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The demonstrated that an E2-2high fraction among common DC progenitors, which are a major source of pDCs and cDCs in the steady state, strictly gave rise to pDCs in the presence of Flt3 (Fms-like tyrosine kinase receptor-3) ligand ex vivo or in the secondary lymphoid organs when transferred in vivo.
Acute myeloid leukemia 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
Data show that conditional deletion of Dnmt3a and simultaneous "knock in" of Flt3ITD/+, cooperate to drive leukemia development at a faster rate than Dnmt3a loss alone.
ATM/G6PD-driven redox metabolism promotes FLT3 inhibitor resistance in acute myeloid leukemia 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), 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 Egfl7 activates the Flt3/Flt3 ligand 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- and Meis1-associated upregulation of Flt3 is a passive event with regard to leukemia development in mice and with limited relevance to the AML pathology.
lineage-specific STAT5 activation in hematopoietic progenitor cells predicts the FLT3(+)-mediated leukemic phenotype in mice
DOCK2 is a potential therapeutic target for novel AML treatments, as this protein regulates the survival of leukemia cells with elevated FLT3 activity and sensitizes FLT3/ITD leukemic cells to conventional antileukemic agents.
Used a genetic model to determine whether miR-155 influences the development of FLT3-ITD-induced myeloproliferative disease. miR-155 promotes FLT3-ITD-induced myeloid expansion in the bone marrow, spleen, and peripheral blood. Mechanistically, miR-155 increases proliferation of the hematopoietic stem and progenitor cell compartments by reducing the growth-inhibitory effects of the interferon response.
Overexpression of Abl-related gene tyrosine kinase ABL2 in pro-B cell line Ba/F3 cells expressing an oncogenic mutant of FLT3 (FLT3-ITD) resulted in partial inhibition of FLT3-ITD-dependent cell proliferation.
Sorafenib-resistant leukemia cells with a FLT3/ITD mutation are sensitive to glycolytic inhibitors.
FLT3-ITD is capable of inhibiting FLT3-ITD+ cell proliferation through the p21/Pbx1 axis
Data indicate that most Fms-like tyrosine kinase-3 (FLT3) tyrosine kinase inhibitors (TKI) effectively target wild-type FLT3 signaling.
DNMT3A haploinsufficiency results in reversible epigenetic alterations that transform FLT3(ITD)-mutant myeloproliferative neoplasm into AML.
murine Fms-like tyrosine kinase 3 (Flt3) ligand was used to generate conventional dendritic cells (FL-cDCs) and plasmacytoid DCs (FL-pDCs) and further evaluated their immunological responses to bacillus Calmette-Guerin (BCG) infection in vitro.
increased number of osteoclasts in Flt3L(-/-) mice may be a consequence of insufficient expression of interferon regulatory factor 8
Authors have shown that the stability of ETV6/FLT3 is regulated by the Hsp90 chaperone. ETV6/FLT3 fusion protein forms a complex with Hsp90 by coimmunoprecipitation analyses using an Hsp90 antibody.
Multivariate Cox's proportional hazards regression analyses revealed that OCT4 mRNA high expression was an independent predictive factor for shorter EFS and OS in AML patients. Conclusion OCT4 correlates with presence of CK, FLT3-ITD mutation and poorer risk stratification, and it could be served as a convincing biomarker for predicting unfavourable prognosis in AML patients.
Results indicate that DNMT3A mutations alone do not affect the clinical outcomes of AML patients undergoing allogeneic HSCT, but when accompanied by FLT3-ITD mutations, the OS was significantly reduced (5-year OS 0% for DNMT3A R882mut/FLT3-ITDpos patients vs. 62% DNMT3A R882wt/FLT3-ITDneg, p=0.025) and the relapse rate increased.
RIPK3-dependent cell death and inflammasome activation in FLT3-internal-tandem-duplication-expressing leukemia-initiating cells
The results suggested that FLT3 ITD mutations could become an indicator of poor prognosis of APL, and these patients should receive more intensive therapy according to current guidelines.
Low FLT3 expression is associated with Pancreatic ductal adenocarcinoma.
DNMT3A R882 mutation plays an important role in CN-AML patients' prognosis and clinical outcomes in the presence and absence of NPM1 and FLT3 mutations.
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.
Acute myeloid leukemia harboring internal tandem duplication of FMS-like tyrosine kinase 3 (AML(FLT3-ITD)) is associated with poor prognosis.
Impact of FLT3-ITD diversity on response to induction chemotherapy in patients with acute myeloid leukemia 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 mutations were evaluated in adult Iranian patients with de novo cytogenetically normal acute myeloid leukemia and its correlations with clinical and laboratory parameters were also assessed.
FLT3 and FLT3-ITD can directly bind and selectively phosphorylate p27kip1 on tyrosine residue 88 in acute myeloid leukemia. Inhibition of FLT3-ITD in cell lines strongly reduced p27 tyrosine 88 phosphorylation and resulted in increased p27 levels and cell cycle arrest
study showed that FLT3 can be targeted by FLT3-CAR T cells for the treatment FLT3(+) AML. FLT3-CAR T cells may provide a new immunotherapeutic approach for AML patients
In the Title.
The high expressions of BCRP mRNA calculated with Pfaffl's rule and FLT3-ITD are independent poor risk factors in adult patients with AML 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