ArticleNature genetics2024
Single-cell multiomics analysis reveals dynamic clonal evolution and targetable phenotypes in acute myeloid leukemia with complex karyotype.
Article in Nature genetics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed.
- A system-level metastable model of cancer evolution: integrating replication stress, cell cycle deregulation and chromosomal instability.Annals of medicine · 2026Review
- Article
- Alterations in 3D-DNA architecture drive unique leukemic profiles in IDH1- and DNMT3A-mutant acute myeloid leukemia.Leukemia · 2026Article
- Long-read sequencing of single cell-derived melanoma sublines reveals divergent and parallel genomic and epigenomic evolutionary trajectories.Nature communications · 2026Article
- Deep learning based individualized cross-platform molecular subtype classification of B-lineage acute lymphoblastic leukemia.NPJ precision oncology · 2026Article
- Multi-omics and artificial intelligence for precision drug discovery and potential clinical applications.Signal transduction and targeted therapy · 2026Review
- Integrated proteogenomic and metabolomic profiling of acute myeloid leukemias to identify molecular subtypes and associated therapy targets.Nature cancer · 2026Article
- Charting single-cell lineages with synthetic and natural barcodes.Nature reviews. Genetics · 2026Review
- Strand-seq and the future of personalized genomics.Nature genetics · 2026Review
- Decoding the archipelago: single-cell biomarkers rechart the molecular geography of acute myeloid leukemia.Cell communication and signaling : CCS · 2026Review
- Review
- Single-cell profiling reveals reprogrammed hierarchy and disrupted immune-stromal ecosystem in TP53-mutated AML.Experimental hematology & oncology · 2026Article
- Hijacking the helpers: platelet and neutrophil trafficking in AML and therapeutic exploitation.Experimental hematology & oncology · 2026Review
- Multidimensional tumor heterogeneity and its role in therapeutic resistance.Frontiers in immunology · 2026Review
- The evolving nosology of myeloid neoplasms: the semi-centennial of the 1976 French-American-British classification.Leukemia · 2025Review
- How to drug a leukemic stem cell: deciphering heterogeneity for better specificity.Blood neoplasia · 2025Review
- Development and validation of a leukemia prognostic model through single-cell RNA sequencing and machine learning approaches.Discover oncology · 2025Article
- Precision oncology to overcome resistance in R/R AML in children and adults requires combinations of cytotoxic, targeted, and immunological treatments.Journal of internal medicine · 2025Review
- Absolute copy number aware CNV calling of sub-megabase segments in ultra-low coverage single-cell DNA sequencing data.Nucleic acids research · 2025Article
- Long-read sequencing of single cell-derived melanoma subclones reveals divergent and parallel genomic and epigenomic evolutionary trajectories.bioRxiv : the preprint server for biology · 2025Article
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26 authors.
Funding
Abstract
Chromosomal instability is a major driver of intratumoral heterogeneity (ITH), promoting tumor progression. In the present study, we combined structural variant discovery and nucleosome occupancy profiling with transcriptomic and immunophenotypic changes in single cells to study ITH in complex karyotype acute myeloid leukemia (CK-AML). We observed complex structural variant landscapes within individual cells of patients with CK-AML characterized by linear and circular breakage-fusion-bridge cycles and chromothripsis. We identified three clonal evolution patterns in diagnosis or salvage CK-AML (monoclonal, linear and branched polyclonal), with 75% harboring multiple subclones that frequently displayed ongoing karyotype remodeling. Using patient-derived xenografts, we demonstrated varied clonal evolution of leukemic stem cells (LSCs) and further dissected subclone-specific drug-response profiles to identify LSC-targeting therapies, including BCL-xL inhibition. In paired longitudinal patient samples, we further revealed genetic evolution and cell-type plasticity as mechanisms of disease progression. By dissecting dynamic genomic, phenotypic and functional complexity of CK-AML, our findings offer clinically relevant avenues for characterizing and targeting disease-driving LSCs.
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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 OpenQuestion graph.