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Chemosensitization of acute myeloid leukemia (AML) following mobilization by the CXCR4 antagonist AMD3100
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AC220 is a uniquely potent and selective inhibitor of FLT3 for the treatment of acute myeloid leukemia (AML)
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RUNX1 and its fusion oncoprotein derivative, RUNX1-ETO, induce senescence-like growth arrest independently of replicative stress
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Internal tandem duplication of FLT3 (FLT3/ITD) induces increased ROS production, DNA damage, and misrepair: implications for poor prognosis in AML
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Incorporating FLT3 inhibitors into acute myeloid leukemia treatment regimens
Keith Pratz et al.
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H-A Hou et al.
LEUKEMIA (2008)
CXCR4 antagonists mobilize childhood acute lymphoblastic leukemia cells into the peripheral blood and inhibit engraftment
J. Juarez et al.
LEUKEMIA (2007)
Prolonged exposure to FLT3 inhibitors leads to resistance via activation of parallel signaling pathways
Obdulio Piloto et al.
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FLT3 inhibition in acute myeloid leukaemia
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Synergistic effect of arsenic trioxide and Flt3 inhibition on cells with Flt3 internal tandem duplication
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Inverse correlation between Flt3 and PU.1 expression in acute myeloblastic leukemias
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Prevalence and prognostic impact of NPM1 mutations in 1485 adult patients with acute myeloid leukemia (AML)
Christian Thiede et al.
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Block of C/EBPα function by phosphorylation in acute myeloid leukemia with FLT3 activating mutations
HS Radomska et al.
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Inhibition of the MEK/MAPK signal transduction pathway strongly impairs the growth of Flt3-ITD cells
S Takahashi
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Clinical resistance to the kinase inhibitor PKC412 in acute myeloid leukemia by mutation of Asn-676 in the FLT3 tyrosine kinase domain
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Genetics of myeloid malignancies:: Pathogenetic and clinical implications
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Human leukemias with mutated FLT3 kinase are synergistically sensitive to FLT3 and Hsp90 inhibitors: the key role of the STAT5 signal transduction pathway
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AML1B transcriptional repressor function is impaired by the Flt3-internal tandem duplication
S Takahashi et al.
BRITISH JOURNAL OF HAEMATOLOGY (2005)
FLT3 tyrosine kinase inhibitors
M Levis et al.
INTERNATIONAL JOURNAL OF HEMATOLOGY (2005)
Runx1/UAML1 in normal and abnormal hematopoiesis
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INTERNATIONAL JOURNAL OF HEMATOLOGY (2005)
AML-associated Flt3 kinase domain mutations show signal transduction differences compared with Flt3 ITD mutations
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FLT3-ITD and tyrosine kinase domain mutants induce 2 distinct phenotypes in a murine bone marrow transplantation model
R Grundler et al.
BLOOD (2005)
FLT-3: a new focus in the understanding of acute leukemia
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Identification of Ki23819, a highly potent inhibitor of kinase activity of mutant FLT3 receptor tyrosine kinase
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FIG ligand and the Flt3 receptor regulate hematopoietic cell migration by modulating the SDF-1α(CXCL12)/CXCR4 axis
S Fukuda et al.
BLOOD (2005)
CHIR-258, a novel, multitargeted tyrosine kinase inhibitor for the potential treatment of t(4;14) multiple myeloma
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Arsenic trioxide: New clinical experience with an old medication in hematologic malignancies
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After chronic myelogenous leukemia: tyrosine kinase inhibitors in other hematofogic malignancies
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Patients with acute myeloid leukemia and an activating mutation in FLT3 respond to a small-molecule FLT3 tyrosine kinase inhibitor, PKC412
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A phase 1 study of SU11248 in the treatment of patients with refractory or resistant acute myeloid leukemia (AML) or not amenable to conventional therapy for the disease
W Fiedler et al.
BLOOD (2005)
Cytoplasmic nucleophosmin in acute myelogenous leukemia with a normal karyotype.
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NEW ENGLAND JOURNAL OF MEDICINE (2005)
FLT3 receptors with internal tandem duplications promote cell viability and proliferation by signaling through Foxo proteins
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ONCOGENE (2004)
CXCR4 regulates migration and development of human acute myelogenous leukemia stem cells in transplanted NOD/SCID mice
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Flt3 mutation activates p21WAF1/CIP1 gene expression through the action of STAT5
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BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS (2004)
Internal tandem duplication mutation of FLT3 blocks myeloid differentiation through suppression of C/EBPα expression
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BLOOD (2004)
Biologic and clinical significance of the FLT3 transcript level in acute myeloid leukemia
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BLOOD (2004)
FLT3 mutations in the activation loop of tyrosine kinase domain are frequently found in infant ALL with MLL rearrangements and pediatric ALL with hyperdiploidy
T Taketani et al.
BLOOD (2004)
Prediction of resistance to small molecule FLT3 inhibitors: Implications for molecularly targeted therapy of acute leukemia
J Cools et al.
CANCER RESEARCH (2004)
Acute myeloid leukemia with t(6;9)(p23;q34) is associated with dysplasia and a high frequency of flt3 gene mutations
MP Oyarzo et al.
AMERICAN JOURNAL OF CLINICAL PATHOLOGY (2004)
In vitro studies of a FM inhibitor combined with chemotherapy: sequence of administration is important to achieve synergistic cytotoxic effects
M Levis et al.
BLOOD (2004)
Synergistic effect of SU11248 with cytarabine or daunorubicin on FLT3 ITD-positive leukemic cells
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BLOOD (2004)
Deletion of an AML1-ETO C-terminal NcoR/SMRT-interacting region strongly induces leukemia development
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PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA (2004)
Relation between CXCR-4 expression, Flt3 mutations, and unfavorable prognosis of adult acute myeloid leukemia
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BLOOD (2004)
FLT3 mutations are associated with other molecular lesions in AML
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The Flt3 internal tandem duplication mutant inhibits the function of transcriptional repressors by blocking interactions with SMRT
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FLT3 ligand causes autocrine signaling in acute myeloid leukemia cells
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Cotreatment with 17-allylamino-demethoxygeldanamycin and FLT-3 kinase inhibitor PKC412 is highly effective against human acute myelogenous leukemia cells with mutant FLT-3
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The role of FLT3 in haematopoietic malignancies
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Selective cytotoxic mechanism of GTP-14564, a novel tyrosine kinase inhibitor in leukemia cells expressing a constitutively active Fms-like tyrosine kinase 3 (FLT3)
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Sensitivity toward tyrosine kinase inhibitors varies between different activating mutations of the FLT3 receptor
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BLOOD (2003)
Comparative analysis of MLL partial tandem duplication and FLT3 internal tandem duplication mutations in 956 adult patients with acute myeloid leukemia
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Tricyclic quinoxalines as potent kinase inhibitors of PDGFR kinase, Flt3 and Kit
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Suppression of myeloid transcription factors and induction of STAT response genes by AML-specific Flt3 mutations
M Mizuki et al.
BLOOD (2003)
The protein tyrosine kinase inhibitor SU5614 inhibits FLT3 and induces growth arrest and apoptosis in AML-derived cell lines expressing a constitutively activated FLT3
K Spiekermann et al.
BLOOD (2003)
Prognostic significance of activating FLT3 mutations in younger adults (16 to 60 years) with acute myeloid leukemia and normal cytogenetics:: a study of the AML Study Group Ulm
S Fröhling et al.
BLOOD (2002)
Alterations of the FLT3 gene in acute promyelocytic leukemia: association with diagnostic characteristics and analysis of clinical outcome in patients treated with the Italian AIDA protocol
N Noguera et al.
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Inhibition of the transforming activity of FLT3 internal tandem duplication mutants from AML patients by a tyrosine kinase inhibitor
KF Tse et al.
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The human promyelocytic leukemia zinc finger gene is regulated by the Evi-1 oncoprotein and a novel guanine-rich site binding protein
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Bis(1 H-2-indolyl)-1-methanones as inhibitors of the hematopoietic tyrosine kinase Flt3
S Teller et al.
LEUKEMIA (2002)
Selective apoptosis of tandemly duplicated FLT3-transformed leukemia cells by Hsp90 inhibitors
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Analysis of FLT3 length mutations in 1003 patients with acute myeloid leukemia:: correlation to cytogenetics, FAB subtype, and prognosis in the AMLCG study and usefulness as a marker for the detection of minimal residual disease
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Analysis of FLT3-activating mutations in 979 patients with acute myelogenous leukemia:: association with FAB subtypes and identification of subgroups with poor prognosis
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PML/RARα and FLT3-ITD induce an APL-like disease in a mouse model
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Inhibition of mutant FLT3 receptors in leukemia cells by the small molecule tyrosine kinase inhibitor PKC412
E Weisberg et al.
CANCER CELL (2002)
A FLT3-targeted tyrosine kinase inhibitor is cytotoxic to leukemia cells in vitro and in vivo
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FLT3 internal tandem duplication mutations associated with human acute myeloid leukemias induce myeloproliferative disease in a murine bone marrow transplant model
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The presence of a FLT3 internal tandem duplication in patients with acute myeloid leukemia (AML) adds important prognostic information to cytogenetic risk group and response to the first cycle of chemotherapy: analysis of 854 patients from the United Kingdom Medical Research Council AML 10 and 12 trials
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BLOOD (2001)
A FLT3 tyrosine kinase inhibitor is selectively cytotoxic to acute myeloid leukemia blasts harboring FLT3 internal tandem duplication mutations
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Inhibition of FLT3-mediated transformation by use of a tyrosine kinase inhibitor
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Activating mutation of D835 within the activation loop of FLT3 in human hematologic malignancies
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Tandem-duplicated Flt3 constitutively activates STAT5 and MAP kinase and introduces autonomous cell growth in IL-3-dependent cell lines
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