الفهرس 
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Abstract
A
cute Myeloid Leukemia (AML) is a life-threatening hematopoietic stem cell tumor characterized by bone marrow infiltration by leukemic cells that replace and suppress normal hematopoiesis, resulting in organ infiltration, fatal infections and/or bleeding.
The etiology of AML is both heterogeneous and complex, but it is widely accepted that environmental, along with genetic factors, are significantly involved in the development of AML. AML transformation is a multistep process that is believed to be triggered by more than one genetic hit
It has been reported that the frequency of Th-17 cells (memory CD4 positive T cells), as well as the plasma levels of IL-17 and its related cytokines, differ significantly between normal cells and leukemic cells; both were significantly higher in AML patients when compared to healthy controls, indicating that Th-17 cells may play a role in the pathophysiological process of AML.
Interleukin-17F is a member of the pro-inflammatory cytokine family secreted by Th-17 cell and polymorphic features located within its gene are accused to be associated with AML susceptibility.
Previous studies have investigated the role of IL-17F gene polymorphism in susceptibility to AML, however the results remained controversial. This prompted us to study the relation between IL-17F gene polymorphism and susceptibility to AML. Furthermore, to evaluate IL-17 plasma levels in AML patients with different IL-17F genotypes.
This study was conducted on 40 newly diagnosed AML patients according to the WHO classification and were recruited from Ain Shams University Hospitals ASUH. The diagnosis of AML was based on standard morphology, cytochemical evaluation, immunophenotyping (flow cytometry) and confirmatory cytogenetic studies according to updated WHO (2016) diagnostic criteria. In addition, 20 age and sex matched adult subjects were incorporated as a control group.
Focusing on the association between IL-17F gene polymorphism and susceptibility to AML, the present study showed no statistically significant difference between cases and control subjects as regards IL-17F genotype distribution, denoting that IL-17F gene polymorphism doesn’t increase susceptibility to AML in this study. However, IL-17 plasma level was significantly higher in the cases group than the control group with a cutoff point >35 pg/mL.
The mutant G allele which was detected in 4 patients who exhibited (AG) genotype, showed significant association with lower TLC values, higher platelet count & higher bone marrow blast cell percentage.
In this study, we also evaluated the association between IL-17F gene polymorphism & the expression of different CD markers. There was a significant association between IL-17F gene polymorphism & the frequency of expression of CD33, CD64 & MPOX; they are all less expressed in the AG heterozygous genotype group than in the AA homozygous group respectively.
In the context of the relationship between the IL-17F gene polymorphism and the level of IL-17 plasma protein, we observed no discernible variations in IL-17 plasma levels across AML patients with various genotypes.
Additionally, we demonstrated a statistically significant positive association between the number of blast cells in the bone marrow and peripheral blood and the IL-17F plasma level.
To conclude, in this study IL-17F gene polymorphism was not proven to be a risk factor for AML, while IL-17 plasma level showed significantly higher level among AML patients.
RECOMMENDATIONS
• A more extended study, including patients from other centers, is recommended to confirm/exclude the liability of subjects with IL-17F gene polymorphism to AML.
• More investigation is encouraged to determine IL-17 protein function as a therapeutic and prognostic marker.
• It is recommended to investigate the effects of IL-17F gene polymorphism on the prognosis and survival of AML patients, putting into consideration other factors affecting prognosis e.g. genetic factors.