6533b861fe1ef96bd12c4f49

RESEARCH PRODUCT

MOZ/TIF2-induced acute myeloid leukaemia in transgenic fish.

Julia ZhuravlevaArlette HammannLaurent DelvaLaurent DelvaJérôme PaggettiJérôme PaggettiJean-noël BastieJean-noël BastieEric SolaryEric SolaryLaurent Martin

subject

MyeloidMicroinjectionsOncogene Proteins FusionTransgeneBiologyKidneyMYST3Fusion geneAnimals Genetically ModifiedNuclear Receptor Coactivator 2hemic and lymphatic diseasesmedicineAnimalsZebrafishGeneZebrafishHistone AcetyltransferasesSPI1Reverse Transcriptase Polymerase Chain ReactionHematologymedicine.diseasebiology.organism_classificationMolecular biologyLeukemiaDisease Models AnimalLeukemia Myeloid Acutemedicine.anatomical_structureembryonic structuresCancer researchGene Fusion

description

The inv(8)(p11q13) chromosomal abnormality, described in acute myeloid leukaemias (AML), fuses the histone acetyl-transferase (HAT) MYST3 (MOZ) gene with another HAT gene, NCOA2 (TIF2). We generated a transgenic zebrafish in which the MYST3/NCOA2 fusion gene was expressed under control of the spi1 promoter. An AML developed in 2 of 180 MYST3/NCOA2-EGFP-expressing embryos, 14 and 26 months after injection of the fusion gene in a one-cell embryo, respectively. This leukaemia was characterised by an extensive invasion of kidneys by myeloid blast cells. This model, which is the first zebrafish model of AML, demonstrates the oncogenic potency of MYST3/NCOA2 fusion gene.

yearjournalcountryeditionlanguage
2008-08-30British journal of haematology
10.1111/j.1365-2141.2008.07362.xhttps://pubmed.ncbi.nlm.nih.gov/18729850