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

2 Article Leukocyte telomere length in relation to pancreatic cancer risk: a prospective study. 2014

Campa, Daniele / Mergarten, Björn / De Vivo, Immaculata / Boutron-Ruault, Marie-Christine / Racine, Antoine / Severi, Gianluca / Nieters, Alexandra / Katzke, Verena A / Trichopoulou, Antonia / Yiannakouris, Nikos / Trichopoulos, Dimitrios / Boeing, Heiner / Quirós, J Ramón / Duell, Eric J / Molina-Montes, Esther / Huerta, José María / Ardanaz, Eva / Dorronsoro, Miren / Khaw, Kay-Tee / Wareham, Nicholas / Travis, Ruth C / Palli, Domenico / Pala, Valeria / Tumino, Rosario / Naccarati, Alessio / Panico, Salvatore / Vineis, Paolo / Riboli, Elio / Siddiq, Afshan / Bueno-de-Mesquita, H B / Peeters, Petra H / Nilsson, Peter M / Sund, Malin / Ye, Weimin / Lund, Eiliv / Jareid, Mie / Weiderpass, Elisabete / Duarte-Salles, Talita / Kong, So Yeon / Stepien, Magdalena / Canzian, Federico / Kaaks, Rudolf. ·Division of Cancer Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany. · Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts. Program in Genetic Epidemiology and Statistical Genetics, Harvard School of Public Health, Boston, Massachusetts. · Institut National de la Santé et de la Recherche Médicale (INSERM), Centre for research in Epidemiology and Population Health (CESP), U1018, Nutrition, Hormones, and Women's Health team, Villejuif, France. Univ Paris Sud, UMRS 1018, Villejuif, France. IGR, Villejuif, France. · Human Genetics Foundation (HuGeF), Torino, Italy. · Center for Chronic Immunodeficiency, University Medical Center Freiburg, Freiburg, Germany. · Hellenic Health Foundation, Athens, Greece. Bureau of Epidemiologic Research, Academy of Athens, Athens, Greece. · Hellenic Health Foundation, Athens, Greece. Harokopio University of Athens, Greece. · Hellenic Health Foundation, Athens, Greece. Bureau of Epidemiologic Research, Academy of Athens, Athens, Greece. Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts. · Department of Epidemiology, German Institute of Human Nutrition Potsdam-Rehbrücke, Nuthetal, Germany. · Public Health Directorate, Asturias, Spain. · Unit of Nutrition, Environment, and Cancer, Cancer Epidemiology Research Program, Bellvitge Biomedical Research Institute (IDIBELL), Catalan Institute of Oncology (ICO), Barcelona, Spain. · Escuela Andaluza de Salud Pública, Instituto de Investigación Biosanitaria de Granada (Granada.ibs), Granada, Spain. CIBER Epidemiology and Public Health CIBERESP, Madrid, Spain. · CIBER Epidemiology and Public Health CIBERESP, Madrid, Spain. Department of Epidemiology, Murcia Regional Health Council, Murcia, Spain. · CIBER Epidemiology and Public Health CIBERESP, Madrid, Spain. Navarre Public Health Institute, Pamplona, Spain. · Public Health Direction and Biodonostia-Ciberesp Basque Regional Health Department, San Sebastian, Spain. · University of Cambridge, School of Clinical Medicine, Cambridge, United Kingdom. · Cancer Epidemiology Unit, University of Oxford, Oxford, United Kingdom. · Molecular and Nutritional Epidemiology Unit, Cancer Research and Prevention Institute, ISPO, Florence, Italy. · Epidemiology and Prevention Unit Fondazione IRCCS Istituto Nazionale dei Tumori, Milan, Italy. · Cancer Registry and Histopathology Unit, "Civic - M.P. Arezzo" Hospital, ASP Ragusa, Ragusa, Italy. · Dipartimento Di Medicina Clinica e Chirurgia Federico II University, Naples, Italy. · Division of Epidemiology, Public Health and Primary Care, Imperial College, London, United Kingdom. · Department of Genomics of Common Disease, School of Public Health, Imperial College London, London, United Kingdom. · National Institute for Public Health and the Environment (RIVM), Bilthoven, the Netherlands. Department of Gastroenterology and Hepatology, University Medical Centre, Utrecht, the Netherlands. The School of Public Health, Imperial College London, London, United Kingdom. · Department of Epidemiology, Julius Center for Health Sciences and Primary Care, University Medical Center, Utrecht, the Netherlands. · Lund University, Department of Clinical Sciences, Skåne University Hospital, Malmö Sweden. · Department of Surgical and Perioperative Sciences, Umeå University, Umeå, Sweden. · Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden. The Medical Biobank at Umeå University, Umeå, Sweden. · Department of Community Medicine, Faculty of Health Sciences, University of Tromso, The Arctic University of Norway, Tromsø, Norway. · Department of Community Medicine, Faculty of Health Sciences, University of Tromso, The Arctic University of Norway, Tromsø, Norway. Department of Research, Cancer Registry of Norway, Oslo, Norway. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden. Samfundet Folkhälsan, Helsinki, Finland. · International Agency for Research on Cancer (IARC-WHO), Lyon, France. · Genomic Epidemiology Group, German Cancer Research Center (DKFZ), Heidelberg, Germany. · Division of Cancer Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany. r.kaaks@dkfz.de. ·Cancer Epidemiol Biomarkers Prev · Pubmed #25103821.

ABSTRACT: BACKGROUND: Several studies have examined leukocyte telomere length (LTL) as a possible predictor for cancer at various organ sites. The hypothesis originally motivating many of these studies was that shorter telomeres would be associated with an increase in cancer risk; the results of epidemiologic studies have been inconsistent, however, and suggested positive, negative, or null associations. Two studies have addressed the association of LTL in relation to pancreatic cancer risk and the results are contrasting. METHODS: We measured LTL in a prospective study of 331 pancreatic cancer cases and 331 controls in the context of the European Prospective Investigation into Cancer and Nutrition (EPIC). RESULTS: We observed that the mean LTL was higher in cases (0.59 ± 0.20) than in controls (0.57 ± 0.17), although this difference was not statistically significant (P = 0.07), and a basic logistic regression model showed no association of LTL with pancreas cancer risk. When adjusting for levels of HbA1c and C-peptide, however, there was a weakly positive association between longer LTL and pancreatic cancer risk [OR, 1.13; 95% confidence interval (CI), 1.01-1.27]. Additional analyses by cubic spline regression suggested a possible nonlinear relationship between LTL and pancreatic cancer risk (P = 0.022), with a statistically nonsignificant increase in risk at very low LTL, as well as a significant increase at high LTL. CONCLUSION: Taken together, the results from our study do not support LTL as a uniform and strong predictor of pancreatic cancer. IMPACT: The results of this article can provide insights into telomere dynamics and highlight the complex relationship between LTL and pancreatic cancer risk.

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 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.

5 Article Plasma antibodies to oral bacteria and risk of pancreatic cancer in a large European prospective cohort study. 2013

Michaud, Dominique S / Izard, Jacques / Wilhelm-Benartzi, Charlotte S / You, Doo-Ho / Grote, Verena A / Tjønneland, Anne / Dahm, Christina C / Overvad, Kim / Jenab, Mazda / Fedirko, Veronika / Boutron-Ruault, Marie Christine / Clavel-Chapelon, Françoise / Racine, Antoine / Kaaks, Rudolf / Boeing, Heiner / Foerster, Jana / Trichopoulou, Antonia / Lagiou, Pagona / Trichopoulos, Dimitrios / Sacerdote, Carlotta / Sieri, Sabina / Palli, Domenico / Tumino, Rosario / Panico, Salvatore / Siersema, Peter D / Peeters, Petra H M / Lund, Eiliv / Barricarte, Aurelio / Huerta, José-María / Molina-Montes, Esther / Dorronsoro, Miren / Quirós, J Ramón / Duell, Eric J / Ye, Weimin / Sund, Malin / Lindkvist, Björn / Johansen, Dorthe / Khaw, Kay-Tee / Wareham, Nick / Travis, Ruth C / Vineis, Paolo / Bueno-de-Mesquita, H Bas / Riboli, Elio. ·Department of Epidemiology, Division of Biology and Medicine, Brown University, Providence, Rhode Island, USA. ·Gut · Pubmed #22990306.

ABSTRACT: OBJECTIVE: Examine the relationship between antibodies to 25 oral bacteria and pancreatic cancer risk in a prospective cohort study. DESIGN: We measured antibodies to oral bacteria in prediagnosis blood samples from 405 pancreatic cancer cases and 416 matched controls, nested within the European Prospective Investigation into Cancer and Nutrition study. Analyses were conducted using conditional logistic regression and additionally adjusted for smoking status and body mass index. RESULTS: Individuals with high levels of antibodies against Porphyromonas gingivalis ATTC 53978, a pathogenic periodontal bacteria, had a twofold higher risk of pancreatic cancer than individuals with lower levels of these antibodies (OR 2.14; 95% CI 1.05 to 4.36; >200 ng/ml vs ≤200 ng/ml). To explore the association with commensal (non-pathogenic) oral bacteria, we performed a cluster analysis and identified two groups of individuals, based on their antibody profiles. A cluster with overall higher levels of antibodies had a 45% lower risk of pancreatic cancer than a cluster with overall lower levels of antibodies (OR 0.55; 95% CI 0.36 to 0.83). CONCLUSIONS: Periodontal disease might increase the risk for pancreatic cancer. Moreover, increased levels of antibodies against specific commensal oral bacteria, which can inhibit growth of pathogenic bacteria, might reduce the risk of pancreatic cancer. Studies are needed to determine whether oral bacteria have direct effects on pancreatic cancer pathogenesis or serve as markers of the immune response.

6 Article Inflammation marker and risk of pancreatic cancer: a nested case-control study within the EPIC cohort. 2012

Grote, V A / Kaaks, R / Nieters, A / Tjønneland, A / Halkjær, J / Overvad, K / Skjelbo Nielsen, M R / Boutron-Ruault, M C / Clavel-Chapelon, F / Racine, A / Teucher, B / Becker, S / Pischon, T / Boeing, H / Trichopoulou, A / Cassapa, C / Stratigakou, V / Palli, D / Krogh, V / Tumino, R / Vineis, P / Panico, S / Rodríguez, L / Duell, E J / Sánchez, M-J / Dorronsoro, M / Navarro, C / Gurrea, A B / Siersema, P D / Peeters, P H M / Ye, W / Sund, M / Lindkvist, B / Johansen, D / Khaw, K-T / Wareham, N / Allen, N E / Travis, R C / Fedirko, V / Jenab, M / Michaud, D S / Chuang, S-C / Romaguera, D / Bueno-de-Mesquita, H B / Rohrmann, S. ·Division of Cancer Epidemiology (c020), German Cancer Research Center (DKFZ), Im Neuenheimer Feld 581, Heidelberg 69120, Germany. ·Br J Cancer · Pubmed #22617158.

ABSTRACT: BACKGROUND: Established risk factors for pancreatic cancer include smoking, long-standing diabetes, high body fatness, and chronic pancreatitis, all of which can be characterised by aspects of inflammatory processes. However, prospective studies investigating the relation between inflammatory markers and pancreatic cancer risk are scarce. METHODS: We conducted a nested case-control study within the European Prospective Investigation into Cancer and Nutrition, measuring prediagnostic blood levels of C-reactive protein (CRP), interleukin-6 (IL-6), and soluble receptors of tumour necrosis factor-α (sTNF-R1, R2) in 455 pancreatic cancer cases and 455 matched controls. Odds ratios (ORs) were estimated using conditional logistic regression models. RESULTS: None of the inflammatory markers were significantly associated with risk of pancreatic cancer overall, although a borderline significant association was observed for higher circulating sTNF-R2 (crude OR=1.52 (95% confidence interval (CI) 0.97-2.39), highest vs lowest quartile). In women, however, higher sTNF-R1 levels were significantly associated with risk of pancreatic cancer (crude OR=1.97 (95% CI 1.02-3.79)). For sTNF-R2, risk associations seemed to be stronger for diabetic individuals and those with a higher BMI. CONCLUSION: Prospectively, CRP and IL-6 do not seem to have a role in our study with respect to risk of pancreatic cancer, whereas sTNF-R1 seemed to be a risk factor in women and sTNF-R2 might be a mediator in the risk relationship between overweight and diabetes with pancreatic cancer. Further large prospective studies are needed to clarify the role of proinflammatory proteins and cytokines in the pathogenesis of exocrine pancreatic cancer.

7 Article Dietary intake of iron, heme-iron and magnesium and pancreatic cancer risk in the European prospective investigation into cancer and nutrition cohort. 2012

Molina-Montes, Esther / Wark, Petra A / Sánchez, María-José / Norat, Teresa / Jakszyn, Paula / Luján-Barroso, Leila / Michaud, Dominique S / Crowe, Francesca / Allen, Naomi / Khaw, Kay-Tee / Wareham, Nicholas / Trichopoulou, Antonia / Adarakis, George / Katarachia, Helen / Skeie, Guri / Henningsen, Maria / Broderstad, Ann Ragnhild / Berrino, Franco / Tumino, Rosario / Palli, Domenico / Mattiello, Amalia / Vineis, Paolo / Amiano, Pilar / Barricarte, Aurelio / Huerta, José-María / Duell, Eric J / Quirós, José-Ramón / Ye, Weimin / Sund, Malin / Lindkvist, Björn / Johansen, Dorthe / Overvad, Kim / Tjønneland, Anne / Roswall, Nina / Li, Kuanrong / Grote, Verena A / Steffen, Annika / Boeing, Heiner / Racine, Antoine / Boutron-Ruault, Marie-Christine / Carbonnel, Franck / Peeters, Petra H M / Siersema, Peter D / Fedirko, Veronika / Jenab, Mazda / Riboli, Elio / Bueno-de-Mesquita, Bas. ·Andalusian School of Public Health. Granada Cancer Registry, Spain. ·Int J Cancer · Pubmed #22438075.

ABSTRACT: Several studies support a protective effect of dietary magnesium against type 2 diabetes, but a harmful effect for iron. As diabetes has been linked to pancreatic cancer, intake of these nutrients may be also associated with this cancer. We examined the association between dietary intake of magnesium, total iron and heme-iron and pancreatic cancer risk in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. In total, 142,203 men and 334,999 women, recruited between 1992 and 2000, were included. After an average follow-up of 11.3 years, 396 men and 469 women developed exocrine pancreatic cancer. Hazard ratios and 95% confidence intervals (CIs) were obtained using Cox regression stratified by age and center, and adjusted for energy intake, smoking status, height, weight, and self-reported diabetes status. Neither intake of magnesium, total iron nor heme-iron was associated with pancreatic cancer risk. In stratified analyses, a borderline inverse association was observed among overweight men (body mass index, ≥ 25 kg/m(2) ) with magnesium (HR(per 100 mg/day increase) = 0.79, 95% CI = 0.63-1.01) although this was less apparent using calibrated intake. In female smokers, a higher intake of heme-iron was associated with a higher pancreatic cancer risk (HR (per 1 mg/day increase) = 1.38, 95% CI = 1.10-1.74). After calibration, this risk increased significantly to 2.5-fold (95% CI = 1.22-5.28). Overall, dietary magnesium, total iron and heme-iron were not associated with pancreatic cancer risk during the follow-up period. Our observation that heme-iron was associated with increased pancreatic cancer risk in female smokers warrants replication in additional study populations.

8 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.

9 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.