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

Mutations in KIT and RAS are frequent events in pediatric core-binding factor acute myeloid leukemia.

Leukemia - 1 Sept 2005

Goemans B F, Zwaan C M, Miller M, Zimmermann M, Harlow A, Meshinchi S, Loonen A H, Hählen K, Reinhardt D, Creutzig U, Kaspers G J L, Heinrich M C

Abstract excerpt

Activating mutations in RAS and receptor tyrosine kinases such as KIT and FLT3 are hypothesized to cooperate with chimeric transcription factors in the pathogenesis of acute myeloid leukemia (AML). To test this hypothesis, we genotyped 150 pediatric AML samples for mutations in KIT (exons 8, 17),...

Read the complete abstract on PubMed

Topics

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

Share to Benzamides
Share to Core Binding Factors
Share to Cytogenetic Analysis

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to fms-Like Tyrosine Kinase 3

Share to Imatinib Mesylate

Share to Leukemia, Myeloid

Share to Piperazines

Share to Proto-Oncogene Proteins c-kit

Source

Identifiers

PMID: 16015387
DOI: 10.1038/sj.leu.2403870

Genes

KIT
FLT3
KRAS
NRAS

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026. Prepared record publication-16015387-2026-09-02.2. Manifest publication-graph-cohort-2026-09-02.2.

Source receipt: PubMed via Helena Literature Corpus, retrieved 2 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Mutations in KIT and RAS are frequent events in pediatric core-binding factor acute myeloid leukemia.PMID 16015387Read ↗

Prevalence and prognostic significance of KIT mutations in pediatric patients with core binding factor AML enrolled on serial pediatric cooperative trials for de novo AML.Semantic proximity Read ↗

KIT mutations correlate with adverse survival in children with core-binding factor acute myeloid leukemia.Semantic proximity Read ↗

Cooperating mutations of receptor tyrosine kinases and Ras genes in childhood core-binding factor acute myeloid leukemia and a comparative analysis on paired diagnosis and relapse samples.Semantic proximity Read ↗

The Prognostic Significance of c-KIT Mutations in Core Binding Factor Acute Myeloid Leukemia.Semantic proximity Read ↗

KIT and FLT3-ITD mutations do not predict outcomes in pediatric core-binding factor acute myeloid leukemia: findings from the C-HUANAN-AML-15 multicenter cohort study.Semantic proximity Read ↗

Prospective Evaluation of KIT Mutations and Long-Term Outcomes in Pediatric Core Binding Factor Acute Myeloid Leukemia: A Single Institutional Study in China.Semantic proximity Read ↗

Incidence and prognostic impact of c-Kit, FLT3, and Ras gene mutations in core binding factor acute myeloid leukemia (CBF-AML).Semantic proximity Read ↗

Core binding factor acute myeloid leukaemia and c-KIT mutations.Semantic proximity Read ↗

Core-binding factor acute myeloid leukemia in pediatric patients enrolled in the AIEOP AML 2002/01 trial: screening and prognostic impact of c-KIT mutations.Semantic proximity Read ↗

Extracellular KIT receptor mutants, commonly found in core binding factor AML, are constitutively active and respond to imatinib mesylate.Semantic proximity Read ↗

KIT exon 17 mutations are predictive of inferior outcome in pediatric acute myeloid leukemia with RUNX1::RUNX1T1.Semantic proximity Read ↗

KIT and FLT3-ITD Mutations Do Not Predict Outcomes in Pediatric Core-Binding Factor Acute Myeloid Leukemia: Findings from the C-HUANAN-AML-15 Multicenter Cohort StudySemantic proximity Read ↗

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