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Pancreatic Neoplasms: HELP
Articles by Lars Engstrand
Based on 3 articles published since 2010
(Why 3 articles?)
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Between 2010 and 2020, Lars Engstrand wrote the following 3 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Article Long-term proton pump inhibitor usage and the association with pancreatic cancer in Sweden. 2019

Brusselaers, Nele / Sadr-Azodi, Omid / Engstrand, Lars. ·Department of Microbiology, Tumor and Cell Biology, Centre for Translational Microbiome Research, Karolinska Institutet, Karolinska Hospital, Visionsgatan 4, 171 64, Stockholm, Sweden. Nele.Brusselaers@ki.se. · Science for Life Laboratory (SciLifeLab), Stockholm, Sweden. Nele.Brusselaers@ki.se. · Department of Head and Skin, Faculty of Medicine, Ghent University, Ghent, Belgium. Nele.Brusselaers@ki.se. · Clinical Epidemiology Division, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden. · Department of Surgery, St Göran Hospital, Stockholm, Sweden. · Department of Microbiology, Tumor and Cell Biology, Centre for Translational Microbiome Research, Karolinska Institutet, Karolinska Hospital, Visionsgatan 4, 171 64, Stockholm, Sweden. · Science for Life Laboratory (SciLifeLab), Stockholm, Sweden. ·J Gastroenterol · Pubmed #31811561.

ABSTRACT: BACKGROUND: The long-term safety of proton pump inhibitors (PPIs) is increasingly questioned. The aim of our study was to assess the risk of pancreatic cancer among long-term PPI users in Sweden. METHODS: This population-based nationwide Swedish cohort study including 796,492 adult long-term PPI users has been used to calculate the standardized incidence rate ratios (SIRs) and 95% confidence intervals (CI) for pancreatic cancer, stratifying by indications of use, age, sex, and duration of use. The risk among all 20,210 long-term H2-receptor antagonist users was assessed as comparison. RESULTS: Pancreatic cancer was found in 1733 long-term PPI users, and 25 H2-receptor antagonist users. For PPI users, the risk of pancreatic cancer was increased overall (SIRs = 2.22; 95% CI 2.12-2.32) and in all subgroup analyses, with the highest risk among PPI-users younger than 40 years (SIR = 8.90, 95% CI 4.26-16.37), and among individuals with a history of Helicobacter pylori (SIR = 2.99, 95% CI 2.54-3.49). After the first year after enrolment (during which PPI use may be because of early symptoms of pancreatic cancer), the risk remained increased over time, with SIR = 1.57 (95% CI 1.38-1.76) after 5 years. No associations were found for H2-receptor antagonists (SIR = 1.02, 95% CI 0.66-1.51). CONCLUSIONS: This large study showed an increased risk of pancreatic cancer in long-term users of PPIs in Sweden, in particular among the youngest users.

2 Article Bioinformatory-assisted analysis of next-generation sequencing data for precision medicine in pancreatic cancer. 2017

Malgerud, Linnéa / Lindberg, Johan / Wirta, Valtteri / Gustafsson-Liljefors, Maria / Karimi, Masoud / Moro, Carlos Fernández / Stecker, Katrin / Picker, Alexander / Huelsewig, Carolin / Stein, Martin / Bohnert, Regina / Del Chiaro, Marco / Haas, Stephan L / Heuchel, Rainer L / Permert, Johan / Maeurer, Markus J / Brock, Stephan / Verbeke, Caroline S / Engstrand, Lars / Jackson, David B / Grönberg, Henrik / Löhr, Johannes Matthias. ·Center for Digestive Diseases, Karolinska University Hospital, Stockholm, Sweden. · Department of Clinical Sciences, Intervention and Technology (CLINTEC), Karolinska Institutet, Stockholm, Sweden. · Department of Medical Epidemiology & Biostatistics (MEB), Karolinska Institutet, Stockholm, Sweden. · Science for Life Laboratory, Department of Microbiology, Tumor and Cell Biology (MTC), Karolinska Institutet, Stockholm, Sweden. · Department of Oncology at Radiumhemmet, Karolinska University Hospital, Stockholm, Sweden. · Department of Pathology, Karolinska University Hospital, Stockholm, Sweden. · Molecular Health GmbH, Heidelberg, Germany. · Innovation Office, Karolinska University Hospital, Stockholm, Sweden. · Department of Laboratory Medicine (LABMED), Karolinska Institutet, Stockholm, Sweden. ·Mol Oncol · Pubmed #28675654.

ABSTRACT: Pancreatic ductal adenocarcinoma (PDAC) is a tumor with an extremely poor prognosis, predominantly as a result of chemotherapy resistance and numerous somatic mutations. Consequently, PDAC is a prime candidate for the use of sequencing to identify causative mutations, facilitating subsequent administration of targeted therapy. In a feasibility study, we retrospectively assessed the therapeutic recommendations of a novel, evidence-based software that analyzes next-generation sequencing (NGS) data using a large panel of pharmacogenomic biomarkers for efficacy and toxicity. Tissue from 14 patients with PDAC was sequenced using NGS with a 620 gene panel. FASTQ files were fed into treatmentmap. The results were compared with chemotherapy in the patients, including all side effects. No changes in therapy were made. Known driver mutations for PDAC were confirmed (e.g. KRAS, TP53). Software analysis revealed positive biomarkers for predicted effective and ineffective treatments in all patients. At least one biomarker associated with increased toxicity could be detected in all patients. Patients had been receiving one of the currently approved chemotherapy agents. In two patients, toxicity could have been correctly predicted by the software analysis. The results suggest that NGS, in combination with an evidence-based software, could be conducted within a 2-week period, thus being feasible for clinical routine. Therapy recommendations were principally off-label use. Based on the predominant KRAS mutations, other drugs were predicted to be ineffective. The pharmacogenomic biomarkers indicative of increased toxicity could be retrospectively linked to reported negative side effects in the respective patients. Finally, the occurrence of somatic and germline mutations in cancer syndrome-associated genes is noteworthy, despite a high frequency of these particular variants in the background population. These results suggest software-analysis of NGS data provides evidence-based information on effective, ineffective and toxic drugs, potentially forming the basis for precision cancer medicine in PDAC.

3 Article Helicobacter pylori infection, chronic corpus atrophic gastritis and pancreatic cancer risk in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort: A nested case-control study. 2017

Huang, Jiaqi / Zagai, Ulrika / Hallmans, Göran / Nyrén, Olof / Engstrand, Lars / Stolzenberg-Solomon, Rachael / Duell, Eric J / Overvad, Kim / Katzke, Verena A / Kaaks, Rudolf / Jenab, Mazda / Park, Jin Young / Murillo, Raul / Trichopoulou, Antonia / Lagiou, Pagona / Bamia, Christina / Bradbury, Kathryn E / Riboli, Elio / Aune, Dagfinn / Tsilidis, Konstantinos K / Capellá, Gabriel / Agudo, Antonio / Krogh, Vittorio / Palli, Domenico / Panico, Salvatore / Weiderpass, Elisabete / Tjønneland, Anne / Olsen, Anja / Martínez, Begoña / Redondo-Sanchez, Daniel / Chirlaque, Maria-Dolores / Hm Peeters, Petra / Regnér, Sara / Lindkvist, Björn / Naccarati, Alessio / Ardanaz, Eva / Larrañaga, Nerea / Boutron-Ruault, Marie-Christine / Rebours, Vinciane / Barré, Amélie / Bueno-de-Mesquita, H B As / Ye, Weimin. ·Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Solna, Sweden. · Department of Public Health and Clinical Nutrition, Umeå University, Umeå, Sweden. · Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden. · Metabolic Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, MD. · Unit of Nutrition and Cancer, Cancer Epidemiology Research Program, Catalan Institute of Oncology (ICO-IDIBELL), Barcelona, Spain. · Department of Public Health, Section for Epidemiology, Aarhus University, Aarhus, Denmark. · Division of Cancer Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany. · Prevention and Implementation Group, Section of Early Detection and Prevention, Section of Nutrition and Metabolism, International Agency for Research on Cancer, Lyon, France. · 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, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece. · Department of Epidemiology, Harvard T. H. Chan School of Public Health, Boston, MA. · Cancer Epidemiology Unit, Nuffield Department of Population Health, University of Oxford, Oxford, United Kingdom. · Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, London, United Kingdom. · Department of Hygiene and Epidemiology, University of Ioannina School of Medicine, Ioannina, Greece. · Translational Research Laboratory, IDIBELL-Catalan Institute of Oncology, Barcelona, Spain. · Unit of Nutrition and Cancer. Cancer Epidemiology Research Program. Catalan Institute of Oncology-IDIBELL. L'Hospitalet de Llobregat, Barcelona, Spain. · Epidemiology and Prevention Unit, Fondazione IRCCS Istituto Nazionale dei Tumori, Milano, Italy. · Cancer Risk Factors and Life-Style Epidemiology Unit, Cancer Research and Prevention Institute - ISPO, Florence, Italy. · Dipartimento di medicina clinica e chirurgia Federico II, Naples, Italy. · Department of Community Medicine, University of Tromsø, The Arctic University of Norway, Tromsø, Norway. · Department of Research, Cancer Registry of Norway, Institute of Population-Based Cancer Research, Oslo, Norway. · Genetic Epidemiology Group, Folkhälsan Research Center, Helsinki, Finland. · Danish Cancer Society Research Center, Copenhagen, Denmark. · Andalusian School of Public Health, Instituto De Investigación Biosanitaria Ibs, Granada, Spain. · CIBER of Epidemiology and Public Health (CIBERESP), Madrid, Spain. · Escuela Andaluza de Salud Pública, Instituto de Investigación Biosanitaria ibs, Granada, Hospitales Universitarios de Granada/Universidad de Granada, Granada, Spain. · Department of Epidemiology, Regional Health Council, IMIB-Arrixaca, Murcia, Spain. · Department of Health and Social Sciences, Universidad de Murcia, Murcia, Spain. · Department of Epidemiology, Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Utrecht, The Netherlands. · Department of Surgery, Institution of Clinical Sciences Malmö, Lund University, Malmö, Sweden. · Department of Medicine, Sahlgrenska University Hospital, Gothenburg, Sweden. · Molecular and Genetic Epidemiology Unit, Human Genetics Foundation, Turin, Italy. · Navarra Public Health Institute, Pamplona, Spain; IdiSNA, Navarra Institute for Health Research, Pamplona, Spain. · Public Health Division of Gipuzkoa, Regional Government of the Basque Country, Spain. · Hormones and Women's Health Team, INSERM, Centre for Research in Epidemiology and Population Health (CESP), U1018, Nutrition, Villejuif, F-94805, France. · Université Paris Sud, UMRS 1018, Villejuif, F-94805, France. · Institut Gustave Roussy, Villejuif, F-94805, France. · Department of Gastroenterology and Pancreatology, Beaujon Hospital, University Paris 7, Clichy, France. · Université Paris Sud and Gastroenterology Unit, Hôpitaux Universitaires Paris Sud, CHU de Bicêtre, AP-HP, Le Kremlin Bicêtre, France. · Department for Determinants of Chronic Diseases (DCD), 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 & Preventive Medicine, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia. · The Medical Biobank at Umeå University, Umeå, Sweden. ·Int J Cancer · Pubmed #28032715.

ABSTRACT: The association between H. pylori infection and pancreatic cancer risk remains controversial. We conducted a nested case-control study with 448 pancreatic cancer cases and their individually matched control subjects, based on the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort, to determine whether there was an altered pancreatic cancer risk associated with H. pylori infection and chronic corpus atrophic gastritis. Conditional logistic regression models were applied to calculate odds ratios (ORs) and corresponding 95% confidence intervals (CIs), adjusted for matching factors and other potential confounders. Our results showed that pancreatic cancer risk was neither associated with H. pylori seropositivity (OR = 0.96; 95% CI: 0.70, 1.31) nor CagA seropositivity (OR = 1.07; 95% CI: 0.77, 1.48). We also did not find any excess risk among individuals seropositive for H. pylori but seronegative for CagA, compared with the group seronegative for both antibodies (OR = 0.94; 95% CI: 0.63, 1.38). However, we found that chronic corpus atrophic gastritis was non-significantly associated with an increased pancreatic cancer risk (OR = 1.35; 95% CI: 0.77, 2.37), and although based on small numbers, the excess risk was particularly marked among individuals seronegative for both H. pylori and CagA (OR = 5.66; 95% CI: 1.59, 20.19, p value for interaction < 0.01). Our findings provided evidence supporting the null association between H. pylori infection and pancreatic cancer risk in western European populations. However, the suggested association between chronic corpus atrophic gastritis and pancreatic cancer risk warrants independent verification in future studies, and, if confirmed, further studies on the underlying mechanisms.