IL-16 polymorphism and risk of renal cell carcinoma: Association in a Chinese population

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Abstract

Objectives: Interleukin-16 (IL-16) plays a fundamental role in inflammatory diseases, as well as in the development and progression of tumors. A T-to-C polymorphism at the -295 position in the promoter region of the IL-16 gene has been described. This variation might lead to altered IL-16 expression, and might modulate an individual's susceptibility to cancer. The objective of the present study was to determine if IL-16 polymorphism is associated with risk of renal cell carcinoma (RCC). Methods: A case-control study including 335 RCC cases and 340 cancer-free controls was carried out. All subjects were genetically unrelated ethnic Han Chinese recruited from a single institution between July 2006 and July 2009. The IL-16 -295 T>C polymorphism was determined by using the polymerase chain reaction-restriction fragment length polymorphism method. Serum samples were available for 70 RCC cases and 96 controls to detect IL-16 concentration. Results: Compared with the IL-16 -295 TT genotype, the CC genotype had a significantly decreased RCC risk (adjusted odds ratio [OR] = 0.34, 95% confidence interval [CI] = 0.18-0.66). Furthermore, a significant decreased risk of RCC was found in the combined variant genotypes CT + CC compared with the TT genotype (adjusted OR = 0.68, 95% CI = 0.50-0.93). In addition, the serum IL-16 levels in RCC patients were significantly lower than those in controls (P < 0.001). Furthermore, patients carrying CC genotype or CT genotype had higher serum IL-16 levels than TT carriers. Conclusion: IL-16 -295 T>C polymorphism is significantly associated with a higher risk of developing RCC in Chinese population. © 2010 The Japanese Urological Association.

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Zhu, J., Qin, C., Yan, F., Wang, M., Ding, Q., Zhang, Z., & Yin, C. (2010). IL-16 polymorphism and risk of renal cell carcinoma: Association in a Chinese population. International Journal of Urology, 17(8), 700–707. https://doi.org/10.1111/j.1442-2042.2010.02559.x

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