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Growth inhibition of leukaemic cells carrying the t(3;21) by the AML1/EVI‐1 ‐specific antisense oligonucleotide
Author(s) -
MITANI KINUKO,
OGAWA SEISHI,
TANAKA TOMOYUKI,
KUROKAWA MINEO,
YAZAKI YOSHIO,
HIRAI HISAMARU
Publication year - 1995
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.1995.tb05606.x
Subject(s) - fusion protein , chromosomal translocation , microbiology and biotechnology , oligonucleotide , biology , cancer research , fusion gene , k562 cells , chemistry , leukemia , gene , immunology , genetics , recombinant dna
Summary. 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 [H]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.