Acute myeloid leukemia (AML) is an aggressive hematologic malignancy characterized by impaired differentiation and accumulation of immature myeloid cells. Aurora kinases and their regulatory genes play key roles in mitotic progression and may contribute to leukemogenesis. This study aimed to evaluate the expression and promoter methylation status of AURKA, AURKB, and AURKC and their regulatory genes, AURKAIP1, E2F1, and E2F4 in AML. Peripheral blood samples from 83 AML patients and 28 age- and sex-matched healthy controls were analyzed using MIQE-compliant RT-qPCR for gene expression and MSRE-qPCR for promoter methylation. Diagnostic performance was assessed using receiver operating characteristic (ROC) curve analysis. Expression levels of AURKA, AURKB, AURKC, and E2F1 were significantly increased in AML patients (p < 0.001), whereas AURKAIP1 expression was significantly reduced (p = 0.001), and E2F4 showed no significant difference. Promoter methylation analysis revealed significantly increased AURKAIP1 methylation in AML (p < 0.001), decreased E2F4 methylation (p = 0.023), and no significant change in E2F1. ROC analysis demonstrated strong diagnostic performance, with AURKB showing the highest accuracy (AUC = 0.95), while a combined biomarker panel achieved an AUC of 0.96. Aurora kinase–related genes are dysregulated in AML and may serve as preliminary peripheral biomarker candidates. However, further validation in independent cohorts and more refined cellular models is required before clinical application.
Kayim et al. (Sun,) studied this question.