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Acute myeloid leukemia (显示 BCL11A 蛋白) 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 (显示 BCL11A 蛋白)
Data show that conditional deletion of Dnmt3a (显示 DNMT3A 蛋白) and simultaneous "knock in" of Flt3ITD/+, cooperate to drive leukemia development at a faster rate than Dnmt3a (显示 DNMT3A 蛋白) loss alone.
ATM (显示 ATM 蛋白)/G6PD (显示 G6PD 蛋白)-driven redox metabolism promotes FLT3 inhibitor resistance in acute myeloid leukemia (显示 BCL11A 蛋白) 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 (显示 TNF 蛋白)), 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 (显示 VEGFA 蛋白) Egfl7 (显示 EGFL7 蛋白) activates the Flt3/Flt3 ligand (显示 FLT3LG 蛋白) 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 (显示 HOXA9 蛋白)- and Meis1 (显示 MEIS1 蛋白)-associated upregulation of Flt3 is a passive event with regard to leukemia development in mice and with limited relevance to the AML (显示 RUNX1 蛋白) pathology.
lineage-specific STAT5 (显示 STAT5A 蛋白) activation in hematopoietic progenitor cells predicts the FLT3(+)-mediated leukemic phenotype in mice
Multivariate Cox's proportional hazards regression analyses revealed that OCT4 (显示 POU5F1 蛋白) mRNA high expression was an independent predictive factor for shorter EFS (显示 EFS 蛋白) and OS in AML (显示 RUNX1 蛋白) patients. Conclusion OCT4 (显示 POU5F1 蛋白) 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 (显示 RUNX1 蛋白) patients.
Results indicate that DNMT3A (显示 DNMT3A 蛋白) mutations alone do not affect the clinical outcomes of AML (显示 RUNX1 蛋白) patients undergoing allogeneic HSCT, but when accompanied by FLT3-ITD mutations, the OS was significantly reduced (5-year OS 0% for DNMT3A (显示 DNMT3A 蛋白) R882mut/FLT3-ITDpos patients vs. 62% DNMT3A (显示 DNMT3A 蛋白) R882wt/FLT3-ITDneg, p=0.025) and the relapse rate increased.
RIPK3 (显示 RIPK3 蛋白)-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 (显示 FASL 蛋白), and these patients should receive more intensive therapy according to current guidelines.
Low FLT3 expression is associated with Pancreatic ductal adenocarcinoma.
DNMT3A (显示 DNMT3A 蛋白) R882 mutation plays an important role in CN-AML (显示 RUNX1 蛋白) patients' prognosis and clinical outcomes in the presence and absence of NPM1 (显示 NPM1 蛋白) 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 (显示 BCL11A 蛋白).
Acute myeloid leukemia (显示 BCL11A 蛋白) harboring internal tandem duplication of FMS-like tyrosine kinase 3 (AML (显示 RUNX1 蛋白)(FLT3-ITD)) is associated with poor prognosis.
Impact of FLT3-ITD diversity on response to induction chemotherapy in patients with acute myeloid leukemia (显示 BCL11A 蛋白) has been described.
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