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Prostate Cancer Risk in Relation to Selected Genetic Polymorphisms in Insulin-like Growth Factor-I, Insulin-like Growth Factor Binding Protein-3, and Insulin-like Growth Factor-I Receptor

¹ Program in Epidemiology, Fred Hutchinson Cancer Research Center; and Departments of ² Epidemiology and ³ Medicine, University of Washington, Seattle, Washington

Requests for reprints: Noel S. Weiss, University of Washington, Box 357236, Seattle, WA 98195. Phone: 206-685-1788; Fax: 206-543-8525. E-mail: nweiss{at}u.washington.edu

We conducted a nested case-control study within a cohort of elderly Americans to examine the role of the insulin-like growth factor (IGF) signaling pathway in prostate cancer etiology. The distribution of genotypes of IGF-I (CA)_n, IGF binding protein-3 (IGFBP-3) A-202C, and of the 2-bp deletion and (AGG)_n polymorphisms in IGF-I receptor (IGF-IR) was compared between men with prostate cancer (n = 213) and equal number of controls matched on year of blood draw, survival until the date of diagnosis, race, and age. Among controls, the number of CA repeats in IGF-I was not correlated to any appreciable degree with plasma IGF-I concentration, whereas the IGFBP-3 CC genotype was associated with a relatively low level of plasma IGFBP-3. There was no association between prostate cancer risk and the number of CA repeats in IGF-I, IGFBP-3 genotype, or the presence of the 2-bp deletion in IGF-IR. There was a small increased risk among men who did not carry two copies of the (AGG)₇ allele of IGF-IR. These results add to the evidence that the number of IGF-I CA repeats is not associated with prostate cancer risk. Our observation that men who do not carry two copies of the IGF-IR (AGG)₇ allele are at increased risk of prostate cancer merits further investigation. (Cancer Epidemiol Biomarkers Prev 2006;15(12):2461–6)

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