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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
DOCK2 is a potential therapeutic target for novel AML (show RUNX1 Proteins) 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 (show MLXIP Proteins)-155 influences the development of FLT3-ITD-induced myeloproliferative disease. miR (show MLXIP Proteins)-155 promotes FLT3-ITD-induced myeloid expansion in the bone marrow, spleen, and peripheral blood. Mechanistically, miR (show MLXIP Proteins)-155 increases proliferation of the hematopoietic stem and progenitor cell compartments by reducing the growth-inhibitory effects of the interferon (show IFNA Proteins) response.
Overexpression of Abl (show ABL1 Proteins)-related gene tyrosine kinase (show TYRO3 Proteins) 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 (show PBX1 Proteins) axis
Data indicate that most Fms-like tyrosine kinase-3 (FLT3) tyrosine kinase (show TYRO3 Proteins) inhibitors (TKI) effectively target wild-type FLT3 signaling.
FLT3/ITD increases aerobic glycolysis through AKT (show AKT1 Proteins)-mediated upregulation of mitochondrial hexokinase (HK2 (show HK2 Proteins)). Inhibition of glycolysis preferentially causes severe ATP depletion and massive cell death in FLT3/ITD leukemia cells.
Our results indicate that CD4 (show CD4 Proteins) expression and older age are adverse prognostic factors in wild-type NPM1 (show NPM1 Proteins), FLT3-ITD-negative CN-AML (show RUNX1 Proteins).
FLT3 mutation is associated with Metaplastic Breast Cancer.
Collectively, we have developed a novel targeted therapeutic strategy, using FLT3L (show FLT3LG Proteins)-guided miR (show MLXIP Proteins)-150-based nanoparticles, to treat FLT3-overexpressing AML (show RUNX1 Proteins) with high efficacy and minimal side effects.
Y842 is critical for FLT3-mediated RAS/ERK (show EPHB2 Proteins) signaling and cellular transformation.
value of FLT3-ITD allelic ratio in AML (show RUNX1 Proteins) in risk assessment and evaluating prognosis
Gedatolisib significantly extended survival of mice in a sorafenib-resistant acute myeloid leukemia (show BCL11A Proteins) (AML (show RUNX1 Proteins)) patient-derived xenograft model. Taken together, our data suggest that aberrant activation of the PI3K (show PIK3CA Proteins)/mTOR (show FRAP1 Proteins) pathway in FLT3-ITD-dependent AML (show RUNX1 Proteins) results in resistance to drugs targeting FLT3.
HHEX (show HHEX Proteins) could replace RUNX1 (show RUNX1 Proteins) in cooperating with FLT3-ITD to induce Acute myeloid leukemia (show BCL11A Proteins) (AML (show RUNX1 Proteins)).
mutated FLT3-ITD and JAK2 (show JAK2 Proteins) augment reactive oxygen species production and homologous recombination, shifting the cellular milieu toward illegitimate recombination.
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