ArticleNature communications2020
Dissecting the early steps of MLL induced leukaemogenic transformation using a mouse model of AML.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed, 59 citations in OpenAlex.
- Article
- The TET protein family interactor PROSER1 sustains hematopoietic stem cell function.Blood advances · 2025Article
- Genetic mutations in lymphocytic variant of hypereosinophilic syndrome: study of five siblings.Frontiers in medicine · 2025Article
- Review
- Modelling acute myeloid leukemia (AML): What's new? A transition from the classical to the modern.Drug delivery and translational research · 2023Review
- Article
- Multi-omics analysis defines highly refractory RAS burdened immature subgroup of infant acute lymphoblastic leukemia.Nature communications · 2022Article
- Lower RNA expression of ALDH1A1 distinguishes the favorable risk group in acute myeloid leukemia.Molecular biology reports · 2022Review
- A rapid CRISPR competitive assay forComputational and structural biotechnology journal · 2021Article
- Interactions between lineage-associated transcription factors govern haematopoietic progenitor states.The EMBO journal · 2020Article
- Exploitable metabolic dependencies in MLL-ENL-induced leukemia.Blood advances · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 3 institutions in 1 country.
Funding
Abstract
Leukaemogenic mutations commonly disrupt cellular differentiation and/or enhance proliferation, thus perturbing the regulatory programs that control self-renewal and differentiation of stem and progenitor cells. Translocations involving the Mll1 (Kmt2a) gene generate powerful oncogenic fusion proteins, predominantly affecting infant and paediatric AML and ALL patients. The early stages of leukaemogenic transformation are typically inaccessible from human patients and conventional mouse models. Here, we take advantage of cells conditionally blocked at the multipotent haematopoietic progenitor stage to develop a MLL-r model capturing early cellular and molecular consequences of MLL-ENL expression based on a clear clonal relationship between parental and leukaemic cells. Through a combination of scRNA-seq, ATAC-seq and genome-scale CRISPR-Cas9 screening, we identify pathways and genes likely to drive the early phases of leukaemogenesis. Finally, we demonstrate the broad utility of using matched parental and transformed cells for small molecule inhibitor studies by validating both previously known and other potential therapeutic targets.
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Registered trials
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