AC220 is a uniquely potent and selective inhibitor of FLT3 for the treatment of acute myeloid leukemia (AML) - Wikidata - wikimedia - TriplyDB

AC220 is a uniquely potent and selective inhibitor of FLT3 for the treatment of acute myeloid leukemia (AML)

AC220 is a uniquely potent and selective inhibitor of FLT3 for the treatment of acute myeloid leukemia (AML)

http://www.wikidata.org/entity/Q37373040

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Downstream molecular pathways of FLT3 in the pathogenesis of acute myeloid leukemia: biology and therapeutic implications Midostaurin: an emerging treatment for acute myeloid leukemia patients Molecular and Cellular Mechanisms of Myelodysplastic Syndrome: Implications on Targeted Therapy Pediatric AML: From Biology to Clinical Management Childhood acute myeloid leukaemia An overview on the role of FLT3-tyrosine kinase receptor in acute myeloid leukemia: biology and treatment FLT3 mutations in acute myeloid leukemia: what is the best approach in 2013?Validation of ITD mutations in FLT3 as a therapeutic target in human acute myeloid leukaemia.FLT3 tyrosine kinase inhibitors in acute myeloid leukemia: clinical implications and limitations Selective Akt inhibitors synergize with tyrosine kinase inhibitors and effectively override stroma-associated cytoprotection of mutant FLT3-positive AML cells The FLT3 inhibitor quizartinib inhibits ABCG2 at pharmacologically relevant concentrations, with implications for both chemosensitization and adverse drug interactions An ensemble based top performing approach for NCI-DREAM drug sensitivity prediction challenge Internal Tandem Duplication in FLT3 Attenuates Proliferation and Regulates Resistance to the FLT3 Inhibitor AC220 by Modulating p21Cdkn1a and Pbx1 in Hematopoietic Cells Identifying kinase dependency in cancer cells by integrating high-throughput drug screening and kinase inhibition data Role of altered growth factor receptor-mediated JAK2 signaling in growth and maintenance of human acute myeloid leukemia stem cells.Functions of flt3 in zebrafish hematopoiesis and its relevance to human acute myeloid leukemia.FLT3-mutant allelic burden and clinical status are predictive of response to FLT3 inhibitors in AML.Using combination therapy to override stromal-mediated chemoresistance in mutant FLT3-positive AML: synergism between FLT3 inhibitors, dasatinib/multi-targeted inhibitors and JAK inhibitors.Discovery of a Diaminopyrimidine FLT3 Inhibitor Active against Acute Myeloid Leukemia.Tyrosine kinase inhibitors targeting FLT3 in the treatment of acute myeloid leukemia.Salvage therapy using FLT3 inhibitors may improve long-term outcome of relapsed or refractory AML in patients with FLT3-ITD FLT3 mutations in myelodysplastic syndrome and chronic myelomonocytic leukemia Targeted therapies in hematology and their impact on patient care: chronic and acute myeloid leukemia.Investigational FMS-like tyrosine kinase 3 inhibitors in treatment of acute myeloid leukemia Emerging FMS-like tyrosine kinase 3 inhibitors for the treatment of acute myelogenous leukemia Treatment with FLT3 inhibitor in patients with FLT3-mutated acute myeloid leukemia is associated with development of secondary FLT3-tyrosine kinase domain mutations.Preclinical evaluation of lestaurtinib (CEP-701) in combination with retinoids for neuroblastoma.The Biology and Targeting of FLT3 in Pediatric Leukemia.Kinase pathway dependence in primary human leukemias determined by rapid inhibitor screening.LAMTOR2 regulates dendritic cell homeostasis through FLT3-dependent mTOR signalling SU11652 Inhibits tyrosine kinase activity of FLT3 and growth of MV-4-11 cells The Future of Targeting FLT3 Activation in AML.Genetic abnormalities and challenges in the treatment of acute myeloid leukemia.Treatment of FLT3-ITD acute myeloid leukemia.Gene mutations and molecularly targeted therapies in acute myeloid leukemia.FLT3 ligand impedes the efficacy of FLT3 inhibitors in vitro and in vivo A new approach for prediction of tumor sensitivity to targeted drugs based on functional data FLT3-internal tandem duplication and age are the major prognostic factors in patients with relapsed acute myeloid leukemia with normal karyotype Pim-1 kinase phosphorylates and stabilizes 130 kDa FLT3 and promotes aberrant STAT5 signaling in acute myeloid leukemia with FLT3 internal tandem duplication FLT3 kinase inhibitor TTT-3002 overcomes both activating and drug resistance mutations in FLT3 in acute myeloid leukemia.

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AC220 is a uniquely potent and selective inhibitor of FLT3 for the treatment of acute myeloid leukemia (AML)

http://www.wikidata.org/entity/Q37373040

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bilimsel makale

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scientific article published on 04 August 2009

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name

AC220 is a uniquely potent and ...... f acute myeloid leukemia (AML)

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AC220 is a uniquely potent and ...... ment of acute myeloid leukemia

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AC220 is a uniquely potent and ...... f acute myeloid leukemia (AML)

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AC220 is a uniquely potent and ...... ment of acute myeloid leukemia

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AC220 is a uniquely potent and ...... f acute myeloid leukemia (AML)

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AC220 is a uniquely potent and ...... ment of acute myeloid leukemia

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BLOOD-2009-05-222034

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AC220 is a uniquely potent and ...... f acute myeloid leukemia (AML)

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Barbara Belli

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Daniel Brigham

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Gabriel Pallares

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Hitesh K Patel

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Joyce James

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Keith W Pratz

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Kelly G Sprankle

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Mark Levis

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Mazen W Karaman

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Merryl D Cramer

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EGFR mutations in lung cancer: correlation with clinical response to gefitinib therapy.

The impact of FLT3 internal tandem duplication mutant level, number, size, and interaction with NPM1 mutations in a large cohort of young adult patients with acute myeloid leukemia.

Mutant FLT3: a direct target of sorafenib in acute myelogenous leukemia.

Mutations and treatment outcome in cytogenetically normal acute myeloid leukemia.

Activating mutations in the epidermal growth factor receptor underlying responsiveness of non-small-cell lung cancer to gefitinib

A FLT3-targeted tyrosine kinase inhibitor is cytotoxic to leukemia cells in vitro and in vivo

A quantitative analysis of kinase inhibitor selectivity

Patterns of somatic mutation in human cancer genomes

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2984-2992

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10.1182/BLOOD-2009-05-222034

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