck, Casper H J / van Hooft, Jeanin E / Schwartz, Matthijs P / Kuipers, Ernst J / Siersema, Peter D / Anonymous5130688. ·Department of Gastroenterology and Hepatology, Erasmus MC-University Medical Center Rotterdam, The Netherlands. s.m.jeurnink@students.uu.nl ·Dig Liver Dis · Pubmed #21376680.

ABSTRACT: BACKGROUND: Gastrojejunostomy and stentplacement are the most commonly used treatments for malignant gastric outlet obstruction (GOO). The preference for either treatment largely depends on the expected survival. Our objective was to investigate predictors of survival in patients with malignant GOO and to develop a model that could aid in the decision for either gastrojejunostomy or stentplacement. METHODS: Prognostic factors for survival were collected from a literature search and evaluated in our patient population, which included 95 retrospectively and 56 prospectively followed cases. All 151 patients were treated with gastrojejunostomy or stentplacement. RESULTS: A higher WHO performance score was the only significant prognostic factor for survival in our multivariable analysis (HR 2.2 95%CI 1.7-2.9), whereas treatment for obstructive jaundice, gender, age, metastases, weight loss, level of obstruction and pancreatic cancer were not. A prognostic model that includes the WHO score was able to distinguish patients with a poor survival (WHO score 3-4, median survival: 31 days) from those with a relatively intermediate or good survival (WHO score 2, median survival: 69 and WHO score 0-1, median survival: 139 days, respectively). CONCLUSIONS: Only the WHO score is a significant predictor of survival in patients with malignant GOO. A simple prognostic model is able to guide the palliative treatment decision for either gastrojejunostomy (WHO score 0-1) or stentplacement (WHO 3-4) in patients with malignant GOO.