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Article

The secondary FLT3-ITD F691L mutation induces resistance to AC220 in FLT3-ITD+ AML but retains in vitro sensitivity to PKC412 and Sunitinib.

Leukemia - 1 Jun 2013

Albers C, Leischner H, Verbeek M, Yu C, Illert A L, Peschel C, von Bubnoff N, Duyster J

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Identifiers

PMID: 23392356
DOI: 10.1038/leu.2013.14

Genes

FLT3

Variants

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Related research

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Research trail→

Click a neighbor to travelStep 1 · 12 closest

The secondary FLT3-ITD F691L mutation induces resistance to AC220 in FLT3-ITD+ AML but retains in vitro sensitivity to PKC412 and Sunitinib.PMID 23392356Read ↗

Selective FLT3 inhibition of FLT3-ITD+ acute myeloid leukaemia resulting in secondary D835Y mutation: a model for emerging clinical resistance patterns.Semantic proximity Read ↗

Secondary mutations as mediators of resistance to targeted therapy in leukemia.Semantic proximity Read ↗

Mechanisms Underlying Resistance to FLT3 Inhibitors in Acute Myeloid LeukemiaSemantic proximity Read ↗

Validation of ITD mutations in FLT3 as a therapeutic target in human acute myeloid leukaemia.Semantic proximity Read ↗

Quizartinib-resistant FLT3-ITD acute myeloid leukemia cells are sensitive to the FLT3-Aurora kinase inhibitor CCT241736Semantic proximity Read ↗

An imidazo[1,2-a]pyridine-pyridine derivative potently inhibits FLT3-ITD and FLT3-ITD secondary mutants, including gilteritinib-resistant FLT3-ITD/F691L.Semantic proximity Read ↗

Identification of a secondary FLT3/A848P mutation in a patient with FLT3-ITD-positive blast phase CMML and response to sunitinib and sorafenib.Semantic proximity Read ↗

Activity of ponatinib against clinically-relevant AC220-resistant kinase domain mutants of FLT3-ITDSemantic proximity Read ↗

Sensitivity toward sorafenib and sunitinib varies between different activating and drug-resistant FLT3-ITD mutations.Semantic proximity Read ↗

A noncanonical FLT3 gatekeeper mutation disrupts gilteritinib binding and confers resistanceSemantic proximity Read ↗

Expression of myeloid Src-family kinases is associated with poor prognosis in AML and influences Flt3-ITD kinase inhibitor acquired resistanceSemantic proximity Read ↗

Clinical and molecular response of AML harboring non-canonical <i>FLT3</i> N676K driver mutations to contemporary FLT3 inhibitorsSemantic proximity Read ↗

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