Growth inhibition of leukaemic cells carrying the t(3;21) by the AML1/EVI-1-specific antisense oligonucleotide.
The t(3;21)(q26;q22) translocation is thought to play an important role in the acute phase transformation of CML. The formation of the AML1/EVI-1 fusion gene by the translocation leads to expression of the AML1/EVI-1 fusion protein. Here we demonstrate that the AML1/EVI-1-specific antisense oligonucleotide markedly decreases the [3H]thymidine incorporation and growth of leukaemic cells carrying the t(3;21) and the t(9;22), but not those of K562 cells. These results indicate that the AML1/EVI-1 fusion protein could contribute to proliferation of the t(3;21)-carrying leukaemic cells after entering the blastic crisis phase of CML.
Mitani
K
K
Third Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan.
Ogawa
S
S
Tanaka
T
T
Kurokawa
M
M
Yazaki
Y
Y
Hirai
H
H
D001483:Base Sequence; D002455:Cell Division; D002891:Chromosomes, Human, Pair 21; D002893:Chromosomes, Human, Pair 3; D006801:Humans; D015470:Leukemia, Myeloid, Acute / Q000235:genetics* / Q000473:pathology; D008969:Molecular Sequence Data; D016376:Oligonucleotides, Antisense / Q000235:genetics*; D015514:Oncogene Proteins, Fusion; D014178:Translocation, Genetic; D014407:Tumor Cells, Cultured
D016376:Oligonucleotides, Antisense; D015514:Oncogene Proteins, Fusion