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Acute myeloid leukemia (show BCL11A Proteins) tumor cell lines expressing the D835Y activation loop mutation of FLT3 failed to form colonies.
Flt3 was heterogeneously expressed by almost all of the hematopoietic stem cell compartments.
SLAP2 acts as a negative regulator of FLT3 signaling and therefore, modulation of SLAP2 expression levels may provide an alternative therapeutic approach for FLT3-ITD positive acute myeloid leukemia (show BCL11A Proteins)
Data show that conditional deletion of Dnmt3a (show DNMT3A Proteins) and simultaneous "knock in" of Flt3ITD/+, cooperate to drive leukemia development at a faster rate than Dnmt3a (show DNMT3A Proteins) loss alone.
ATM (show ATM Proteins)/G6PD (show G6PD Proteins)-driven redox metabolism promotes FLT3 inhibitor resistance in acute myeloid leukemia (show BCL11A Proteins) that can be successfully reversed.
Flt3 and cooperating Flt3/Runx1 mutations cause hematopoietic stem cell depletion and myeloid progenitor expansion during adult but not fetal stages of murine development.
Tumor necrosis factor (TNF (show TNF Proteins)), a cell-extrinsic potent negative regulator of hematopoietic stem cells (HSCs), was overexpressed in bone marrow niche cells from FLT3 internal tandem duplications (FLT3 ITDs) mice.
the angiogenic factor (show VEGFA Proteins) Egfl7 (show EGFL7 Proteins) activates the Flt3/Flt3 ligand (show FLT3LG Proteins) pathway and is a key molecular driver enforcing thymus progenitor generation and thereby directly links endothelial cell biology to the production of T cell-based adaptive immunity
the Hoxa9 (show HOXA9 Proteins)- and Meis1 (show MEIS1 Proteins)-associated upregulation of Flt3 is a passive event with regard to leukemia development in mice and with limited relevance to the AML (show RUNX1 Proteins) pathology.
lineage-specific STAT5 (show STAT5A Proteins) activation in hematopoietic progenitor cells predicts the FLT3(+)-mediated leukemic phenotype in mice
the FLT3 inhibitor AC220 inhibited glutamine flux into the antioxidant factor glutathione profoundly due to defective glutamine import.
Mutation in FLT3 gene is associated with Acute Myeloid Leukemia (show BCL11A Proteins).
Acute myeloid leukemia (show BCL11A Proteins) harboring internal tandem duplication of FMS-like tyrosine kinase 3 (AML (show RUNX1 Proteins)(FLT3-ITD)) is associated with poor prognosis.
Impact of FLT3-ITD diversity on response to induction chemotherapy in patients with acute myeloid leukemia (show BCL11A Proteins) has been described.
The results of the present study showed that the overexpression of FLT3 is a potential risk factor in leukemia.
In this study, FLT3 and NPM1 (show NPM1 Proteins) mutations were evaluated in adult Iranian patients with de novo cytogenetically normal acute myeloid leukemia (show BCL11A Proteins) and its correlations with clinical and laboratory parameters were also assessed.
FLT3 and FLT3-ITD can directly bind and selectively phosphorylate p27kip1 (show CDKN1B Proteins) on tyrosine residue 88 in acute myeloid leukemia (show BCL11A Proteins). Inhibition of FLT3-ITD in cell lines strongly reduced p27 (show PAK2 Proteins) tyrosine 88 phosphorylation and resulted in increased p27 (show PAK2 Proteins) levels and cell cycle arrest
study showed that FLT3 can be targeted by FLT3-CAR T cells for the treatment FLT3(+) AML (show RUNX1 Proteins). FLT3-CAR T cells may provide a new immunotherapeutic approach for AML (show RUNX1 Proteins) patients
The high expressions of BCRP mRNA calculated with Pfaffl's rule and FLT3-ITD are independent poor risk factors in adult patients with AML (show RUNX1 Proteins) and intermediate or normal karyotype.
The new and recurrent FLT3 juxtamembrane deletion mutation shows a dominant negative effect on the wild-type FLT3 receptor.
This gene encodes a class III receptor tyrosine kinase that regulates hematopoiesis. The receptor consists of an extracellular domain composed of five immunoglobulin-like domains, one transmembrane region, and a cytoplasmic kinase domain split into two parts by a kinase-insert domain. The receptor is activated by binding of the fms-related tyrosine kinase 3 ligand to the extracellular domain, which induces homodimer formation in the plasma membrane leading to autophosphorylation of the receptor. The activated receptor kinase subsequently phosphorylates and activates multiple cytoplasmic effector molecules in pathways involved in apoptosis, proliferation, and differentiation of hematopoietic cells in bone marrow. Mutations that result in the constitutive activation of this receptor result in acute myeloid leukemia and acute lymphoblastic leukemia.
fms-related tyrosine kinase 3
, FL cytokine receptor-like
, FL cytokine receptor
, fetal liver kinase 2
, receptor-type tyrosine-protein kinase FLT3
, tyrosine-protein kinase FLT3
, tyrosine-protein kinase receptor flk-2
, CD135 antigen
, fms-like tyrosine kinase 3
, growth factor receptor tyrosine kinase type III
, stem cell tyrosine kinase 1
, FMS-like tyrosine kinase 3