Background: The development and progression of prostate cancer may be influenced by systemic inflammation. Environmental influences, such as dietary factors and genetic polymorphisms mediate chronic inflammation. Particularly, high fructose corn syrup, which is associated with elevation of uric acid and metabolic syndrome, and single nucleotide polymorphisms in immune response and inflammatory pathways may promote prostate cancer by promoting systemic inflammation.
Methods: The current analysis utilized a hospital-based case-control study of 241 prostate cancer patients and 155 controls recruited from 1994 to 1997 at the Memorial Sloan Kettering Cancer Center. Using genotyping results of CRP rs1205 and 1800947, FGFR2 rs1219648 and rs2981582, and IFNGR1 rs11914, the associations of high fructose corn syrup and inflammation-related polymorphisms with prostate cancer susceptibility and overall survival were analyzed. Adjusted odds ratios and 95% confidence intervals were calculated using unconditional logistic regression models. The Cox proportional hazards model was used to generate estimates of survival among prostate cancer patients.
Results: No polymorphisms were found associated with prostate cancer susceptibility. However, the CRP rs1205 CT genotype was associated with poorer prognosis among prostate cancer patients with a primary diagnosis (HR: 2.99; 95% CI: 1.06-8.44). FGFR2 rs1219648 and rs2981582 polymorphisms were associated with more favorable survival (HR: 0.07; 95% CI: 0.01-0.43 and HR: 0.04, 95%CI:0.01-0.28), with the latter more pronounced in nonsmokers. High fructose corn syrup was not associated with prostate cancer susceptibility, but correlated with reduced survival among smokers when considering all patients with a prostate cancer diagnosis (HR: 2.31, 95% CI:1.12 - 4.76). No interaction was observed between high fructose intake and inflammation-related SNPs.
Conclusion: The results of this study highlight potential inflammation-related polymorphisms associated with poorer prognosis of prostate cancer, and provide a basis for which to confirm and identify inflammation-related polymorphisms in larger studies of prostate cancer risk and progression.