caa a22 4500 445314982 CHVBK 20180317142643.0 cr unu---uuuuu 170323e20110701xx s 000 0 eng 10.1007/s10552-011-9774-z doi (NATIONALLICENCE)springer-10.1007/s10552-011-9774-z Low levels of apolipoprotein A-I and HDL are associated with risk of prostate cancer in the Swedish AMORIS study [Elektronische Daten] [Mieke Van Hemelrijck, Göran Walldius, Ingmar Jungner, Niklas Hammar, Hans Garmo, Elisa Binda, Adrian Hayday, Mats Lambe, Lars Holmberg] Background: A detailed analysis of lipid profiles, using apolipoproteins, has not yet been conducted for prostate cancer (PCa). Since several etiological pathways have been proposed for PCa and lipids, we aimed to study this in a large Swedish cohort with 1,469 primary prostate cancers. Methods: A cohort (n=69,735) of all men aged 35years or older, whose levels of triglycerides (TG) (mmol/L), total cholesterol (mmol/L), glucose (mmol/L), LDL (mmol/L), HDL (mmol/L), apoB (g/L), and apoA-I (g/L) were measured at baseline, was selected from the Apolipoprotein MOrtality RISk (AMORIS) database. About 2,008 men developed PCa. Multivariate Cox proportional hazard models were used to analyze associations between lipid components and PCa. Results: ApoA-I and HDL were inversely associated with PCa risk (e.g., HR for HDL: 0.93 (95% CI: 0.81-1.07), 0.88 (0.76-1.01), 0.81 (0.70-0.94), for second, third, and fourth quartiles compared with the first quartile; with p for trend: 0.004; HR for apoA-I: 1.00 (0.88-1.13), 0.93 (0.82-1.05), 0.88 (0.77-0.99),), for second, third, and fourth quartiles compared with the first quartile; with p for trend: 0.022). ApoB, LDL, and non-HDL were not associated with PCa risk. Conclusions: Our results show that low HDL and ApoA-I as well as increased lipid ratios are related to increased PCa risk. Experimental studies are required to tease out the underlying biological mechanisms linking these lipid components to PCa. Springer Science+Business Media B.V., 2011 Prostate cancer nationallicence Hypercholesterolemia nationallicence Hypertriglyceridemia nationallicence Apolipoproteins nationallicence Lipids nationallicence Cholesterol nationallicence Van Hemelrijck Mieke King's College London, School of Medicine, Division of Cancer Studies, Cancer Epidemiology Group, Research Oncology, Bermondsey Wing, Guy's Hospital, 3rd Floor, SE1 9RT, London, UK aut Walldius Göran Department of Medicine and Department of Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden aut Jungner Ingmar Department of Medicine, Clinical Epidemiological Unit, Karolinska Institutet and CALAB Research, Stockholm, Sweden aut Hammar Niklas Department of Epidemiology, Insitute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden aut Garmo Hans King's College London, School of Medicine, Division of Cancer Studies, Cancer Epidemiology Group, Research Oncology, Bermondsey Wing, Guy's Hospital, 3rd Floor, SE1 9RT, London, UK aut Binda Elisa King's College London, School of Medicine, Division of Immunology, Infection and Inflammatory Disease, Peter Gorer Department of Immunobiology, London, UK aut Hayday Adrian King's College London, School of Medicine, Division of Immunology, Infection and Inflammatory Disease, Peter Gorer Department of Immunobiology, London, UK aut Lambe Mats Regional Oncologic Centre, Uppsala University, Uppsala, Sweden aut Holmberg Lars King's College London, School of Medicine, Division of Cancer Studies, Cancer Epidemiology Group, Research Oncology, Bermondsey Wing, Guy's Hospital, 3rd Floor, SE1 9RT, London, UK aut Cancer Causes & Control Springer Netherlands 22/7(2011-07-01), 1011-1019 0957-5243 22:7<1011 2011 22 10552 https://doi.org/10.1007/s10552-011-9774-z text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/s10552-011-9774-z text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Van Hemelrijck Mieke King's College London, School of Medicine, Division of Cancer Studies, Cancer Epidemiology Group, Research Oncology, Bermondsey Wing, Guy's Hospital, 3rd Floor, SE1 9RT, London, UK aut NATIONALLICENCE 700 1- Walldius Göran Department of Medicine and Department of Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden aut NATIONALLICENCE 700 1- Jungner Ingmar Department of Medicine, Clinical Epidemiological Unit, Karolinska Institutet and CALAB Research, Stockholm, Sweden aut NATIONALLICENCE 700 1- Hammar Niklas Department of Epidemiology, Insitute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden aut NATIONALLICENCE 700 1- Garmo Hans King's College London, School of Medicine, Division of Cancer Studies, Cancer Epidemiology Group, Research Oncology, Bermondsey Wing, Guy's Hospital, 3rd Floor, SE1 9RT, London, UK aut NATIONALLICENCE 700 1- Binda Elisa King's College London, School of Medicine, Division of Immunology, Infection and Inflammatory Disease, Peter Gorer Department of Immunobiology, London, UK aut NATIONALLICENCE 700 1- Hayday Adrian King's College London, School of Medicine, Division of Immunology, Infection and Inflammatory Disease, Peter Gorer Department of Immunobiology, London, UK aut NATIONALLICENCE 700 1- Lambe Mats Regional Oncologic Centre, Uppsala University, Uppsala, Sweden aut NATIONALLICENCE 700 1- Holmberg Lars King's College London, School of Medicine, Division of Cancer Studies, Cancer Epidemiology Group, Research Oncology, Bermondsey Wing, Guy's Hospital, 3rd Floor, SE1 9RT, London, UK aut NATIONALLICENCE 773 0- Cancer Causes & Control Springer Netherlands 22/7(2011-07-01), 1011-1019 0957-5243 22:7<1011 2011 22 10552 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer