ArticleMolecular cancer2022
Longitudinal single-cell transcriptomics reveals distinct patterns of recurrence in acute myeloid leukemia.
Article in Molecular cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 46 citations in OpenAlex.
- Global bibliometric analysis of TP53-mutated acute myeloid leukemia: research hotspots and evolution.Translational cancer research · 2026Article
- Diving into the transcriptional landscape of leukemic stem cells in acute myeloid leukemia at single-cell resolution.Journal of cancer research and clinical oncology · 2026Review
- BCL6B suppresses acute myeloid leukemia progression by transcriptionally repressing GGT5 and modulating MAPK signaling.Biology direct · 2026Article
- Targeting LAPTM5 enhances AML sensitivity to cytarabine through autophagy inhibition.Cell death & disease · 2026Article
- Longitudinal omics data analysis: approaches and applications.Computational and structural biotechnology journal · 2026Review
- Defining the role of natural killer cells in acute myeloid leukemia through the lens of single-cell omics.Frontiers in immunology · 2026Review
- The AML cellular state space unveils NPM1 immune evasion subtypes with distinct clinical outcomes.Nature communications · 2025Article
- How to drug a leukemic stem cell: deciphering heterogeneity for better specificity.Blood neoplasia · 2025Review
- Joint representation and visualization of derailed cell states with Decipher.Genome biology · 2025Article
- Significance of targeting DNMT3A mutations in AML.Annals of hematology · 2025Review
- Metabolic reprogramming and immune regulation in acute myeloid leukemia.Frontiers in immunology · 2025Review
- The tumor microenvironment across four dimensions: assessing space and time in cancer biology.Frontiers in immunology · 2025Review
- Identification of single-cell blasts in pediatric acute myeloid leukemia using an autoencoder.Life science alliance · 2024Article
- Single-cell landscape of innate and acquired drug resistance in acute myeloid leukemia.Nature communications · 2024Article
- Establishment and verification of a TME prognosis scoring model based on the acute myeloid leukemia single-cell transcriptome.Scientific reports · 2024Article
- Application of omics in the diagnosis, prognosis, and treatment of acute myeloid leukemia.Biomarker research · 2024Review
- Single-cell and spatial transcriptomics reveal alterations in trophoblasts at invasion sites and disturbed myometrial immune microenvironment in placenta accreta spectrum disorders.Biomarker research · 2024Article
- From hypoxia single-cell gene signatures to HIF targeting of AML leukemic stem cells.HemaSphere · 2024Article
- Leukemic stem cells activate lineage inappropriate signalling pathways to promote their growth.Nature communications · 2024Article
- Prognostic value of postinduction medullary myeloid recovery by flow cytometry in acute myeloid leukemia.EJHaem · 2024Article
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Authors and funding
14 authors at 8 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAcute myeloid leukemia (AML) is a heterogeneous and aggressive blood cancer that results from diverse genetic aberrations in the hematopoietic stem or progenitor cells (HSPCs) leading to the expansion of blasts in the hematopoietic system. The heterogeneity and evolution of cancer blasts can render therapeutic interventions ineffective in a yet poorly understood patient-specific manner. In this study, we investigated the clonal heterogeneity of diagnosis (Dx) and relapse (Re) pairs at genetic and transcriptional levels, and unveiled the underlying pathways and genes contributing to recurrence.
methodsWhole-exome sequencing was used to detect somatic mutations and large copy number variations (CNVs). Single cell RNA-seq was performed to investigate the clonal heterogeneity between Dx-Re pairs and amongst patients.
resultsscRNA-seq analysis revealed extensive expression differences between patients and Dx-Re pairs, even for those with the same -presumed- initiating events. Transcriptional differences between and within patients are associated with clonal composition and evolution, with the most striking differences in patients that gained large-scale copy number variations at relapse. These differences appear to have significant molecular implications, exemplified by a DNMT3A/FLT3-ITD patient where the leukemia switched from an AP-1 regulated clone at Dx to a mTOR signaling driven clone at Re. The two distinct AML1-ETO pairs share genes related to hematopoietic stem cell maintenance and cell migration suggesting that the Re leukemic stem cell-like (LSC-like) cells evolved from the Dx cells.
conclusionsIn summary, the single cell RNA data underpinned the tumor heterogeneity not only amongst patient blasts with similar initiating mutations but also between each Dx-Re pair. Our results suggest alternatively and currently unappreciated and unexplored mechanisms leading to therapeutic resistance and AML recurrence.
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