Interleukin gene polymorphisms (IL1B, IL6, IL10, IL16, IL28B) increase prostate cancer risk and associate with...

Prostate cancer is one of the most frequently diagnosed cancers in men globally. Chronic inflammation is a major contributor to the development of cancer, with interleukins as key players in regulating inflammatory pathways. This study aims to explore the association between IL1, IL6, IL10, IL16, and IL28 gene polymorphisms and the risk of prostate cancer in the Iraqi population.

This case-control study included 290 histologically confirmed prostate cancer patients and 350 age-matched healthy controls recruited from Al-Diwaniyah Teaching Hospital between February 2024 and December 2024. Genotyping for IL1B-511 C>T (rs16944), IL6-174 G>C (rs1800795), IL10-1082 A>G (rs1800896), IL16-295 T > C (rs4778889), and IL28B C>T (rs12979860) polymorphisms was performed using tetra-primer amplification refractory mutation system-polymerase chain reaction (T-ARMS-PCR). Statistical analyses included odds ratios (ORs) with 95 % confidence intervals (CIs) and haplotype analysis.

Significant associations with prostate cancer risk were observed for the IL1B-511 TT genotype (OR=1.76, 95 % CI: 1.18-2.63, p = 0.006), IL6-174 GG genotype (OR=1.66, 95 % CI: 1.12-2.45, p = 0.011), IL10-1082 GG genotype (OR=1.82, 95 % CI: 1.20-2.76, p = 0.005), IL16-295 CC genotype (OR=1.88, 95 % CI: 1.27-2.79, p = 0.002), and IL28B TT genotype (OR=1.79, 95 % CI: 1.22-2.63, p = 0.003). Haplotype analysis revealed that the TGGCT haplotype was associated with a 2.35-fold increased risk of prostate cancer (OR=2.35, 95 % CI: 1.51-3.66, p < 0.001). Stratified analyses demonstrated stronger associations between these polymorphisms and aggressive disease characteristics, including higher Gleason scores, advanced tumor stages, and elevated PSA levels.

In this study, we identified proliferative inflammatory lesions of the prostate in Iraqi patients, suggesting that polymorphisms in the IL1B, IL6, IL10, IL16, and IL28B genes significantly increased prostate cancer risk and exacerbated aggressive disease features. These findings suggest the key role of these gene variants in modulating inflammatory and immune responses in the prostate carcinogenesis. Additional research is necessary to investigate these findings in other populations and examine the possibility of using them as risk assessment and personalized treatment biomarkers.