Crenolanib is active against models of drug-resistant FLT3-ITD-positive acute myeloid leukemia. - Wikidata - awgldk - TriplyDB

Crenolanib is active against models of drug-resistant FLT3-ITD-positive acute myeloid leukemia.

Crenolanib is active against models of drug-resistant FLT3-ITD-positive acute myeloid leukemia.

http://www.wikidata.org/entity/Q37334711

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Midostaurin: an emerging treatment for acute myeloid leukemia patients An advanced preclinical mouse model for acute myeloid leukemia using patients' cells of various genetic subgroups and in vivo bioluminescence imaging Discovery of a Diaminopyrimidine FLT3 Inhibitor Active against Acute Myeloid Leukemia.Tyrosine kinase inhibitors targeting FLT3 in the treatment of acute myeloid leukemia.The Cytokine Flt3-Ligand in Normal and Malignant Hematopoiesis Investigational FMS-like tyrosine kinase 3 inhibitors in treatment of acute myeloid leukemia Small-molecule inhibitors of the receptor tyrosine kinases: promising tools for targeted cancer therapies BET protein antagonist JQ1 is synergistically lethal with FLT3 tyrosine kinase inhibitor (TKI) and overcomes resistance to FLT3-TKI in AML cells expressing FLT-ITD.FLT3 kinase inhibitor TTT-3002 overcomes both activating and drug resistance mutations in FLT3 in acute myeloid leukemia.Current Approaches in the Treatment of Relapsed and Refractory Acute Myeloid Leukemia.Computer aided drug discovery of highly ligand efficient, low molecular weight imidazopyridine analogs as FLT3 inhibitors.Identification of an orally available compound with potent and broad FLT3 inhibition activity Characterizing and Overriding the Structural Mechanism of the Quizartinib-Resistant FLT3 "Gatekeeper" F691L Mutation with PLX3397 Pim kinases modulate resistance to FLT3 tyrosine kinase inhibitors in FLT3-ITD acute myeloid leukemia.FLT3 mutational status is an independent risk factor for adverse outcomes after allogeneic transplantation in AML Evaluation of artemisinins for the treatment of acute myeloid leukemia.Molecular therapeutic approaches for pediatric acute myeloid leukemia.Crenolanib is a selective type I pan-FLT3 inhibitor Will FLT3 inhibitors fulfill their promise in acute meyloid leukemia?FLT3 inhibitors in AML: are we there yet?A critical review of which children with acute myeloid leukaemia need stem cell procedures.The evolving role of FLT3 inhibitors in acute myeloid leukemia: quizartinib and beyond.Novel drugs for older patients with acute myeloid leukemia.Targeting FLT3 to treat leukemia.Is allogeneic transplantation really the best treatment for FLT3/ITD-positive acute myeloid leukemia? A systematic review.Investigational therapies up to Phase II which target PDGF receptors: potential anti-cancer therapeutics.New approaches for the immunotherapy of acute myeloid leukemia.FLT3 Inhibitors in Acute Myeloid Leukemia: Current Status and Future Directions.Platelet-derived growth factor regulates YAP transcriptional activity via Src family kinase dependent tyrosine phosphorylation.FLT3 activating mutations display differential sensitivity to multiple tyrosine kinase inhibitors.Bone marrow fibrosis at diagnosis predicts survival for primary acute myeloid leukemia.Synthesis and anti-cancer screening of novel heterocyclic-(2H)-1,2,3-triazoles as potential anti-cancer agents.Chemotherapy Options for Poor Responders to Neoadjuvant Chemotherapy for Orbital Granulocytic Sarcoma.Reversal of acquired drug resistance in FLT3-mutated acute myeloid leukemia cells via distinct drug combination strategies.Treatment of Relapsed/Refractory Acute Myeloid Leukemia.Predicting Chemotherapy Resistance in AML.Mechanisms of Resistance to FLT3 Inhibitors and the Role of the Bone Marrow Microenvironment.Crenolanib, a PDGFR inhibitor, suppresses lung cancer cell proliferation and inhibits tumor growth in vivo Emerging therapies for acute myeloid leukemia: translating biology into the clinic.Gilteritinib, a FLT3/AXL inhibitor, shows antileukemic activity in mouse models of FLT3 mutated acute myeloid leukemia.

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Crenolanib is active against models of drug-resistant FLT3-ITD-positive acute myeloid leukemia.

http://www.wikidata.org/entity/Q37334711

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article científic

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bilimsel makale

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scientific article published on 17 September 2013

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vedecký článok

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vetenskaplig artikel

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videnskabelig artikel

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vědecký článek

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name

Crenolanib is active against m ...... sitive acute myeloid leukemia.

@en

Crenolanib is active against m ...... sitive acute myeloid leukemia.

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type

label

Crenolanib is active against m ...... sitive acute myeloid leukemia.

@en

Crenolanib is active against m ...... sitive acute myeloid leukemia.

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prefLabel

Crenolanib is active against m ...... sitive acute myeloid leukemia.

@en

Crenolanib is active against m ...... sitive acute myeloid leukemia.

@nl

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Crenolanib is active against m ...... sitive acute myeloid leukemia.

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Abhijit Ramachandran

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Clinton F Stewart

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David C Turner

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Eric I Zimmerman

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Hiroto Inaba

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Jassada Buaboonnam

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Laura J Janke

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Michael S Roberts

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Shelley Orwick

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Shuiying Hu

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P2860

Phase I study of the safety, tolerability, and pharmacokinetics of oral CP-868,596, a highly specific platelet-derived growth factor receptor tyrosine kinase inhibitor in patients with advanced cancers

KIT kinase mutants show unique mechanisms of drug resistance to imatinib and sunitinib in gastrointestinal stromal tumor patients

Sorafenib treatment of FLT3-ITD(+) acute myeloid leukemia: favorable initial outcome and mechanisms of subsequent nonresponsiveness associated with the emergence of a D835 mutation.

Validation of ITD mutations in FLT3 as a therapeutic target in human acute myeloid leukaemia.

Crenolanib inhibits the drug-resistant PDGFRA D842V mutation associated with imatinib-resistant gastrointestinal stromal tumors.

Activity of ponatinib against clinically-relevant AC220-resistant kinase domain mutants of FLT3-ITD

Emergence of polyclonal FLT3 tyrosine kinase domain mutations during sequential therapy with sorafenib and sunitinib in FLT3-ITD-positive acute myeloid leukemia.

FLT3 as a therapeutic target in AML: still challenging after all these years

Comprehensive analysis of kinase inhibitor selectivity

Rational design of inhibitors that bind to inactive kinase conformations

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10.1182/BLOOD-2013-07-513044

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Sharyn D. Baker

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