ArticleClinical and translational science2019
Uncovering the Genomic Landscape in Newly Diagnosed and Relapsed Pediatric Cytogenetically Normal FLT3-ITD AML.
Article in Clinical and translational science, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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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
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.
- Molecular Landscape of Acute Myeloid Leukemia in Pediatric Patient-Age-Related Correlations: A Systematic Review.International journal of molecular sciences · 2025Pooled it
- Genomic landscape of patients with FLT3-mutated acute myeloid leukemia (AML) treated within the CALGB 10603/RATIFY trial.Leukemia · 2022Trial
- Impact of Wilms' tumor 1 gene (WT1) mutation on outcome of allogeneic hematopoietic-cell transplantation for acute myeloid leukemia: a retrospective multicenter cohort study from the ALWP/EBMT registry.Bone marrow transplantation · 2026Article
- CanID: A Robust and Accurate RNA-seq Expression-based Diagnostic Classification Scheme for Pediatric Malignancies.Genomics, proteomics & bioinformatics · 2025Article
- Fusion oncoproteins and cooperating mutations define disease phenotypes in NUP98-rearranged leukemia.Blood · 2025Article
- Characteristics and prognosis of paediatric normal karyotype acute myeloid leukaemia: A NOPHO-DBH AML study.British journal of haematology · 2025Article
- Case Report: Pediatric AML withFrontiers in oncology · 2025Article
- A new genomic framework to categorize pediatric acute myeloid leukemia.Nature genetics · 2024Article
- Etiology of oncogenic fusions in 5,190 childhood cancers and its clinical and therapeutic implication.Nature communications · 2023Article
- Preclinical and Pilot Study of Type I FLT3 Tyrosine Kinase Inhibitor, Crenolanib, with Sorafenib in Acute Myeloid Leukemia and FLT3-Internal Tandem Duplication.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022Article
- Integrated Genomic Analysis Identifies UBTF Tandem Duplications as a Recurrent Lesion in Pediatric Acute Myeloid Leukemia.Blood cancer discovery · 2022Article
- Integrative Genomic Analysis of Pediatric Myeloid-Related Acute Leukemias Identifies Novel Subtypes and Prognostic Indicators.Blood cancer discovery · 2021Article
- Article
- Genomic characterization of relapsed acute myeloid leukemia reveals novel putative therapeutic targets.Blood advances · 2021Article
- TP-0903 is active in models of drug-resistant acute myeloid leukemia.JCI insight · 2020Article
- Hotspots mutational analysis of Wilms tumor 1 gene in acute myeloid leukaemia; prevalence and clinical correlation in North Indian population.American journal of blood research · 2020Article
Corrections and comments
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Authors and funding
19 authors at 2 institutions in 1 country.
Funding
Abstract
Fms-like tyrosine kinase 3 (FLT3) internal tandem duplication (ITD) mutations, common in pediatric acute myeloid leukemia (AML), associate with early relapse and poor prognosis. Past studies have suggested additional cooperative mutations are required for leukemogenesis in FLT3-ITD+ AML. Using RNA sequencing and a next-generation targeted gene panel, we broadly characterize the co-occurring genomic alterations in pediatric cytogenetically normal (CN) FLT3-ITD+ AML to gain a deeper understanding of the clonal patterns and heterogeneity at diagnosis and relapse. We show that chimeric transcripts were present in 21 of 34 (62%) of de novo samples, 2 (6%) of these samples included a rare reoccurring fusion partner BCL11B. At diagnosis, the median number of mutations other than FLT3 per patient was 1 (range 0-3), which involved 8 gene pathways; WT1 and NPM1 mutations were frequently observed (35% and 24%, respectively). Fusion transcripts and high variant allele frequency (VAF) mutants, which included WT1, NPM1, SMARCA2, RAD21, and TYK2, were retained from diagnosis to relapse. We did observe reduction in VAF of simple or single mutation clones, but VAFs were preserved or expanded in more complex clones with multiple mutations. Our data provide the first insight into the genomic complexity of pediatric CN FLT3-ITD+ AML and could help stratify future targeted treatment strategies.
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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 Socratic graph.