Abstract Background Acute myeloid leukemia represents the highest percentage of all adult acute variants. Runt-related transcription factor1 ( RUNX1 ), a factor with known tumor suppressor function, was recently reported as promoter in (AML). We investigated role gene expression level Egyptian AML patients and delineated its clinical significance. Results measured using reverse transcription-qu...

Nucleophosmin (NPM1) exon-12 gene mutations are the hallmark of a large acute myelogenous leukemia (AML) subgroup with normal karyotype, but their prognostic value in this AML subset has not yet been determined. We screened 401 AML patients with normal karyotype treated within the German AML Cooperative Group Protocol 99 (AMLCG99) study for NPM1 mutations. Results were related with partial tand...

Mutations of Fms-like tyrosine kinase 3 (FLT3) are among the most frequently detected molecular abnormalities in AML patients. Internal tandem duplications (ITDs) are found in approximately 25% and point mutations within the second tyrosine kinase domain (TKD) in approximately 7% of AML patients. Patients carrying the FLT3-ITD but not the FLT3-TKD mutation have a significantly worse prognosis. ...

Correspondence To the Editor: Sorafenib is a novel, orally available inhibitor of multiple kinases. It has been used in relapsed and refractory FMS‑like tyrosine kinase (FLT)‑3‑positive acute myeloid leukemia (AML) in recent years with favorable outcomes. Thyroiditis and hypothyroidism as side effects have been reported in treatment on renal cell cancer. [1] Here, we report a case of FLT3‑inter...

Fms-like tyrosine kinase 3 ligand (Flt3L) is known as the primary differentiation and survival factor for dendritic cells (DCs). Furthermore, Flt3L is involved in the homeostatic feedback loop between DCs and regulatory T cell (Treg). We have previously shown that Flt3L accumulates in the synovial fluid in rheumatoid arthritis (RA) and that local exposure to Flt3L aggravates arthritis in mice, ...

Fms-like tyrosine kinase 3 ligand (FLT3L) plays a major role in dendritic cell (DC) biology. Deficiency of FLT3L causes a dramatic decrease in DC numbers, whereas increasing its availability (by repetitive injections for 7-10 days) leads to a 10-fold increase in DC numbers. In this study, we show that FLT3L treatment indirectly leads to an expansion of peripheral naturally occurring T regulator...