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Association between Genetic Polymorphisms of Macrophage Scavenger Receptor 1 Gene and Risk of Prostate Cancer in the Health Professionals Follow-up Study

¹ Channing Laboratory, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School; Departments of ² Nutrition and ³ Epidemiology and ⁴ Program in Molecular and Genetic Epidemiology, Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts; and ⁵ Research Center for Genes, Environment, and Human Health, and Graduate Institute of Epidemiology, College of Public Health, National Taiwan University, Taipei, Taiwan, Republic of China

Requests for reprints: Yen-Ching Chen, Channing Laboratory, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, 181 Longwood Avenue, Boston, MA 02115. Phone: 617-525-2279; Fax: 617-525-2008. E-mail: karen.chen{at}channing.harvard.edu

Background: Macrophage scavenger receptor 1 (MSR1) is involved in chronic inflammation, which is a risk factor for prostate cancer. Association studies assessing the relationship between sequence variants of MSR1 and prostate cancer are inconsistent. We hypothesized that sequence variants of MSR1 were associated with prostate cancer risk.

Methods: In a nested case-control design within the Health Professionals Follow-up Study, we identified 700 participants with prostate cancer diagnosed after they had provided a blood specimen in 1993 and before January 2000. Controls were 700 age-matched men without prostate cancer who had had a prostate-specific antigen test after providing a blood specimen. We genotyped three common (>5%) single nucleotide polymorphisms (SNP) that have been reported previously to be associated with risk of prostate cancer.

Results: None of these MSR1 SNPs nor estimated haplotypes were associated with prostate cancer risk (P for the global test for haplotypes = 0.89). These MSR1 SNPs also did not appear to be associated with higher-grade or advanced-stage prostate cancer.

Conclusion: The association between these sequence variants of MSR1 and the risk of prostate cancer was null. Further study of aggressive prostate cancer may be warranted, as we had limited power to assess these. (Cancer Epidemiol Biomarkers Prev 2008;17(4):1001–3)