GENETIC ASSOCIATION OF IL-17A GENE POLYMORPHISM (rs2275913) WITH SUSCEPTIBILITY TO ORAL CANCER - A CASE CONTROL STUDY IN SOUTH INDIAN POPULATION

Abstract

Background Interleukin-17A (IL-17A), encoded by the IL-17A gene on chromosome 6p12, is a pro-inflammatory cytokine that plays a crucial role in immune regulation, inflammation, and carcinogenesis. The rs2275913 (G>A) polymorphism in the promoter region of the IL-17A gene has been implicated in susceptibility to various inflammatory and malignant conditions, including oral cancer. Oral squamous cell carcinoma represents one of the most common malignancies worldwide, and genetic predisposition may contribute to its development. Aim To determine the genotype and allele frequencies of IL-17A gene polymorphism (rs2275913) and to evaluate its association with susceptibility to oral cancer in a South Indian population. Materials and Methods A case-control study was conducted including 50 participants (25 oral cancer cases and 25 healthy controls). Genomic DNA was extracted from peripheral blood samples and genotyping was performed using PCR-RFLP analysis. The amplified product size was 102 bp, with digestion patterns identifying AA (102 bp), AG (68 + 34 bp), and GG (102 + 68 + 34 bp) genotypes. Statistical analysis was carried out using the Chi-square test, and Hardy–Weinberg equilibrium (HWE) was assessed. Results Among cases, the genotype distribution was AA (28%), AG (24%), and GG (48%), while in controls it was AA (24%), AG (20%), and GG (56%). The allele frequencies in cases were A (0.40) and G (0.60), and in controls were A (0.44) and G (0.56). No statistically significant association was observed between IL-17A rs2275913 polymorphism and oral cancer susceptibility (p > 0.05). Allele frequencies were comparable to those reported in the South Indian population. Conclusion The present study found no significant association between IL-17A rs2275913 polymorphism and oral cancer risk in the studied South Indian population. Although genotype distributions were assessed with respect to HWE, larger sample sizes are required to draw definitive conclusions regarding the role of this polymorphism in oral carcinogenesis.