Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Reversal of acquired drug resistance in FLT3-mutated acute myeloid leukemia cells via distinct drug combination strategies.

Clinical cancer research : an official journal of the American Association for Cancer Research - 1 May 2014

Zhang Weiguo, Gao Chen, Konopleva Marina, Chen Ye, Jacamo Rodrigo O, Borthakur Gautam, Cortes Jorge E, Ravandi Farhad, Ramachandran Abhijit, Andreeff Michael

Abstract excerpt

PURPOSE: FMS-like tyrosine kinase-3 (FLT3) internal tandem duplication (FLT3-ITD) mutations are common in patients with acute myeloid leukemia (AML). These patients regularly develop resistance to FLT3 inhibitors suggesting that targeted combination drug strategies are needed to enhance AML therapy efficacy. EXPERIMENTAL DESIGN: Acquired point mutations of FLT3-ITD gene were screened using cDNA-based sequencing...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Drug Synergism
Share to fms-Like Tyrosine Kinase 3

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Gene Duplication

Share to Niacinamide

Share to Phenylurea Compounds

Share to Protein Interaction Domains and Motifs

Share to Sorafenib

Share to Tandem Repeat Sequences

Source

Open in PubMed Open full text

Identifiers

PMID: 24619500
DOI: 10.1158/1078-0432.CCR-13-2052
PMCID: PMC4073635

Genes

FLT3

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Reversal of acquired drug resistance in FLT3-mutated acute myeloid leukemia cells via distinct drug combination strategies.PMID 24619500Read ↗

Mutant FLT3: a direct target of sorafenib in acute myelogenous leukemia.Semantic proximity Read ↗

Patterns of molecular response to and relapse after combination of sorafenib, idarubicin, and cytarabine in patients with FLT3 mutant acute myeloid leukemia.Semantic proximity Read ↗

Decitabine and Sorafenib Therapy in FLT-3 ITD-Mutant Acute Myeloid Leukemia.Semantic proximity Read ↗

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

Mutations of FLT3/ITD confer resistance to multiple tyrosine kinase inhibitors.Semantic proximity Read ↗

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

Aberrant activation of the PI3K/mTOR pathway promotes resistance to sorafenib in AML.Semantic proximity Read ↗

FLT3 activating mutations display differential sensitivity to multiple tyrosine kinase inhibitors.Semantic proximity Read ↗

FMS-like tyrosine kinase 3-internal tandem duplication tyrosine kinase inhibitors display a nonoverlapping profile of resistance mutations in vitro.Semantic proximity Read ↗

[Efficacy and safety of Sorafenib as monotherapy to FLT3-ITD positive acute myeloid leukemia].Semantic proximity Read ↗

Sorafenib induces paradoxical phosphorylation of the extracellular signal-regulated kinase pathway in acute myeloid leukemia cells lacking FLT3-ITD mutation.Semantic proximity Read ↗

Inhibition of FLT3 in AML: a focus on sorafenib.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.