Correlation of FLT3 Gene Mutations and mRNA Expression with FLT3 Receptor Protein (CD135) Expression in Acute Myeloid Leukemia

Abstract

SUMMARY A cute myeloid leukemia (AML) is a malignant disorder of the haematopoeitic system characterized by marked genetic heterogeneity. Multiple molecular aberrations are thought to contribute to the process of leukemic transformation. Alterations of the FLT3 have been shown to play a significant role in AML pathogenesis. FLT3 is a receptor tyrosine kinase expressed mainly on myeloid and lymphoid progenitor cells in the BM. Interaction of FLT3 receptor with its ligand results in receptor phosphorylation and mediates several downstream effects resulting in cellular proliferation and inhibition of apoptosis. The aim of the current study was to evaluate FLT3 gene mutations (ITD and TKD) and mRNA expression in de novo AML patients and correlate them with surface FLT3 receptor protein (CD135) expression. The present study was conducted on 40 de novo AML patients and 10 age and sex-matched controls with non-malignant haematological disorders. The overall incidence of FLT3 ITD mutation detected at diagnosis of our studied AML patients was 22.5%, while none of the studied patients carried the FLT3 TKD mutation. FLT3 mRNA and FLT3 receptor protein were detected in all the studied AML patients with the expression levels of both mRNA and protein being higher in AML patients as compared to