Association of selected ELAC2, MSR1, RNASEL and KLK3 polymorphisms with prostate cancer susceptibility in a Hungarian cohort

Abstract

Background Prostate cancer (PCa) remains a leading malignancy among men worldwide, with inherited genetic susceptibility playing a pivotal role in its pathogenesis. Although numerous single nucleotide polymorphisms (SNPs) within immune response, inflammatory, and apoptotic pathways have been linked to PCa risk, these associations often exhibit substantial inconsistency across diverse populations. This study aimed to evaluate the association of selected polymorphisms within the RNASEL, ELAC2, MSR1, and KLK3 genes with PCa susceptibility in a Hungarian cohort. Methods This case-control study included 103 histologically confirmed prostate cancer patients and 103 healthy controls recruited at the University of Pécs Department of Urology. Genotyping of selected polymorphisms was performed by PCR and Sanger sequencing at the Department of Medical Genetics. Statistical associations were evaluated using chi-square tests, odds ratios, and logistic regression. Results A statistically nominally significant association with prostate cancer susceptibility was observed for the RNASEL rs486907 polymorphism, demonstrating a potential protective effect under the dominant model in the studied population (OR = 0.53, 95% CI: 0.30–0.92, p = 0.025). In the age-adjusted logistic regression analysis, this association remained statistically significant (OR = 0.56, 95% CI: 0.32–0.99, p = 0.046), suggesting that the observed effect was independent of age. In contrast, no statistically significant associations were identified between prostate cancer risk and the investigated polymorphisms in the KLK3, MSR1, or ELAC2 genes. Conclusion The present study demonstrated a significant association between the RNASEL rs486907 polymorphism and prostate cancer susceptibility in a Hungarian cohort, suggesting a potential protective effect of this variant. These findings support the possible role of inherited genetic factors in prostate cancer development and highlight the importance of population-specific genetic association studies. Further investigations involving larger cohorts are warranted to validate these observations.