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

Point mutations in the juxtamembrane domain of FLT3 define a new class of activating mutations in AML

12 Jan 2006

Abstract excerpt

In acute myeloid leukemia (AML), two clusters of activating mutations are known in the FMS-like tyrosine kinase-3 (FLT3) gene: FLT3-internal tandem duplications (FLT3-ITDs) in the juxtamembrane (JM) domain in 20% to 25% of patients, and FLT3 point mutations in the tyrosine-kinase domain (FLT3-TKD) in 7% to 10% of patients, respectively. Here, we have characterized a new class of activating point mutations (PMs)...

Read the complete abstract on PubMed

Topics

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

Share to Acute Myeloid Leukemia Research
Share to Chronic Myeloid Leukemia Treatments
Share to Cytokine Signaling Pathways and Interactions

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

Source

Identifiers

PMID: 16410449
DOI: 10.1182/blood-2005-06-2596

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

Point mutations in the juxtamembrane domain of FLT3 define a new class of activating mutations in AMLPMID 16410449Read ↗

Identifying and characterizing a novel activating mutation of the FLT3 tyrosine kinase in AML.Semantic proximity Read ↗

Internal tandem duplication mutations in the tyrosine kinase domain of FLT3 display a higher oncogenic potential than the activation loop D835Y mutation.Semantic proximity Read ↗

Activating FLT3 mutants show distinct gain-of-function phenotypes in vitro and a characteristic signaling pathway profile associated with prognosis in acute myeloid leukemia.Semantic proximity Read ↗

Targeting FLT3 mutations in AML: review of current knowledge and evidenceSemantic proximity Read ↗

FLT3 Mutations in Acute Myeloid Leukemia: Unraveling the Molecular Mechanisms and Implications for Targeted TherapiesSemantic proximity Read ↗

Current knowledge about FLT3 gene mutations, exploring the isoforms, and protein importance in AML.Semantic proximity Read ↗

Differential signaling of Flt3 activating mutations in acute myeloid leukemia: a working model.Semantic proximity Read ↗

FLT3 mutations in acute myeloid leukemia: Therapeutic paradigm beyond inhibitor developmentSemantic proximity Read ↗

Biology, clinical relevance, and molecularly targeted therapy in acute leukemia with FLT3 mutation.Semantic proximity Read ↗

Clinical and molecular features of FLT3 juxtamembrane domain missense mutations in acute myeloid leukaemia.Semantic proximity Read ↗

Deletions in FLT-3 juxtamembrane domain define a new class of pathogenic mutations: case report and systematic analysis.Semantic proximity Read ↗

Downstream molecular pathways of FLT3 in the pathogenesis of acute myeloid leukemia: biology and therapeutic implications.Semantic proximity Read ↗

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