Prognostic impact of inhibitors of DNA binding proteins1 and inhibitors of DNA binding proteins4 genes expression on adult Egyptian patients with acute myeloid leukemia

Abstract

Background Acute myeloid leukemia (AML) pathogenesis and treatment are currently being better understood at an accelerated rate. Determining genetic and epigenetic changes that can identify patients who are at risk of poor outcomes is therefore desired to optimize treatment options. Many solid tumors have been reported to overexpress Inhibitors of DNA binding proteins (ID1), but few research has looked at the clinical significance of ID1 expression in AML. Additionally, little research has been focused on the direct role of ID4 in myeloid malignancies, as well as its expression and methylation patterns. The aim of the current study was to assess ID1 and ID4 gene expression in bone marrow (BM) aspiration specimens of 91 AML patients, compared with 14 control donors of bone marrow transplantation (BMT), using real-time polymerase chain reaction (RT-PCR). Data were correlated with patients’ clinicopathological features, response to treatment, disease-free survival (DFS), and overall survival (OS) rates. Results ID1 transcript level was significantly increased in AML bone marrow samples compared with normal controls (P = 0.002), while ID4 gene expression showed a nonsignificant difference (P = 0.717). In addition, there was a significant increase in ID1 gene expression in fms-like tyrosine kinase 3 (FLT3) mutant group than fms-like tyrosine kinase 3 wild group (P = 0.010). The total leukocytic count (TLC) was significantly higher in patients with high ID1 expression (P = 0.038) and patients with undetected ID4 expression (P = 0.025). No significant associations were detected between ID1 and ID4 expression levels and patients’ clinicopathological characteristics and OS rates. Conclusion In contrast to ID4, overexpressed ID1 can be adopted as a genetic biomarker for diagnosing AML. ID1 and ID4 expressions did not affect the patients’ OS or DFS.