Objective: STK15 is a serine threonine kinase which assists chromosomal separation and mitotic spindle stability through interaction with the centrosome during mitosis. We hypothesized that STK15 polymorphisms might modulate the risk of uterine cancer.
Methods: We used a hospital-based case-control study to assess the association between STK15 polymorphisms and risk of uterine cancer. Cases and controls were matched on age, race, and smoking status. Two common STK15 single nucleotide polymorphisms (SNPs), F31I (T/A), and V57I (G/A), were genotyped. Odds ratios (OR) and 95% confidence intervals (CI) were obtained using unconditional logistic regression analysis.
Results: A total of 193 women with uterine cancer and 218 controls were genotyped for both SNPs. After adjustment for age, race, and smoking status for the F31I SNP, the homozygous variant genotype (AA) was associated with a significantly increased uterine cancer risk (OR 10.2; 95% CI 2.23-46.5). Individuals with the heterozygous genotype (TA) and a history of tobacco use also exhibited an increased risk for uterine cancer (OR 2.63; 95% CI 1.20-5.76). For the V57I SNP, neither the homozygous (AA) nor the heterozygous (GA) variant genotypes were associated with significantly altered risk for uterine cancer (OR 0.76; 95% CI 0.18-3.25 and OR 0.88; 95% CI 0.52-1.49).
Conclusion: Our study demonstrates that STK15 F31I SNP is associated with an increased risk for uterine cancer. Confirmation of this pilot study is needed in a larger case-control population to evaluate this genetic variant with other known risk factors for uterine cancer.