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

Prolonged exposure to FLT3 inhibitors leads to resistance via activation of parallel signaling pathways.

Blood - 15 Feb 2007

Piloto Obdulio, Wright Melissa, Brown Patrick, Kim Kyu-Tae, Levis Mark, Small Donald

Abstract excerpt

Continuous treatment of malignancies with tyrosine kinase inhibitors (TKIs) may select for resistant clones (ie, imatinib mesylate). To study resistance to TKIs targeting FLT3, a receptor tyrosine kinase that is frequently mutated in acute myelogenous leukemia (AML), we developed resistant human cell lines through prolonged coculture with FLT3 TKIs. FLT3 TKI-resistant cell lines and primary samples still exhibit...

Read the complete abstract on PubMed

Topics

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

Share to Benzamides
Share to Drug Resistance, Neoplasm
Share to fms-Like Tyrosine Kinase 3

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Imatinib Mesylate

Share to Piperazines

Share to Protein-Tyrosine Kinases

Share to Pyrimidines

Share to ras Proteins

Source

Open in PubMed Open full text

Identifiers

PMID: 17047150
DOI: 10.1182/blood-2006-05-023804
PMCID: PMC1794049

Genes

FLT3

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Prolonged exposure to FLT3 inhibitors leads to resistance via activation of parallel signaling pathways.PMID 17047150Read ↗

Reversible resistance induced by FLT3 inhibition: a novel resistance mechanism in mutant FLT3-expressing cells.Semantic proximity Read ↗

Resistance to FLT3 inhibitors in acute myeloid leukemia: Molecular mechanisms and resensitizing strategiesSemantic proximity Read ↗

Drug resistance in mutant FLT3-positive AML.Semantic proximity Read ↗

Resistance to tyrosine kinase inhibition therapy for chronic myelogenous leukemia: a clinical perspective and emerging treatment options.Semantic proximity Read ↗

FLT3 Inhibitors in Acute Myeloid Leukemia: Challenges and Recent Developments in Overcoming Resistance.Semantic proximity Read ↗

Targeting Oncogenic Signaling in Mutant FLT3 Acute Myeloid Leukemia: The Path to Least ResistanceSemantic proximity Read ↗

Overcoming Resistance to FLT3 Inhibitors in the Treatment of FLT3-Mutated AML.Semantic proximity Read ↗

Co-expression of wild-type FLT3 attenuates the inhibitory effect of FLT3 inhibitor on FLT3 mutated leukemia cells.Semantic proximity Read ↗

Resistance to targeted therapies: delving into FLT3 and IDH.Semantic proximity Read ↗

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

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

Targeting Oncogenic Signaling in Mutant FLT3 Acute Myeloid Leukemia: the Path to Least ResistanceSemantic proximity Read ↗

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