Document Type : Original articles
Authors
1 Department of Pathology, College of Medicine, University of Mosul, Mosul, Iraq.
2 Department of Internal Medicine, College of Medicine, University of Mosul, Mosul, Iraq.
Abstract
Background: The FMS-like tyrosine kinase 3 mutation is one of the most prevalent recurrent genetic aberrations in acute myeloid leukemia (AML). Two modules of mutation are subsumed under the term FLT3 mutation, including internal tandem duplication (ITD) within the juxtamembrane domain and point mutations in the tyrosine kinase domain (TKD).
Objectives: To determine the frequency of FLT3 mutations in adults with newly diagnosed AML and to find any correlation between the existence of FLT3 mutations and the clinical or laboratory findings of the disease.
Materials and methods: Fifty newly diagnosed AML patients were investigated prospectively in this study. A complete blood count, peripheral blood film, bone marrow aspirate, and flow cytometry study were conducted for each patient. The detection of FLT3 mutations was performed using next-generation sequencing technology.
Results: Out of 50 AML patients, FLT3 mutations were detected in 12 (24%). 8 (16%) of them expressed FLT3-ITD, whereas FLT3-TKD was expressed in 4 (8%). There was a non-significant rise in the medians of the total leucocyte count and the peripheral blood blast percentage in both FLT3-ITD and FLT3-TKD mutated patients compared to those without mutation (P-value = 0.15, 0.28, 0.74, and 0.66, respectively). Most cases of both FLT3-ITD and FLT3-TKD mutations were female (65.8% and 75%, respectively). The majority of FLT3-ITD mutations were found in the FAB classification M5 subtype (37.5%), followed by the M1 subtype (25%). FLT3-TKD mutations were mostly detected in the M3 subtype (50%), followed by M4 and M5 (25%).
Conclusion: The FLT3 mutations were frequently seen in patients with AML disease. They were associated with a higher white blood cell count and peripheral blood blast percentage; therefore, they are considered a predictive and prognostic marker in AML disease.
Keywords
Main Subjects
)