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Pancreatic Neoplasms: HELP
Articles by Dora Romaguera
Based on 5 articles published since 2010
(Why 5 articles?)
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Between 2010 and 2020, D. Romaguera wrote the following 5 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Article Sweet-beverage consumption and risk of pancreatic cancer in the European Prospective Investigation into Cancer and Nutrition (EPIC). 2016

Navarrete-Muñoz, Eva M / Wark, Petra A / Romaguera, Dora / Bhoo-Pathy, Nirmala / Michaud, Dominique / Molina-Montes, Esther / Tjønneland, Anne / Olsen, Anja / Overvad, Kim / Boutron-Ruault, Marie-Christine / Clavel-Chapelon, Françoise / Fagherazzi, Guy / Katzke, Verena A / Kühn, Tilman / Steffen, Annika / Trichopoulou, Antonia / Klinaki, Eleni / Papatesta, Eleni-Maria / Masala, Giovanna / Krogh, Vittorio / Tumino, Rosario / Naccarati, Alessio / Mattiello, Amalia / Peeters, Petra H / Rylander, Charlotta / Parr, Christine L / Skeie, Guri / Weiderpass, Elisabete / Quirós, J Ramón / Duell, Eric J / Dorronsoro, Miren / Huerta, José María / Ardanaz, Eva / Wareham, Nick / Khaw, Kay-Tee / Travis, Ruth C / Key, Tim / Stepien, Magdalena / Freisling, Heinz / Riboli, Elio / Bueno-de-Mesquita, H Bas. ·Department of Public Health, Faculty of Medicine, Miguel Hernández University, Alicante, Spain; The Spanish Biomedical Research Centre in Epidemology and Public Health (CIBERESP), Health Institute Carlos III, Madrid, Spain; · Global eHealth Unit, Department of Primary Care and Public Health. · Department of Epidemiology and Biostatistics, and The Spanish Biomedical Research Centre in Physiopathology of Obesity and Nutrition (CIBEROBN), Health Institute Carlos III, Madrid, Spain; Medical Research Institute of Palma, University Hospital Son Espases, Palma de Mallorca, Spain; mariaadoracion.romaguera@ssib.es. · Julius Centre University of Malaya, Department of Social and Preventive Medicine, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia; · Department of Public Health and Community Medicine, Tufts University School of Medicine, Boston, MA; · The Spanish Biomedical Research Centre in Epidemology and Public Health (CIBERESP), Health Institute Carlos III, Madrid, Spain; Andalusian School of Public Health. Biomedical Research Institute of Granada; University Hospital of Granada/Granada University, Granada, Spain; · Diet, Genes and Environment, Danish Cancer Society Research Center, Copenhagen Ø, Denmark; · Department of Public Health, Section for Epidemiology, Aarhus University, Aarhus C, Denmark; · Centre for Research in Epidemiology and Population Health, U1018, Nutrition, Hormones and Women's Health team, National Institute for Health and Medical Research, Villejuif, France; UMRS 1018, Université Paris Sud, Villejuif, France; Institut Gustave Roussy, Villejuif, France; · Division of Cancer Epidemiology, German Cancer Research Center, Heidelberg, Germany; · Department of Epidemiology, German Institute of Human Nutrition, Potsdam-Rehbrücke, Nuthetal, Germany; · Hellenic Health Foundation, Athens, Greece; Bureau of Epidemiologic Research, Academy of Athens, Athens, Greece; · Hellenic Health Foundation, 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, Milan, Italy; · Cancer Registry and Histopathology Unit, "Civic - M.P. Arezzo" Hospital, ASP Ragusa, Italy; · Human Genetics Foundation,Torino, Molecular and Genetic Epidemiology Unit, Torino, Italy; · Dipartamento di Medicina Clinica e Chirurgia, Federico II University of Naples, Naples, Italy; · MRC-PHE Centre for Environment and Health, Department of Epidemiology and Biostatistics, 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, Netherlands; · Department of Community Medicine, University of Tromsø-the Arctic University of Norway, Tromsø, Norway; · Department of Chronic Diseases, Division of Epidemiology, Norwegian Institute of Public Health, Oslo, Norway; · Department of Community Medicine, University of Tromsø-the Arctic University of Norway, Tromsø, Norway; Department of Research, Cancer Registry of Norway, Oslo, Norway; Department of Medical Epidemiology and Biostatistics, Karolinska Institute, Stockholm, Sweden; Samfundet Folkhälsan, Helsinki, Finland; · Public Health Directorate, Asturias, Spain; · Unit of Nutrition and Cancer, Cancer Epidemiology Research Program, Bellvitge Biomedical Research Institute, Catalan Institute of Oncology, Barcelona, Spain; · The Spanish Biomedical Research Centre in Epidemology and Public Health (CIBERESP), Health Institute Carlos III, Madrid, Spain; Public Health Direction Biodonostia Basque Regional Health Department, San Sebastian, Spain; · The Spanish Biomedical Research Centre in Epidemology and Public Health (CIBERESP), Health Institute Carlos III, Madrid, Spain; Department of Epidemiology, Murcia Regional Health Council, IMIB-Arrixaca, Murcia, Spain; · The Spanish Biomedical Research Centre in Epidemology and Public Health (CIBERESP), Health Institute Carlos III, Madrid, Spain; Navarre Public Health Institute, Pamplona, Spain; · Medical Research Council Epidemiology Unit. · Department of Public Health and Primary Care, and Clinical Gerontology Unit, School of Clinical Medicine, University of Cambridge, Cambridge, United Kingdom; · Cancer Epidemiology Unit, Nuffield Department of Population Health, University of Oxford, Oxford, United Kingdom; · Nutrition and Metabolism Section, International Agency for Research on Cancer, Lyon, France; · Department for Determinants of Chronic Diseases, National Institute for Public Health and the Environment, Bilthoven, Netherlands; and. · Department of Epidemiology and Biostatistics, and. · Department of Epidemiology and Biostatistics, and Julius Centre University of Malaya, Department of Social and Preventive Medicine, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia; Department for Determinants of Chronic Diseases, National Institute for Public Health and the Environment, Bilthoven, Netherlands; and Department of Gastroenterology and Hepatology, University Medical Center, Utrecht, Netherlands. ·Am J Clin Nutr · Pubmed #27510540.

ABSTRACT: BACKGROUND: The consumption of sweet beverages has been associated with greater risk of type 2 diabetes and obesity, which may be involved in the development of pancreatic cancer. Therefore, it has been hypothesized that sweet beverages may increase pancreatic cancer risk as well. OBJECTIVE: We examined the association between sweet-beverage consumption (including total, sugar-sweetened, and artificially sweetened soft drink and juice and nectar consumption) and pancreatic cancer risk. DESIGN: The study was conducted within the European Prospective Investigation into Cancer and Nutrition cohort. A total of 477,199 participants (70.2% women) with a mean age of 51 y at baseline were included, and 865 exocrine pancreatic cancers were diagnosed after a median follow-up of 11.60 y (IQR: 10.10-12.60 y). Sweet-beverage consumption was assessed with the use of validated dietary questionnaires at baseline. HRs and 95% CIs were obtained with the use of multivariable Cox regression models that were stratified by age, sex, and center and adjusted for educational level, physical activity, smoking status, and alcohol consumption. Associations with total soft-drink consumption were adjusted for juice and nectar consumption and vice versa. RESULTS: Total soft-drink consumption (HR per 100 g/d: 1.03; 95% CI: 0.99, 1.07), sugar-sweetened soft-drink consumption (HR per 100 g/d: 1.02; 95% CI: 0.97, 1.08), and artificially sweetened soft-drink consumption (HR per 100 g/d: 1.04; 95% CI: 0.98, 1.10) were not associated with pancreatic cancer risk. Juice and nectar consumption was inversely associated with pancreatic cancer risk (HR per 100 g/d: 0.91; 95% CI: 0.84, 0.99); this association remained statistically significant after adjustment for body size, type 2 diabetes, and energy intake. CONCLUSIONS: Soft-drink consumption does not seem to be associated with pancreatic cancer risk. Juice and nectar consumption might be associated with a modest decreased pancreatic cancer risk. Additional studies with specific information on juice and nectar subtypes are warranted to clarify these results.

2 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.

3 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.

4 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.

5 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.