ArticleFrontiers in genetics2024
Multi-omic analysis of longitudinal acute myeloid leukemia patient samples reveals potential prognostic markers linked to disease progression.
Article in Frontiers in genetics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Multiomic State-Transitions Reveal Post-Treatment Transcriptome Desynchronization in Acute Myeloid Leukemia.bioRxiv : the preprint server for biology · 2026Article
- NPM1c⁺-driven lncRNA dysregulation in AML: Mechanisms, Controversies and translational roadblocks.Translational oncology · 2026Review
- Chromatin accessibility of circulating CD8⁺ T cells differentiates disease severity in IgA nephropathy.Scientific reports · 2025Article
- Gene expression analysis reveals genes related to heavy metals and produced water exposure in Synechococcus elongatus.International microbiology : the official journal of the Spanish Society for Microbiology · 2025Article
- Liquid Biopsy and Epigenetic Signatures in AML, ALL, and CNS Tumors: Diagnostic and Monitoring Perspectives.International journal of molecular sciences · 2025Review
- Editorial: Screening and discovering novel biological biomarkers by omic-data to revolutionize tumor management.Frontiers in genetics · 2025Article
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Authors and funding
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Abstract
Relapse remains a determinant of treatment failure and contributes significantly to mortality in acute myeloid leukemia (AML) patients. Despite efforts to understand AML progression and relapse mechanisms, findings on acquired gene mutations in relapse vary, suggesting inherent genetic heterogeneity and emphasizing the role of epigenetic modifications. We conducted a multi-omic analysis using Omni-C, ATAC-seq, and RNA-seq on longitudinal samples from two adult AML patients at diagnosis and relapse. Herein, we characterized genetic and epigenetic changes in AML progression to elucidate the underlying mechanisms of relapse. Differential interaction analysis showed significant 3D chromatin landscape reorganization between relapse and diagnosis samples. Comparing global open chromatin profiles revealed that relapse samples had significantly fewer accessible chromatin regions than diagnosis samples. In addition, we discovered that relapse-related upregulation was achieved either by forming new active enhancer contacts or by losing interactions with poised enhancers/potential silencers. Altogether, our study highlights the impact of genetic and epigenetic changes on AML progression, underlining the importance of multi-omic approaches in understanding disease relapse mechanisms and guiding potential therapeutic interventions.
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