ArticleBlood advances2022
Allelic complexity of KMT2A partial tandem duplications in acute myeloid leukemia and myelodysplastic syndromes.
Article in Blood advances, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 20 citations in OpenAlex.
- CPX-351 selectively benefits patients with AML and myelodysplasia-related mutations in the pivotal randomized trial.Blood advances · 2026Trial
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- Aberrant CD25 and Increased CD123 Expression Are Common in Acute Myeloid Leukemia withCancers · 2026Article
- An innovative full-size pathogenic tandem duplication mutation precise detection system based on next-generation sequencing.Experimental biology and medicine (Maywood, N.J.) · 2025Article
- Detection ofCancers · 2024Article
- Unveiling the Complexity ofCancers · 2024Article
- Characterizing the allele-specific gene expression landscape in high hyperdiploid acute lymphoblastic leukemia with BASE.Scientific reports · 2024Article
- Histone methyltransferase KMT2A: Developmental regulation to oncogenic transformation.The Journal of biological chemistry · 2024Review
- Article
- Targeting the deubiquitinaseOncology reports · 2023Review
- Allogeneic Hematopoietic Cell Transplantation Improves Outcome in Myelodysplastic Syndrome Across High-Risk Genetic Subgroups: Genetic Analysis of the Blood and Marrow Transplant Clinical Trials Network 1102 Study.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2023Article
- Prospective evaluation of genome sequencing to compare conventional cytogenetics in acute myeloid leukemia.Blood cancer journal · 2023Article
- Outlier Expression of Isoforms by Targeted or Total RNA Sequencing Identifies Clinically Significant Genomic Variants in Hematolymphoid Tumors.The Journal of molecular diagnostics : JMD · 2023Article
- Predicting leukemic transformation in myelodysplastic syndrome using a transcriptomic signature.Frontiers in genetics · 2023Article
Corrections and comments
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Authors and funding
10 authors at 6 institutions in 1 country.
Funding
Abstract
KMT2A partial tandem duplication (KMT2A-PTD) is an adverse risk factor in acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS), a potential therapeutic target, and an attractive marker of measurable residual disease. High initial KMT2A-PTD RNA levels have been linked to poor prognosis, but mechanisms regulating KMT2A-PTD expression are not well understood. Although KMT2A-PTD has been reported to affect only a single allele, it has been theorized but not proven that genomic gains of a monoallelic KMT2A-PTD may occur, thereby potentially driving high expression and disease progression. In this study, we identified 94 patients with KMT2A-PTDs using targeted DNA next-generation sequencing (NGS) and found that 16% (15/94) had complex secondary events, including copy-neutral loss of heterozygosity and selective gain involving the KMT2A-PTD allele. High copy numbers indicating complexity were significantly enriched in AML vs MDS and correlated with higher RNA expression. Moreover, in serial samples, complexity was associated with relapse and secondary transformation. Taken together, we provide approaches to integrate quantitative and allelic assessment of KMT2A-PTDs into targeted DNA NGS and demonstrate that secondary genetic events occur in KMT2A-PTD by multiple mechanisms that may be linked to myeloid disease progression by driving increased expression from the affected allele.
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