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(28-03-12) Modulation of the association between plasma intercellular adhesion molecule-1 and cancer risk by n−3 PUFA intake



Modulation of the association between plasma intercellular adhesion molecule-1 and cancer risk by n−3 PUFA intake: a nested case-control study 1,2,3

1. Mathilde Touvier,
2. Emmanuelle Kesse-Guyot,
3. Valentina A Andreeva,
4. L?opold Fezeu,
5. Nathalie Charnaux,
6. Angela Sutton,
7. Nathalie Druesne-Pecollo,
8. Serge Hercberg,
9. Pilar Galan,
10. Laurent Zelek,
11. Paule Latino-Martel, and
12. S?bastien Czernichow
+Author Affiliations
1. 1From INSERM U557, National Institute of Health and Medical Research, Inra, Cnam, Paris 13 University (UREN), Bobigny, France (MT, EK-G, VAA, LF, ND-P, SH, PG, LZ, and PL-M); Jean Verdier Hospital, Biochemistry Department, Bondy, France (NC and AS); INSERM U698, Paris 13 University, Bobigny, France (NC, AS); the Public Health Department, Avicenne Hospital, Paris 13 University, Bobigny, France (SH); and the Department of Nutrition, Ambroise Par? Hospital, INSERM U1018?Centre for Research in Epidemiology and Population Health, University Versailles St-Quentin, Boulogne-Billancourt, France (SC).
+Author Notes
? ↵2 Supported by a grant from the French National Cancer Institute (Institut National du Cancer, INCa, 2007-1-SPC-3).
? ↵3 Address correspondence to M Touvier, INSERM U557, UREN, SMBH Paris 13, 74 rue Marcel Cachin, F-93017, Bobigny, France. E-mail: [email protected].
Abstract
Background: Mechanistic data suggest that n−3 PUFAs and endothelial function may interact and play a role in carcinogenesis, but epidemiologic evidence is lacking.
Objective: Our objective was to investigate whether the prospective association between soluble intercellular adhesion molecule-1 (sICAM-1) and cancer risk is modulated by n−3 PUFA intake.
Design: A nested case-control study was designed to include all first-incident cancer cases diagnosed in the SUppl?mentation en VItamines et Min?raux AntioXydants cohort between 1994 and 2007, with available dietary data from 24-h records (n = 408). Cases were matched with 1 or 2 randomly selected controls (n = 760). Conditional logistic regression was used to estimate ORs and 95% CIs for the association between prediagnostic plasma concentrations of sICAM-1 and cancer risk, stratified by n−3 PUFA intake. The interactions between sICAM-1 and n−3 PUFA intake were tested.
Results: An interaction was observed between sICAM-1 and n−3 PUFA intake, which was consistent across the studied cancer locations (P-interaction = 0.036 for overall, 0.038 for breast, and 0.020 for prostate cancer risk). sICAM-1 concentrations were positively associated with cancer risk among subjects with n−3 PUFA intakes below the median (multivariate ORTertile3vsTertile1: 2.8; 95% CI: 1.5, 5.2; P-trend = 0.001), whereas this association was not observed for subjects with n−3 PUFA intakes above the median (ORTertile3vsTertile1: 1.3; 95% CI: 0.8, 2.3; P-trend = 0.3).
Conclusion: These findings suggest that n−3 PUFA intake may counteract the procarcinogenic actions of sICAM-1. This trial was registered at clinicaltrials.gov asNCT00272428.

Source: Am J Clin Nutr April 2012 vol. 95 no. 4 944-950

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