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• W73768536 abstract "Acute myeloid leukemia (AML) is a clonal hematopoietic disorder that is frequently associated with genetic instability characterized by a diversity of chromosomal and molecular changes. One of the most common mutations in AML is DNA duplications in the FLT3 gene. FLT3 mutations result in downstream activation of a number of signaling pathways, of these, the STAT5 pathway appears to be most differentially regulated in FLT3-(internal tandem duplication) cells compared to FLT3-WT (wild) cells. FLT3-ITD potently activates the STAT5 pathway. STAT5 induces its target genes such as cyclin D1, c-myc and the anti-apoptotic gene p21, which are important for cell growth. These effects may indicate a role of FLT3-ITD in the aberrant cell growth of leukemia cells. The aim of the current study was to determine the frequency of FLT3 mutation and the level of STAT5 phosphorylation among acute myeloid leukemia (AML) Egyptian patients. Also, to evaluate the relation between FLT3 mutation, STAT5 phosphorylation and treatment outcome. The study was conducted on 50 newly diagnosed adult AML patients presenting to the Hematology Unit of Alexandria Main University Hospital (group I) and 30 age and sex matched healthy volunteers (group II). Group I patients were subjected to history taking, clinical examination, routine investigations, complete blood picture, bone marrow aspirate and immunophenotyping study. FLT3/ITD mutation by Polymerase chain reaction (PCR) and activation status of STAT5 by Western blotting were done to all subjects. The activation status of STAT5 was reevaluated one month from the first day of induction chemotherapy using 3 and 7 regimen. Heterozygous mutation of FLT3-ITDs was found in 50% of AML patients and absent in the control group. FLT3-ITDs was present in 60% of t(15;17) subgroup, and 54.5% of the normal cytogenetic subgroup. The highest frequency in FLT3-ITD cases was in M3 (60%). No significant difference was detected between the FLT3-ITD and FLT3-WT groups as regards response to induction chemotherapy, in responsive or non-responsive patients 50 AML cases or in normal cytogenetic cases (n=33). There was a significant difference in P-STAT5 levels between patients and control subjects. There was a significant reduction in post chemotherapyP-STAT5 levels in responders and non-responders. After induction chemotherapy, all FAB classes showed significant reductions in P-STAT5 levels except M6 class. On the other hand, M2 and M4 classes had shown highly significant reductions in P-STAT5 levels after chemotherapy. There was a significant reduction in P-STAT5 levels after chemotherapy in normal cytogenetic and favorable cytogenetic groups. ROC curve analysis showed that the sensitivity of FLT3-ITD post chemotherapy in AML patients with normal cytogenetics (n=33) increased from 68.18% to 81.82% if it is combined with P-STAT5 levels. Conclusions: FLT3-ITD is a frequent mutation in Egyptian AML patients, however it could not predict for bad response to induction chemotherapy in those patients. Its sensitivity to predict bad response to induction chemotherapy in AML patients with normal cytogenetics is increased when combined with P-STAT5.STAT5 is an important signal transducer in AML, where it is highly phosphorylated in response to a variety of mediators and not only the FLT3-ITD.P-STAT5 is decreased significantly after chemotherapy especially in the good prognostic groups and not in the bad prognostic groups, thus it might account partly for the prognosis in AML patients." @default.
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• W73768536 date "2015-01-01" @default.
• W73768536 modified "2023-09-26" @default.
• W73768536 title "FLT3 Gene Mutation and STAT5 Protein Activation in Egyptian Acute Myeloid Leukemia Patients" @default.
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