ArticleLeukemia2008
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.
Article in Leukemia, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 2 of them syntheses that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
39 citing papers in PubMed, 2 syntheses or guidelines pooled it, 79 citations in OpenAlex.
- Prognostic significance of cytogenetic and molecular features in pediatric acute myeloid leukemia: a meta-analysis.BMC cancer · 2025Pooled it
- Prognostic Significance of KIT Mutations in Core-Binding Factor Acute Myeloid Leukemia: A Systematic Review and Meta-Analysis.PloS one · 2016Pooled it
- Trial
- Prognostic Impact of Sequential Measurable Residual Disease andAnnals of laboratory medicine · 2026Observational
- 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.Annals of hematology · 2026Article
- Fusion-specific co-mutational architecture and treatment-response associations in pediatric core-binding factor acute myeloid leukemia: a multicenter exome-profiled cohort.Frontiers in oncology · 2026Article
- Prognostic Factors of Pediatric Acute Myeloid Leukemia Patients with t(8;21) (q22;q22): A Single-Center Retrospective Study.Children (Basel, Switzerland) · 2024Article
- Molecular dissection of a hyper-aggressive CBFB-MYH11/FLT3-ITD-positive acute myeloid leukemia.Journal of translational medicine · 2022Article
- A somatic mutation in moesin drives progression into acute myeloid leukemia.Science advances · 2022Article
- Influence of KIT mutations on prognosis of pediatric patients with core-binding factor acute myeloid leukemia: a systematic review and meta-analysis.Translational pediatrics · 2020Article
- Targeting transcription factors in cancer - from undruggable to reality.Nature reviews. Cancer · 2019Review
- Functional Properties ofClinical cancer research : an official journal of the American Association for Cancer Research · 2019Article
- [Study of clinical outcome and prognosis in pediatric core binding factor-acute myeloid leukemia].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2019Article
- Detection of KIT mutations in core binding factor acute myeloid leukemia.Leukemia research reports · 2018Article
- Molecular and genetic alterations associated with therapy resistance and relapse of acute myeloid leukemia.Journal of hematology & oncology · 2017Review
- High level of miR-196b at newly diagnosed pediatric acute myeloid leukemia predicts a poor outcome.EXCLI journal · 2017Article
- Significance of KIT exon 17 mutation depends on mutant level rather than positivity in core-binding factor acute myeloid leukemia.Blood cancer journal · 2016Article
- Clinical Impact of Additional Cytogenetic Aberrations, cKIT and RAS Mutations, and Treatment Elements in Pediatric t(8;21)-AML: Results From an International Retrospective Study by the International Berlin-Frankfurt-Münster Study Group.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2015Article
- Article
- Chemical biology. A small-molecule inhibitor of the aberrant transcription factor CBFβ-SMMHC delays leukemia in mice.Science (New York, N.Y.) · 2015Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
c-KIT mutations have been described in core-binding factor (CBF) acute myeloid leukemia (AML) at diagnosis. The role of c-KIT mutations in the relapse of CBF-AML is not clear. The role of CSF1R mutation in the pathogenesis of AML remains to be determined. We analyzed receptor tyrosine kinases (RTKs) and Ras mutations on 154 children with AML. Also, we examined the paired diagnosis and relapse samples in CBF-AML. CBF-AML accounted for 27% (41/154). c-KIT mutations were detected in 41.5% of CBF-AML at diagnosis (6 in exon 8, 10 in exon 17 and 1 in both exons 8 and 17) , FLT3-TKD 2.7%, N-Ras mutations 7.3% and K-Ras mutations 4.9%. FLT3-LM and CSF1R mutations were not found in CBF-AML. The mutations of RTKs and Ras were mutually exclusive except for one patient who had both c-KIT and N-Ras mutations. Eight of the 41 CBF-AML patients relapsed; four patients retained the identical c-KIT mutation patterns as those at diagnosis, the remaining four without c-KIT mutations at diagnosis did not acquire c-KIT mutations at relapse. Our study showed that 54% of childhood CBF-AML had RTKs and/or Ras mutations; c-KIT but not CSF1R mutations play a role in the leukemogenesis of childhood CBF-AML.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.