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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.

Fms-related tyrosine kinase 3

FLT3, Flk2
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. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: B23, HAD, FMS, CAN, AGE
Papers using FLT3 antibodies
Curcumin Sensitizes Acute Promyelocytic Leukemia Cells to Unfolded Protein Response-induced Apoptosis by Blocking the Loss of Misfolded N-CoR Protein.
Defossez Pierre-Antoine, In PLoS ONE, 2010
... Flt3 (C-20) and Flt3 (8H5) antibodies were from Santa Cruz Biotechnology (California, USA) while FITC-conjugated ...
Mislocalized Activation of Oncogenic RTKs Switches Downstream Signaling Outcomes.
Kalinichenko Vladimir V., In PLoS ONE, 2008
... The human leukemic cell lines MV4-11 and MOLM-13, (homozygous and heterozygous for the FLT3-ITD mutation, respectively) as well as HL-60, were maintained in RPMI 1640 medium supplemented with 10% fetal calf serum, 2mM L-glutamine and 1% penicillin/streptomycin (all from Sigma Aldrich, Dublin, Ireland) in a humidified ...
Gastrointestinal stromal tumors: chemotherapy and imatinib
K. Breuhahn et al., In Rare Tumors, 2001
... (PDGFR-β, 1:100, Calbiochem, Schwalbach/Ts, Germany), and stem cell tyrosine kinase 1 (FLT3, 1:100, Abcam, Cambridge, UK), as ...
Papers on FLT3
Induced Apoptosis Investigation in Wild-Type and FLT3-ITD Acute Myeloid Leukemia Cells by Nanochannel Electroporation and Single Cell qRT-PCR.
Lee et al., Columbus, United States. In Mol Ther, Feb 2016
UNASSIGNED: Nanochannel electroporation (NEP) was applied to deliver precise dosages of myeloid cell leukemia-1 (Mcl-1) specific siRNA and molecular beacons to two types of acute myeloid leukemia (AML) cells, FMS-like tyrosine kinase-3 wild type (WT) and internal tandem duplications (ITD) type at the single cell level.
Residual disease detected by multidimensional flow cytometry shows prognostic significance in childhood acute myeloid leukemia with intermediate cytogenetics and negative FLT3-ITD: a report from the Tokyo Children's Cancer Study Group.
Ohara et al., Kawasaki, Japan. In Int J Hematol, Feb 2016
However, IR cytogenetics and negative FLT3-ITD patients with RD levels ≥0.1 % exhibited significantly lower 3y-EFS and 3y-OS than those with RD levels <0.1 % (33.3 versus 83.3 %, P = 0.02 and 20.0 versus 76.9 %, P = 0.005, respectively).
Influence of XPC, XPD, XPF, and XPG gene polymorphisms on the risk and the outcome of acute myeloid leukemia in a Romanian population.
Lazar et al., Târgu-Mureş, Romania. In Tumour Biol, Feb 2016
Also cytogenetic analyses besides FLT3 and DNMT3A mutations status were investigated.
Allogeneic Hematopoietic Stem Cell Transplant in FLT3-ITD-Positive AML: The Role for FLT3 Tyrosine Kinase Inhibitors Post Transplant.
Desai et al., Los Angeles, United States. In Biol Blood Marrow Transplant, Feb 2016
Patients with AML who have internal tandem duplication mutations in the tyrosine kinase receptor FLT3 (FLT3-ITD) face particularly poor outcomes, even after alloHSCT, which appears to only partially mitigate the poor prognosis associated with this mutation.
A transcriptional miRNA-gene network associated with lung adenocarcinoma metastasis based on the TCGA database.
He et al., Chongqing, China. In Oncol Rep, Feb 2016
Our data suggested that some of the genes including PKM2, STRAP and FLT3, may participate in the pathology of lung adenocarcinoma metastasis and could be applied as potential markers or therapeutic targets for lung adenocarcinoma.
Molecular therapy for acute myeloid leukaemia.
Levine et al., New York City, United States. In Nat Rev Clin Oncol, Jan 2016
Indeed, risk status in patients with this disease has classically been based on cytogenetic findings; however, additional molecular characteristics have been shown to inform risk assessment, including FLT3, NPM1, KIT, and CEBPA mutation status.
Sharan et al., Tel Aviv-Yafo, Israel. In Pac Symp Biocomput, Dec 2015
Finally, we focus on the largest AML patient subgroup (~30%) which is characterized by an FLT3 mutation, and utilize our prediction score to rank patient sensitivity to inhibition of each predicted target, reproducing previous findings of in-vitro experiments.
[Research Progress on Treating Acute Myeloid Leukemia by Midostaurin].
Sun et al., Beijing, China. In Zhongguo Shi Yan Xue Ye Xue Za Zhi, Dec 2015
FLT3 gene mutations occurred in approximately 30% of acute myeloid leukemia (AML) patients, which is closely associated with the occurrence, development and poor prognosis of AML.
PI3-Kinase-γ Has a Distinct and Essential Role in Lung-Specific Dendritic Cell Development.
Kopf et al., Zürich, Switzerland. In Immunity, Nov 2015
Furthermore, we show that in lymphoid organs such as the spleen, DCs depended on a similar signaling network to respond to FLT3 ligand with overlapping and partially redundant roles for kinases PI3Kγ and PI3Kδ.
Clonal evolution and resistance to EGFR blockade in the blood of colorectal cancer patients.
Bardelli et al., Torino, Italy. In Nat Med, Jul 2015
We identified alterations in ctDNA of patients with primary or acquired resistance to EGFR blockade in the following genes: KRAS, NRAS, MET, ERBB2, FLT3, EGFR and MAP2K1.
Cooperative loss of RAS feedback regulation drives myeloid leukemogenesis.
Lowe et al., New York City, United States. In Nat Genet, May 2015
RAS network activation is common in human cancers, and in acute myeloid leukemia (AML) this activation is achieved mainly through gain-of-function mutations in KRAS, NRAS or the receptor tyrosine kinase FLT3.
Mutational cooperativity linked to combinatorial epigenetic gain of function in acute myeloid leukemia.
Levine et al., New York City, United States. In Cancer Cell, May 2015
Specific combinations of acute myeloid leukemia (AML) disease alleles, including FLT3 and TET2 mutations, confer distinct biologic features and adverse outcome.
Relation of clinical response and minimal residual disease and their prognostic impact on outcome in acute myeloid leukemia.
Estey et al., Seattle, United States. In J Clin Oncol, May 2015
Although pretreatment covariates such as cytogenetics, monosomal karyotype, relapsed or refractory rather than newly diagnosed AML, and FLT3 internal tandem duplication were associated with relapse, their prognostic effect was much lower once MRD and response were taken into account, the univariable statistical effect of which was not materially affected by inclusion of pretreatment covariates.
Identification of novel pathogenic gene mutations in pediatric acute myeloid leukemia by whole-exome resequencing.
Shiba, In Rinsho Ketsueki, 2014
Many of the recurrent mutations identified in this study involved previously reported targets in AML, such as FLT3, CEBPA, KIT, CBL, NRAS, WT1 and EZH2.
Goryainova, In Lik Sprava, 2014
In addition to the conventional risk factors molecular genetic alterations, such as mutations of NPM1, CEBPA, c-KIT, AML1/RUNX1, WT1, FLT3 and others, are also important prognostic factors in AML patients.
SOCS1 cooperates with FLT3-ITD in the development of myeloproliferative disease by promoting the escape from external cytokine control.
Study Alliance Leukemia (SAL) et al., Frankfurt am Main, Germany. In Blood, 2012
Socs1 accelerates the onset of Flt3-internal tandem duplication - induced myeloproliferative disease by promoting the escape from external cytokine control.
Patient-specific analysis of FLT3 internal tandem duplications for the prognostication and monitoring of acute myeloid leukemia.
Kreuzer et al., Köln, Germany. In Eur J Haematol, 2012
We conclude that individualized monitoring of FLT3-ITD in patients with AML may guide treatment decisions and should be evaluated for the indication for allo-SCT.
[Establishment of a rapid and easy method for simultaneous detection of FLT3-ITD and NPM1 gene mutations in acute myeloid leukemia].
Jin et al., Ningbo, China. In Zhonghua Yi Xue Yi Chuan Xue Za Zhi, 2012
FLT3-mut (420 bp) is longer than FLT3-wt (327-332 bp), and NPM1-mut (172 bp) is longer than NPM1-wt (168 bp).
Role of misfolded N-CoR mediated transcriptional deregulation of Flt3 in acute monocytic leukemia (AML)-M5 subtype.
Khan et al., Singapore, Singapore. In Plos One, 2011
Findings suggest that N-CoR-induced repression of Flt3 might be crucial for limiting the contribution of the Flt3 signaling pathway on the growth potential of leukemic cells.
Cytogenetic and FMS-like tyrosine kinase 3 mutation analyses in acute promyelocytic leukemia patients.
Ghaffari et al., Tehrān, Iran. In Iran Biomed J, 2011
study found in acute promyelocytic leukemia (APL) patients, about 13% had FLT3 internal tandem duplications (ITD); 26% had D835 point mutation; FLT3 ITD mutation was associated with poor prognosis
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