ArticleNature communications2021
Acute myeloid leukemia maturation lineage influences residual disease and relapse following differentiation therapy.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Dual-functional Nanocarrier for Improved Immunochemotherapy of Acute Myeloid Leukemia.Research square · 2026Article
- Ficoll-based isolation biases the profiling of immune cells and leukemic blasts in AML samples.Frontiers in immunology · 2026Article
- Differentiation therapy in acute myeloid leukaemia: molecular basis, clinical progress, and future perspectives.Frontiers in medicine · 2026Review
- Article
- Review
- Proteinase 3 depletion attenuates leukemia by promoting myeloid differentiation.Cell death and differentiation · 2024Article
- PRL2 inhibition elevates PTEN protein and ameliorates progression of acute myeloid leukemia.JCI insight · 2023Article
- Pediatric Myeloid Sarcoma, More than Just a Chloroma: A Review of Clinical Presentations, Significance, and Biology.Cancers · 2023Review
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute myeloid leukemia (AML) is a malignancy of immature progenitor cells. AML differentiation therapies trigger leukemia maturation and can induce remission, but relapse is prevalent and its cellular origin is unclear. Here we describe high resolution analysis of differentiation therapy response and relapse in a mouse AML model. Triggering leukemia differentiation in this model invariably produces two phenotypically distinct mature myeloid lineages in vivo. Leukemia-derived neutrophils dominate the initial wave of leukemia differentiation but clear rapidly and do not contribute to residual disease. In contrast, a therapy-induced population of mature AML-derived eosinophil-like cells persists during remission, often in extramedullary organs. Using genetic approaches we show that restricting therapy-induced leukemia maturation to the short-lived neutrophil lineage markedly reduces relapse rates and can yield cure. These results indicate that relapse can originate from therapy-resistant mature AML cells, and suggest differentiation therapy combined with targeted eradication of mature leukemia-derived lineages may improve disease outcome.
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Registered trials
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