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Pancreatic Neoplasms: HELP
Articles by Teresa Norat
Based on 7 articles published since 2010
(Why 7 articles?)
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Between 2010 and 2020, T. Norat wrote the following 7 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Review Height and pancreatic cancer risk: a systematic review and meta-analysis of cohort studies. 2012

Aune, Dagfinn / Vieira, Ana Rita / Chan, Doris Sau Man / Navarro Rosenblatt, Deborah A / Vieira, Rui / Greenwood, Darren C / Cade, Janet E / Burley, Victoria J / Norat, Teresa. ·Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, St. Mary's Campus, Norfolk Place, Paddington, London, UK. d.aune@imperial.ac.uk ·Cancer Causes Control · Pubmed #22689322.

ABSTRACT: BACKGROUND: Greater height has been associated with increased risk of several cancers, but epidemiological data on height and pancreatic cancer are inconclusive. We conducted a systematic review and meta-analysis of prospective studies to clarify these results. METHODS: PubMed and several other databases were searched up to September 2011. Prospective studies of height and pancreatic cancer were included. Summary relative risks were estimated by the use of a random effects model. RESULTS: We identified twelve cohort studies that were included in the meta-analysis. The summary RR per 5-cm increase in height was 1.07 (95 % CI: 1.03-1.12, I (2) = 57 %). The results were similar among men and women. The summary estimate was attenuated when we included results from two pooled analyses together with these studies, summary RR = 1.03 (95 % CI: 1.00-1.07, I (2) = 44 %). CONCLUSIONS: This meta-analysis of cohort studies provides further evidence that greater adult attained height is associated with increased pancreatic cancer risk. However, given the unexplained heterogeneity, further studies are needed before a conclusion can be drawn.

2 Review Dietary fructose, carbohydrates, glycemic indices and pancreatic cancer risk: a systematic review and meta-analysis of cohort studies. 2012

Aune, D / Chan, D S M / Vieira, A R / Navarro Rosenblatt, D A / Vieira, R / Greenwood, D C / Cade, J E / Burley, V J / Norat, T. ·Department of Epidemiology and Biostatistics, School of Public Health, Imperial College, London, UK. d.aune@imperial.ac.uk ·Ann Oncol · Pubmed #22539563.

ABSTRACT: BACKGROUND: Dietary carbohydrates, glycemic load and glycemic index have been hypothesized to influence pancreatic cancer risk, but epidemiological studies have been inconsistent. We conducted a systematic review and meta-analysis of prospective studies to clarify these results. METHODS: PubMed and several other databases were searched for prospective studies of intake of carbohydrates, glycemic index and glycemic load and pancreatic cancer up to September 2011. Summary relative risks were estimated using a random effects model. RESULTS: Ten cohort studies (13 publications) were included in the meta-analysis. The summary relative risk (RR) per 10 glycemic index units was 1.02 [95% confidence interval (CI): 0.93-1.12, I(2) = 0%], per 50 glycemic load units was 1.03 (95% CI: 0.93-1.14, I(2) = 10%), per 100 g/day of total carbohydrates was 0.97 (95% CI: 0.81-1.16, I(2) = 35%), and per 25 g/day of sucrose intake was 1.05 (95% CI: 0.85-1.23, I(2) = 53%). A positive association was observed with fructose intake, summary RR = 1.22 (95% CI: 1.08-1.37, I(2) = 0%) per 25 g/day. CONCLUSIONS: This meta-analysis does not support an association between diets high in glycemic index, glycemic load, total carbohydrates or sucrose and pancreatic cancer risk. The finding of an increased risk with fructose intake warrants further investigation in studies with better adjustment for confounding and in non-American populations.

3 Review Body mass index, abdominal fatness and pancreatic cancer risk: a systematic review and non-linear dose-response meta-analysis of prospective studies. 2012

Aune, D / Greenwood, D C / Chan, D S M / Vieira, R / Vieira, A R / Navarro Rosenblatt, D A / Cade, J E / Burley, V J / Norat, T. ·Department of Epidemiology and Biostatistics, Imperial College London, London, UK. d.aune@imperial.ac.uk ·Ann Oncol · Pubmed #21890910.

ABSTRACT: BACKGROUND: Questions remain about the shape of the dose-response relationship between body mass index (BMI) and pancreatic cancer risk, possible confounding by smoking, and differences by gender or geographic location. Whether abdominal obesity increases risk is unclear. METHODS: We conducted a systematic review and meta-analysis of prospective studies of the association between BMI, abdominal fatness and pancreatic cancer risk and searched PubMed and several other databases up to January 2011. Summary relative risks (RRs) were calculated using a random-effects model. RESULTS: Twenty-three prospective studies of BMI and pancreatic cancer risk with 9504 cases were included. The summary RR for a 5-unit increment was 1.10 [95% confidence interval (CI) 1.07-1.14, I(2) = 19%] and results were similar when stratified by gender and geographic location. There was evidence of a non-linear association, P(non-linearity) = 0.005; however, among nonsmokers, there was increased risk even within the 'normal' BMI range. The summary RR for a 10-cm increase in waist circumference was 1.11 (95% CI 1.05-1.18, I(2) = 0%) and for a 0.1-unit increment in waist-to-hip ratio was 1.19 (95% CI 1.09-1.31, I(2) = 11%). CONCLUSIONS: Both general and abdominal fatness increases pancreatic cancer risk. Among nonsmokers, risk increases even among persons within the normal BMI range.

4 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

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

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

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

6 Article 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.

7 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.