Cancer Causes & Control

, Volume 22, Issue 7, pp 1011–1019

Low levels of apolipoprotein A-I and HDL are associated with risk of prostate cancer in the Swedish AMORIS study

  • Mieke Van Hemelrijck
  • Göran Walldius
  • Ingmar Jungner
  • Niklas Hammar
  • Hans Garmo
  • Elisa Binda
  • Adrian Hayday
  • Mats Lambe
  • Lars Holmberg
Original paper

DOI: 10.1007/s10552-011-9774-z

Cite this article as:
Van Hemelrijck, M., Walldius, G., Jungner, I. et al. Cancer Causes Control (2011) 22: 1011. doi:10.1007/s10552-011-9774-z

Abstract

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 35 years 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.

Keywords

Prostate cancer Hypercholesterolemia Hypertriglyceridemia Apolipoproteins Lipids Cholesterol 

Copyright information

© Springer Science+Business Media B.V. 2011

Authors and Affiliations

  • Mieke Van Hemelrijck
    • 1
  • Göran Walldius
    • 2
  • Ingmar Jungner
    • 3
  • Niklas Hammar
    • 4
    • 5
  • Hans Garmo
    • 1
    • 6
  • Elisa Binda
    • 7
  • Adrian Hayday
    • 7
    • 8
  • Mats Lambe
    • 6
    • 9
  • Lars Holmberg
    • 1
    • 6
  1. 1.King’s College London, School of Medicine, Division of Cancer StudiesCancer Epidemiology Group, Research Oncology, Bermondsey Wing, Guy’s HospitalLondonUK
  2. 2.Department of Medicine and Department of EpidemiologyInstitute of Environmental Medicine, Karolinska InstitutetStockholmSweden
  3. 3.Department of Medicine, Clinical Epidemiological UnitKarolinska Institutet and CALAB ResearchStockholmSweden
  4. 4.Department of EpidemiologyInsitute of Environmental Medicine, Karolinska InstitutetStockholmSweden
  5. 5.AstraZeneca SverigeSödertaljeSweden
  6. 6.Regional Oncologic CentreUppsala UniversityUppsalaSweden
  7. 7.King’s College London, School of Medicine, Division of Immunology, Infection and Inflammatory Disease, Peter Gorer Department of ImmunobiologyLondonUK
  8. 8.London Research InstituteCancer ResearchLondonUK
  9. 9.Department of Medical Epidemiology and BiostatisticsKarolinska InstitutetStockholmSweden

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