ArticleNature genetics2023
Single-cell multi-omics identifies chronic inflammation as a driver of TP53-mutant leukemic evolution.
Article in Nature genetics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 116 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
116 citing papers in PubMed, 133 citations in OpenAlex.
- ADORE: an open platform study of ruxolitinib in combination with other novel therapies in patients with myelofibrosis.Blood advances · 2025Trial
- Azacitidine, Venetoclax, and Magrolimab in Newly Diagnosed and Relapsed Refractory Acute Myeloid Leukemia: Phase Ib/II Study and Correlative Analysis.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025Trial
- Second primary cancers following hematologic malignancies: Epidemiology, pathobiology and clinical management.Human vaccines & immunotherapeutics · 2026Review
- Immune and cellular determinants of response to HMA-venetoclax regimens in acute myeloid leukemia.HemaSphere · 2026Article
- Type 1 interferon perturbates clonal competition by reshaping human blood development.Nature genetics · 2026Article
- A single-cell lens into the co-evolution of genotypes and phenotypes in cancer.Nature reviews. Cancer · 2026Review
- A PBD dimer-containing antibody-drug conjugate targeting CCRL2 for high-risk MDS/AML including TP53-mutated disease.Blood advances · 2026Article
- Article
- Single-cell long-read genotyping of transcripts reveals discrete mechanisms of clonal evolution in post-MPN AML.Blood advances · 2026Article
- Scalable genotyping in fixed transcriptomes resolves clonal heterogeneity via single-cell sequencing.bioRxiv : the preprint server for biology · 2026Article
- Real-world treatment patterns and outcomes in accelerated and blast-phase myeloproliferative neoplasms: Insights from a large multi-centre cohort analysis in the United Kingdom.British journal of haematology · 2026Article
- Global bibliometric analysis of TP53-mutated acute myeloid leukemia: research hotspots and evolution.Translational cancer research · 2026Article
- Clonal Metamorphosis: Deconstructing MPN Evolution with Single-Cell and Spatial Multi-Omics.Clinical and experimental medicine · 2026Review
- Inflammatory Signatures in MDS: The Missing Link Between Genetics, Microenvironment, and Therapy.Cells · 2026Review
- Macrophage Plasticity: Phenotypic and Functional Profiles Across Pathological Microenvironments.International journal of molecular sciences · 2026Review
- Distinct stem cell identities converge into shared erythroid stress in ERCC6L2 disease and Shwachman-Diamond syndrome.HemaSphere · 2026Article
- Charting single-cell lineages with synthetic and natural barcodes.Nature reviews. Genetics · 2026Review
- Clonal haematopoiesis and cardiovascular disease, defining risk, filling gaps, and framing the future.NPJ cardiovascular health · 2026Review
- Prognostic significance of inflammatory cytokine polymorphisms in AML: a study of IFNG, TNFA, and IL1B polymorphisms.BMC immunology · 2026Article
- Immune-Genomic Evolution in AML Spontaneous Remission: A 66-Patient Pooled Analysis and Longitudinal Clonal Tracking.Cancers · 2026Article
56 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
34 authors at 11 institutions in 5 countries.
Funding
Abstract
Understanding the genetic and nongenetic determinants of tumor protein 53 (TP53)-mutation-driven clonal evolution and subsequent transformation is a crucial step toward the design of rational therapeutic strategies. Here we carry out allelic resolution single-cell multi-omic analysis of hematopoietic stem/progenitor cells (HSPCs) from patients with a myeloproliferative neoplasm who transform to TP53-mutant secondary acute myeloid leukemia (sAML). All patients showed dominant TP53 'multihit' HSPC clones at transformation, with a leukemia stem cell transcriptional signature strongly predictive of adverse outcomes in independent cohorts, across both TP53-mutant and wild-type (WT) AML. Through analysis of serial samples, antecedent TP53-heterozygous clones and in vivo perturbations, we demonstrate a hitherto unrecognized effect of chronic inflammation, which suppressed TP53 WT HSPCs while enhancing the fitness advantage of TP53-mutant cells and promoted genetic evolution. Our findings will facilitate the development of risk-stratification, early detection and treatment strategies for TP53-mutant leukemia, and are of broad relevance to other cancer types.
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Registered trials
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.