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Pancreatic Neoplasms: HELP
Articles by Yunxia Lu
Based on 4 articles published since 2010
(Why 4 articles?)
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Between 2010 and 2020, Yunxia Lu wrote the following 4 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Article Flavonoid and lignan intake and pancreatic cancer risk in the European prospective investigation into cancer and nutrition cohort. 2016

Molina-Montes, Esther / Sánchez, María-José / Zamora-Ros, Raul / Bueno-de-Mesquita, H B As / Wark, Petra A / Obon-Santacana, Mireia / Kühn, Tilman / Katzke, Verena / Travis, Ruth C / Ye, Weimin / Sund, Malin / Naccarati, Alessio / Mattiello, Amalia / Krogh, Vittorio / Martorana, Caterina / Masala, Giovanna / Amiano, Pilar / Huerta, José-María / Barricarte, Aurelio / Quirós, José-Ramón / Weiderpass, Elisabete / Angell Åsli, Lene / Skeie, Guri / Ericson, Ulrika / Sonestedt, Emily / Peeters, Petra H / Romieu, Isabelle / Scalbert, Augustin / Overvad, Kim / Clemens, Matthias / Boeing, Heiner / Trichopoulou, Antonia / Peppa, Eleni / Vidalis, Pavlos / Khaw, Kay-Tee / Wareham, Nick / Olsen, Anja / Tjønneland, Anne / Boutroun-Rualt, Marie-Christine / Clavel-Chapelon, Françoise / Cross, Amanda J / Lu, Yunxia / Riboli, Elio / Duell, Eric J. ·Andalusian School of Public Health, Instituto De Investigación Biosanitaria Ibs, GRANADA, Hospitales Universitarios De Granada/Universidad De Granada, Granada, Spain. · CIBERESP, CIBER Epidemiología Y Salud Pública, Spain. · Section of Nutrition and Metabolism, International Agency for Research on Cancer (IARC), Lyon, France. · National Institute for Public Health and the Environment (RIVM), Bilthoven, The Netherlands. · Department of Gastroenterology and Hepatology, University Medical Centre, Utrecht, The Netherlands. · Department of Epidemiology and Biostatistics, the School of Public Health, Imperial College London, London, United Kingdom. · Department of Social and Preventive Medicine, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia. · Global eHealth Unit, Department of Primary Care and Public Health, the School of Public Health, Imperial College London, London, United Kingdom. · Unit of Nutrition and Cancer, Catalan Institute of Oncology (ICO-Idibell), Barcelona, Spain. · Division of Cancer Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany. · Cancer Epidemiology Unit, Nuffield Department of Population Health, University of Oxford, Oxford, United Kingdom. · Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden. · The Medical Biobank at Umeå University, Umeå, Sweden. · Molecular and Genetic Epidemiology Unit, HuGeF-Human Genetics Foundation, Torino, Italy. · Dipartimento Di Medicina Clinica E Chirurgia, Federico II University, Naples, Italy. · Epidemiology and Prevention Unit Fondazione IRCCS Istituto Nazionale Dei Tumori, Milan, Italy. · Cancer Registry ASP, Ragusa, Italy. · Molecular and Nutritional Epidemiology Unit, Cancer Research and Prevention Institute-ISPO, Florence, Italy. · Public Health Division of Gipuzkoa, BioDonostia Research Institute, San Sebastián, Spain. · Department of Epidemiology, Murcia Regional Health Council, IMIB-Arrixaca, Murcia, Spain. · Public Health Institute of Navarra, Pamplona, Spain. · Public Health Directorate, Asturias, Spain. · Department of Community Medicine, Faculty of Health Sciences, University of Tromsø, the Arctic University of Norway, Tromsø, Norway. · Department of Research, Cancer Registry of Norway, Oslo, Norway. · Genetic Epidemiology Group, Folkhälsan Research Center, Helsinki, Finland. · Department of Clinical Sciences in Malmö, Lund University, Lund, Sweden. · Department of Epidemiology, Julius Center for Health Sciences and Primary Care, University Medical Center, Utrecht, The Netherlands. · Department of Public Health, Section for Epidemiology, Aarhus University, Aarhus, Denmark. · Department of Epidemiology, German Institute of Human Nutrition Potsdam-Rehbruecke, Nuthetal, Germany. · Hellenic Health Foundation, Athens, Greece. · WHO Collaborating Center for Nutrition and Health, Unit of Nutritional Epidemiology and Nutrition in Public Health, Department of Hygiene, Epidemiology, and Medical Statistics, University of Athens Medical School, Athens, Greece. · University of Cambridge School of Clinical Medicine, Cambridge, United Kingdom. · Epidemiology Unit, Medical Research Council, Cambridge, United Kingdom. · Danish Cancer Society Research Center, Copenhagen, Denmark. · Inserm, CESP Centre for Research in Epidemiology and Population Health, France. ·Int J Cancer · Pubmed #27184434.

ABSTRACT: Despite the potential cancer preventive effects of flavonoids and lignans, their ability to reduce pancreatic cancer risk has not been demonstrated in epidemiological studies. Our aim was to examine the association between dietary intakes of flavonoids and lignans and pancreatic cancer risk in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. A total of 865 exocrine pancreatic cancer cases occurred after 11.3 years of follow-up of 477,309 cohort members. Dietary flavonoid and lignan intake was estimated through validated dietary questionnaires and the US Department of Agriculture (USDA) and Phenol Explorer databases. Hazard ratios (HR) and 95% confidence intervals (CIs) were calculated using age, sex and center-stratified Cox proportional hazards models, adjusted for energy intake, body mass index (BMI), smoking, alcohol and diabetes status. Our results showed that neither overall dietary intake of flavonoids nor of lignans were associated with pancreatic cancer risk (multivariable-adjusted HR for a doubling of intake = 1.03, 95% CI: 0.95-1.11 and 1.02; 95% CI: 0.89-1.17, respectively). Statistically significant associations were also not observed by flavonoid subclasses. An inverse association between intake of flavanones and pancreatic cancer risk was apparent, without reaching statistical significance, in microscopically confirmed cases (HR for a doubling of intake = 0.96, 95% CI: 0.91-1.00). In conclusion, we did not observe an association between intake of flavonoids, flavonoid subclasses or lignans and pancreatic cancer risk in the EPIC cohort.

2 Article New-onset type 2 diabetes, elevated HbA1c, anti-diabetic medications, and risk of pancreatic cancer. 2015

Lu, Yunxia / García Rodríguez, Luis Alberto / Malgerud, Linnéa / González-Pérez, Antonio / Martín-Pérez, Mar / Lagergren, Jesper / Bexelius, Tomas S. ·Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm 171 76, Sweden. · Department of Epidemiology and Biostatistics, Imperial College London, London W2 1PG, UK. · Centro Español de Investigación Farmacoepidemiológica, Madrid 28004, Spain. · Department of Clinical Sciences, Intervention and Technology (CLINTEC), Karolinska Institutet, Stockholm 171 77, Sweden. · Division of Cancer Studies, King's College London, London WC2R 2LS, UK. · Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm 171 77, Sweden. ·Br J Cancer · Pubmed #26575601.

ABSTRACT: BACKGROUND: Associations between type 2 diabetes, anti-diabetic medications and pancreatic cancer are controversial. This study aims to clarify such associations with new-onset type 2 diabetes and repeated measurements of glycated haemoglobin (HbA1c) levels. METHODS: A nested case-control study was initiated from the Health Improvement Network (THIN) in UK from 1996 to 2010. Information of pancreatic cancer cases was retrieved electronically from the medical records and manually validated. Control subjects were randomly selected and frequency-matched to the cases on sex, age, and calendar years. Multivariable unconditional logistic regression was performed to estimate odds ratios (OR) and 95% confidence intervals (CI), and adjusted for potential confounders. RESULTS: Among 1,574,768 person-years of follow-up, 529 pancreatic cancer cases and 5000 controls were identified. Type 2 diabetes, or changed HbA1c levels (rather than HbA1c levels at diabetes diagnosis) in diabetes patients (⩾4 mmol mol(-1) compared with <0 mmol mol(-1)) were followed by an increased OR of pancreatic cancer (OR, 2.16, 95% CI 1.72-2.72 and OR, 5.06, 95% CI 1.52-16.87, respectively). Among the anti-diabetic medications in diabetes patients, the OR for insulin users was 25.57 (95% CI 11.55-56.60), sulphonylureas 2.22 (95% CI 1.13, 4.40), and metformin users 1.46 (95% CI 0.85-2.52), compared with no use of any anti-diabetic medications. CONCLUSIONS: New-onset type 2 diabetes and, particularly, diabetes with rising HbA1c seem to be independent risk factors for pancreatic cancer. The relation between different anti-diabetic medications and pancreatic cancer seems to vary in strength, with the highest risk among users of insulin.

3 Article Sex differences in the incidence of gastrointestinal adenocarcinoma in Sweden 1970-2006. 2010

Rutegård, Martin / Shore, Richard / Lu, Yunxia / Lagergren, Pernilla / Lindblad, Mats. ·Upper Gastrointestinal Research (UGIR), Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden. martin.rutegard@ki.se ·Eur J Cancer · Pubmed #20188539.

ABSTRACT: BACKGROUND: Oesophageal and gastric adenocarcinoma share a male predominance not seen for other adenocarcinomas of the gastrointestinal tract. These sex differences are not explained by known risk factors. An endogenous factor, such as premenopausal oestrogen exposure, may act protectively in favour of women and might be detected by scrutinising sex ratios and incidence rates stratified by age. METHODS: The Swedish Cancer Register was used to collect primary oesophageal, gastric cardia, non-cardia gastric, colonic and pancreatic adenocarcinoma cases aged 25-84, during the study period of 1970-2006. Cases were divided into five-year age groups and crude incidence rates and male: female ratios were calculated. Evaluating potential time period effect, the corresponding results from 1970-1986 and 1987-2006 were also derived. RESULTS: The sex ratio for oesophageal adenocarcinoma ranged from approximately 10:1 to 4:1, presenting a seemingly consistent decline with age. The sex ratio for non-cardia gastric adenocarcinoma, however, increased with age to reach 2:1 at a point one to two decades after menopause, where the ratio levelled off and eventually declined. There was no discernible time period effect concerning any type of adenocarcinoma. The ratios for gastric cardia, colonic and pancreatic adenocarcinoma were stable with age. CONCLUSION: This study indicates separate patterns of age-dependency of the sex difference in oesophageal and non-cardia gastric adenocarcinoma incidence. The non-cardia gastric adenocarcinoma pattern might be due to a protective effect during premenopausal years for the female population, while the seemingly steady decline in sex ratio in oesophageal adenocarcinoma indicates a mechanism independent of menopause.

4 Minor Reply to 'Comment on 'New-onset type 2 diabetes, elevated HbA1c, anti-diabetic medications, and risk of pancreatic cancer''. 2016

Lu, Yunxia / Rodríguez, Luis Alberto García / Malgerud, Linnéa / González-Pérez, Antonio / Martín-Pérez, Mar / Lagergren, Jesper / Bexelius, Tomas S. ·Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm 171 76, Sweden. · Department of Epidemiology and Biostatistics, Imperial College London, London W2 1PG, UK. · Centro Español de Investigación Farmacoepidemiológica, Madrid 28004, Spain. · Department of Clinical Sciences, Intervention and Technology (CLINTEC), Karolinska Institutet, Stockholm 171 77, Sweden. · King's College London, Division of Cancer Studies, London WC2R 2LS, UK. · Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm 171 77, Sweden. ·Br J Cancer · Pubmed #27219289.

ABSTRACT: -- No abstract --