ArticleLeukemia2017
Modeling human MLL-AF9 translocated acute myeloid leukemia from single donors reveals RET as a potential therapeutic target.
Article in Leukemia, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 22 citations in OpenAlex.
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- Comparative small molecule screening of primary human acute leukemias, engineered human leukemia and leukemia cell lines.Leukemia · 2025Article
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- Targeting IGF2BP3 enhances antileukemic effects of menin-MLL inhibition in MLL-AF4 leukemia.Blood advances · 2024Article
- The biology of SCUBE.Journal of biomedical science · 2023Review
- Signal peptide-CUB-EGF-like repeat-containing protein 1-promoted FLT3 signaling is critical for the initiation and maintenance of MLL-rearranged acute leukemia.Haematologica · 2023Article
- Defining the elusive oncogenic role of the methyltransferase TMT1B.Frontiers in oncology · 2023Review
- Dissection of the MEF2D-IRF8 transcriptional circuit dependency in acute myeloid leukemia.iScience · 2022Article
- Epigenetic changes in human model KMT2A leukemias highlight early events during leukemogenesis.Haematologica · 2022Article
- Article
- CXCR4 Inhibition Enhances Efficacy of FLT3 Inhibitors in FLT3-Mutated AML Augmented by Suppressed TGF-b Signaling.Cancers · 2020Article
- Human models of NUP98-KDM5A megakaryocytic leukemia in mice contribute to uncovering new biomarkers and therapeutic vulnerabilities.Blood advances · 2019Article
- Dual lysosomal-mitochondrial targeting by antihistamines to eradicate leukaemic cells.EBioMedicine · 2019Article
- The developmental stage of the hematopoietic niche regulates lineage inThe Journal of experimental medicine · 2019Article
- RET-mediated autophagy suppression as targetable co-dependence in acute myeloid leukemia.Leukemia · 2018Article
- Article
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Authors and funding
17 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute myeloid leukemias (AMLs) result from a series of genetic events occurring in a stem or progenitor hematopoietic cell that gives rise to their clonal expansion and an impaired capacity to differentiate. To circumvent the genetic heterogeneity of AML patient cohorts, we have developed a model system, driven by the MLL-AF9 (MA9) oncogene, to generate multiple human leukemias using progenitor cells from a single healthy donor. Through stepwise RNA-sequencing data generated using this model and AML patients, we have identified consistent changes associated with MA9-driven leukemogenesis and demonstrate that no recurrent secondary mutations are required. We identify 39 biomarkers whose high expression level is specific to this genetic subtype of AML and validate that many of these have diagnostic utility. We further examined one biomarker, the receptor tyrosine kinase (RTK) RET, and show through shRNA knockdowns that its expression is essential for in vivo and in vitro growth of MA9-AML. These results highlight the value of novel human models of AML derived from single donors using specific oncogenic fusions to understand their biology and to uncover potential therapeutic targets.
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