ArticleScientific reports2020
High-fat diet intensifies MLL-AF9-induced acute myeloid leukemia through activation of the FLT3 signaling in mouse primitive hematopoietic cells.
Article in Scientific reports, 2020. 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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Who cites it
8 citing papers in PubMed, 16 citations in OpenAlex.
- The gut-bone marrow axis in acute leukemia: an evidence-graded review of microbiota-immune crosstalk and therapeutic implications.Frontiers in cellular and infection microbiology · 2026Review
- The influence of high-fat diet and energy-restricted diet on hematopoietic stem cells: mechanisms and implications.Frontiers in immunology · 2025Review
- Bidirectional interplay between metabolism and epigenetics in hematopoietic stem cells and leukemia.The EMBO journal · 2023Review
- Microbiota, Diet and Acute Leukaemia: Tips and Tricks on Their Possible Connections.Nutrients · 2023Review
- Variation in Lipid Species Profiles among Leukemic Cells Significantly Impacts Their Sensitivity to the Drug Targeting of Lipid Metabolism and the Prognosis of AML Patients.International journal of molecular sciences · 2023Article
- Untargeted metabolomic and lipidomic analyses reveal lipid dysregulation in the plasma of acute leukemia patients.Frontiers in molecular biosciences · 2023Article
- Acute lymphoblastic leukemia-derived extracellular vesicles affect quiescence of hematopoietic stem and progenitor cells.Cell death & disease · 2022Article
- Translating energy balance research from the bench to the clinic to the community: Parallel animal-human studies in cancer.CA: a cancer journal for cliniciansReview
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Using a MLL-AF9 knock-in mouse model, we discovered that consumption of a high-fat diet (HFD) accelerates the risk of developing acute myeloid leukemia (AML). This regimen increases the clusterization of FLT3 within lipid rafts on the cell surface of primitive hematopoietic cells, which overactivates this receptor as well as the downstream JAK/STAT signaling known to enhance the transformation of MLL-AF9 knock-in cells. Treatment of mice on a HFD with Quizartinib, a potent inhibitor of FLT3 phosphorylation, inhibits the JAK3/STAT3, signaling and finally antagonizes the accelerated development of AML that occurred following the HFD regimen. We can therefore conclude that, on a mouse model of AML, a HFD enforces the FLT3 signaling pathway on primitive hematopoietic cells and, in turn, improves the oncogenic transformation of MLL-AF9 knock-in cells and the leukemia initiation.
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Registered trials
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