Insulin-Like Growth Factor 1 and Prostate Cancer Risk: A Population-Based, Case-Control Study

Abstract

Background. Recent epidemiologic investigations have suggested an association between increased blood levels of insulin-like growth factor 1 (IGF-1) and increased risk of prostate cancer Our goal was to determine whether an association exists between serum levels of IGF-1 and one of its binding proteins, insulin-like growth factorbinding protein 3 (IGFBP-3), and prostate cancer risk. Methods: An immunoradiometric assay was used to quantify IGF-1 levels and IGFBP-3 levels in serum samples as part of a populationbased, case-control study in Sweden. The study population comprised 210 patients with newly diagnosed, untreated prostate cancer and 224 frequency-matched control subjects. Data were analyzed by use of unconditional logistic regression to calculate odds ratios (ORs) and 95% confidence intervals (CIs). Reported P values are twosided. Results: The mean serum IGF-1 level for case patients (158.4 ng/mL) was significantly higher than that for control subjects (147.4 ng/mL) (P =.02); corresponding mean serum IGFBP-3 levels were not significantly different between case patients (2668 ng/mL) and control subjects (2518 ng/ mL) (P =.09). We found a moderately strong and statistically significant (P = .04) positive association between serum levels of IGF-1 levels and risk of prostate cancer (OR = 1.51; 95% CI = 1.0-2.26 per 100 ng/mL increment); the association was particularly strong for men younger than 70 years of age (OR = 2.93; 95% CI = 1.43–5.97). No association was found between serum IGF-1 levels and disease stage. Serum IGFBP-3 levels were not significantly associated with increased risk of disease, and adjustment for IGFBP-3 had little effect on the association between IGF-1 levels and risk of prostate cancer. Conclusion Elevated serum IGF-1 levels may be an important predictor of risk for prostate cancer. However, our results do not support an important role for serum IGFBP-3 as a predictor of risk for this disease. [J Nall Cancer Inst 1998;90:911-5]