ArticleBlood cancer journal2014
Copy-neutral loss of heterozygosity is prevalent and a late event in the pathogenesis of FLT3/ITD AML.
Article in Blood cancer journal, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 37 citations in OpenAlex.
- Evaluation of acute myeloid leukemia using genomic proximity mapping-based next generation cytogenomics.Haematologica · 2026Article
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- Evaluation of Acute Myeloid Leukemia Genomes using Genomic Proximity Mapping.medRxiv : the preprint server for health sciences · 2024Article
- COMPASS: joint copy number and mutation phylogeny reconstruction from amplicon single-cell sequencing data.Nature communications · 2023Article
- Article
- Poor outcome of pediatric patients with acute myeloid leukemia harboring high FLT3/ITD allelic ratios.Nature communications · 2022Article
- Article
- A comparative study of next-generation sequencing and fragment analysis for the detection and allelic ratio determination of FLT3 internal tandem duplication.Diagnostic pathology · 2022Article
- Whole genome, exon mutation and transcriptomic profiling of acute myeloid leukemia: A case report.Oncology letters · 2021Article
- Pan cancer patterns of allelic imbalance from chromosomal alterations in 33 tumor types.Genetics · 2021Article
- Descriptive and Functional Genomics in Acute Myeloid Leukemia (AML): Paving the Road for a Cure.Cancers · 2021Review
- Blocking DNA Damage Repair May Be Involved in Stattic (STAT3 Inhibitor)-Induced FLT3-ITD AML Cell Apoptosis.Frontiers in cell and developmental biology · 2021Article
- POLQ suppresses interhomolog recombination and loss of heterozygosity at targeted DNA breaks.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Genetic Characterization and Prognostic Relevance of Acquired Uniparental Disomies in Cytogenetically Normal Acute Myeloid Leukemia.Clinical cancer research : an official journal of the American Association for Cancer Research · 2019Article
- Article
- Tumor heterogeneity of acute myeloid leukemia: insights from single-cell sequencing.Blood science (Baltimore, Md.) · 2019Article
- Knock-in of theOncotarget · 2018Article
- Distinct age-associated molecular profiles in acute myeloid leukemia defined by comprehensive clinical genomic profiling.Oncotarget · 2018Article
- Article
- Genomic instability is a principle pathologic feature of FLT3 ITD kinase activity in acute myeloid leukemia leading to clonal evolution and disease progression.Leukemia & lymphoma · 2017Review
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Patients with high FLT3 internal tandem duplication allelic ratios (FLT3/ITD-ARs) have a poor prognosis. Single-nucleotide polymorphism/comparative genomic hybridization, single-cell PCR and colony-forming assays were used to evaluate genotypic evolution of high FLT3/ITD-ARs in 85 acute myeloid leukemia (AML) patients. Microarrays were used to examine molecular pathways disrupted in leukemic blasts with high FLT3/ITD-ARs. Copy-neutral loss of heterozygosity (CN-LOH) was identified at the FLT3 locus in diagnostic samples with high FLT3/ITD-ARs (N=11), but not in samples with low FLT3/ITD-ARs (N=24), FLT3-activating loop mutations (N=11) or wild-type FLT3 (N=39). Single-cell assays showed that homozygous FLT3/ITD genotype was present in subsets of leukemic blasts at diagnosis but became the dominant clone at relapse. Less differentiated CD34(+)/CD33(-) progenitor colonies were heterozygous for FLT3/ITD, whereas more differentiated CD34(+)/CD33(+) progenitor colonies were homozygous for FLT3/ITD. Expression profiling revealed that samples harboring high FLT3/ITD-ARs aberrantly expressed genes within the recombination/DNA repair pathway. Thus, the development of CN-LOH at the FLT3 locus, which results in high FLT3/ITD-ARs, likely represents a late genomic event that occurs after the acquisition of the FLT3/ITD. Although the etiology underlying the development of CN-LOH remains to be clarified, the disruption in recombination/DNA repair pathway, which is present before the development of LOH, may have a role.
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