ArticleProceedings of the National Academy of Sciences of the United States of America2009
A Drosophila model identifies calpains as modulators of the human leukemogenic fusion protein AML1-ETO.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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31 citing papers in PubMed, 50 citations in OpenAlex.
- Notch Signaling in Drosophila Tumor Models.Advances in experimental medicine and biology · 2025Review
- The human leukemic oncogene MLL-AF4 promotes hyperplastic growth of hematopoietic tissues iniScience · 2023Article
- Descriptive and Functional Genomics in Acute Myeloid Leukemia (AML): Paving the Road for a Cure.Cancers · 2021Review
- Drosophila Hox genes induce melanized pseudo-tumors when misexpressed in hemocytes.Scientific reports · 2021Article
- Genetic Screening for Potential New Targets in Chronic Myeloid Leukemia Based on Drosophila Transgenic for Human BCR-ABL1.Cancers · 2021Article
- Amalgam regulates the receptor tyrosine kinase pathway through Sprouty in glial cell development in theJournal of cell science · 2020Article
- The Leukemic Fly: Promises and Challenges.Cells · 2020Review
- The Posterior Signaling Center Is an Important Microenvironment for Homeostasis of theFrontiers in cell and developmental biology · 2020Review
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- The Oncogenic Transcription Factor RUNX1/ETO Corrupts Cell Cycle Regulation to Drive Leukemic Transformation.Cancer cell · 2018Article
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- Genetic dissection of leukemia-associated IDH1 and IDH2 mutants and D-2-hydroxyglutarate in Drosophila.Blood · 2015Article
- Esculetin Downregulates the Expression of AML1-ETO and C-Kit in Kasumi-1 Cell Line by Decreasing Half-Life of mRNA.Journal of oncology · 2015Article
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- Drosophila as a model to study the role of blood cells in inflammation, innate immunity and cancer.Frontiers in cellular and infection microbiology · 2014Review
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- Calpain A modulates Toll responses by limited Cactus/IκB proteolysis.Molecular biology of the cell · 2013Article
- Animal models of leukemia: any closer to the real thing?Cancer metastasis reviews · 2013Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The t(8:21)(q22;q22) translocation is 1 of the most common chromosomal abnormalities linked to acute myeloid leukemia (AML). AML1-ETO, the product of this translocation, fuses the N-terminal portion of the RUNX transcription factor AML1 (also known as RUNX1), including its DNA-binding domain, to the almost entire transcriptional corepressor ETO (also known as MTG8 or RUNX1T1). This fusion protein acts primarily by interfering with endogenous AML1 function during myeloid differentiation, although relatively few genes are known that participate with AML1-ETO during leukemia progression. Here, we assessed the consequences of expressing this chimera in Drosophila blood cells. Reminiscent of what is observed in AML, AML1-ETO specifically inhibited the differentiation of the blood cell lineage whose development depends on the RUNX factor Lozenge (LZ) and induced increased numbers of LZ(+) progenitors. Using an in vivo RNAi-based screen for suppressors of AML1-ETO, we identified calpainB as required for AML1-ETO-induced blood cell disorders in Drosophila. Remarkably, calpain inhibition triggered AML1-ETO degradation and impaired the clonogenic potential of the human t(8;21) leukemic blood cell line Kasumi-1. Therefore Drosophila provides a promising genetically tractable model to investigate the conserved basis of leukemogenesis and to open avenues in AML therapy.
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