title: Low levels of apolipoprotein A-I and HDL are associated with risk of prostate cancer in the Swedish AMORIS study.
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.
authors.affiliation: King's College London, School of Medicine, Division of Cancer Studies, Cancer Epidemiology Group, Research Oncology, Bermondsey Wing, Guy's Hospital, London, SE1 9RT, UK. mieke.vanhemelrijck@kcl.ac.uk
authors.forename: Mieke
authors.initials: M
authors.lastname: Van Hemelrijck
authors.forename: Göran
authors.initials: G
authors.lastname: Walldius
authors.forename: Ingmar
authors.initials: I
authors.lastname: Jungner
authors.forename: Niklas
authors.initials: N
authors.lastname: Hammar
authors.forename: Hans
authors.initials: H
authors.lastname: Garmo
authors.forename: Elisa
authors.initials: E
authors.lastname: Binda
authors.forename: Adrian
authors.initials: A
authors.lastname: Hayday
authors.forename: Mats
authors.initials: M
authors.lastname: Lambe
authors.forename: Lars
authors.initials: L
authors.lastname: Holmberg
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D016632:Apolipoprotein A-I / Q000097:blood*; D002277:Carcinoma / Q000097:blood / Q000453:epidemiology / Q000209:etiology*; D008076:Cholesterol, HDL / Q000097:blood*; D015331:Cohort Studies; D016208:Databases, Factual; D015536:Down-Regulation / Q000502:physiology; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D011471:Prostatic Neoplasms / Q000097:blood / Q000453:epidemiology / Q000209:etiology*; D012307:Risk Factors; D013548:Sweden / Q000453:epidemiology
chemical_list: D016632:Apolipoprotein A-I; D008076:Cholesterol, HDL