PUBLICATION

MOZ/TIF2-induced acute myeloid leukaemia in transgenic fish

Authors
Zhuravleva, J., Paggetti, J., Martin, L., Hammann, A., Solary, E., Bastie, J.N., and Delva, L.
ID
ZDB-PUB-080902-17
Date
2008
Source
British journal of haematology   143(3): 378-382 (Journal)
Registered Authors
Keywords
MYST3/NCOA2, histone acetyl-transferase, acute myeloid leukaemia, zebrafish, animal model
MeSH Terms
  • Animals
  • Animals, Genetically Modified
  • Disease Models, Animal
  • Gene Fusion
  • Histone Acetyltransferases/genetics*
  • Histone Acetyltransferases/metabolism
  • Kidney/pathology
  • Leukemia, Myeloid, Acute/genetics*
  • Leukemia, Myeloid, Acute/metabolism
  • Leukemia, Myeloid, Acute/pathology
  • Microinjections/methods
  • Nuclear Receptor Coactivator 2/genetics*
  • Nuclear Receptor Coactivator 2/metabolism
  • Oncogene Proteins, Fusion/genetics*
  • Oncogene Proteins, Fusion/metabolism
  • Reverse Transcriptase Polymerase Chain Reaction/methods
  • Zebrafish/genetics
PubMed
18729850 Full text @ Br. J. Haematol.
Abstract
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.
Genes / Markers
Figures
Show all Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping