Amy Moore1, Wen-Yi Huang2, Kim Danforth3, Roni Falk2, Allison Meade4, Rachel Bagni4, Sonja I Berndt2. 1. Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD, 20892, USA. amy.moore@nih.gov. 2. Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD, 20892, USA. 3. Department of Research and Evaluation, Kaiser Permanente Southern California, Pasadena, CA, USA. 4. Protein Expression Laboratory, Cancer Research and Technology Program, Frederick National Laboratory for Cancer Research, Frederick, MD, USA.
Abstract
BACKGROUND: Sexually transmitted infections and chronic inflammation have been associated with an increased risk of prostate cancer. Inflammatory mediators, such as cytokines and free radicals, have been hypothesized to play a role. METHODS: To explore the role of inflammation in prostate cancer risk further, we examined the association between pre-diagnostic serum levels of interleukin-16 (IL-16), an important pleiotropic cytokine, and prostate cancer risk among 932 Caucasian cases and 942 controls and 154 African-American cases and 302 controls in the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial. Serum IL-16 was quantified using enzyme-linked immunoassay. Logistic regression was used to estimate associations between IL-16 and prostate cancer risk, separately by race. RESULTS: Although no association between IL-16 and prostate cancer overall was observed among Caucasians (p = 0.27), a significantly increased risk of high-grade prostate cancer, defined as Gleason ≥ 7 (phet = 0.02), was observed with increasing levels of IL-16 (OR3rd vs. 1st tertile = 1.37, 95% CI 1.04-1.81, ptrend = 0.02). We also discovered a significant interaction between IL-16 and history of gonorrhea (p = 0.04). Among Caucasian men with a history of gonorrhea, elevated IL-16 levels were associated with an increased risk of prostate cancer (OR3rd vs. 1st tertile = 3.64, 95% CI 1.14-11.6) but no association was seen among those without a history of gonorrhea (OR3rd vs. 1st tertile = 1.06, 95% CI 0.83-1.34). No associations were observed among African-Americans. CONCLUSIONS: This study found evidence that higher pre-diagnostic IL-16 levels may be associated with increased risk of high-grade disease, supporting inflammation as potential mechanism by which sexually transmitted diseases may increase risk.
RCT Entities:
BACKGROUND: Sexually transmitted infections and chronic inflammation have been associated with an increased risk of prostate cancer. Inflammatory mediators, such as cytokines and free radicals, have been hypothesized to play a role. METHODS: To explore the role of inflammation in prostate cancer risk further, we examined the association between pre-diagnostic serum levels of interleukin-16 (IL-16), an important pleiotropic cytokine, and prostate cancer risk among 932 Caucasian cases and 942 controls and 154 African-American cases and 302 controls in the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial. Serum IL-16 was quantified using enzyme-linked immunoassay. Logistic regression was used to estimate associations between IL-16 and prostate cancer risk, separately by race. RESULTS: Although no association between IL-16 and prostate cancer overall was observed among Caucasians (p = 0.27), a significantly increased risk of high-grade prostate cancer, defined as Gleason ≥ 7 (phet = 0.02), was observed with increasing levels of IL-16 (OR3rd vs. 1st tertile = 1.37, 95% CI 1.04-1.81, ptrend = 0.02). We also discovered a significant interaction between IL-16 and history of gonorrhea (p = 0.04). Among Caucasian men with a history of gonorrhea, elevated IL-16 levels were associated with an increased risk of prostate cancer (OR3rd vs. 1st tertile = 3.64, 95% CI 1.14-11.6) but no association was seen among those without a history of gonorrhea (OR3rd vs. 1st tertile = 1.06, 95% CI 0.83-1.34). No associations were observed among African-Americans. CONCLUSIONS: This study found evidence that higher pre-diagnostic IL-16 levels may be associated with increased risk of high-grade disease, supporting inflammation as potential mechanism by which sexually transmitted diseases may increase risk.