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Generation of the AML1-EVI-1 fusion gene in the t(3;21)(q26;q22) causes blastic crisis in chronic myelocytic leukemia.

1994; Springer Nature; Volume: 13; Issue: 3 Linguagem: Inglês

10.1002/j.1460-2075.1994.tb06288.x

1460-2075

Kinuko Mitani, Seishi Ogawa, Tetsuhiro Tanaka, Hiroyuki Miyoshi, Mineo Kurokawa, Hiroyuki Mano, Y Yazaki, Masafumi Ohki, Hisamaru Hirai,

Chronic Myeloid Leukemia Treatments

Research Article1 February 1994free access Generation of the AML1-EVI-1 fusion gene in the t(3;21)(q26;q22) causes blastic crisis in chronic myelocytic leukemia. K. Mitani K. Mitani Third Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan. Search for more papers by this author S. Ogawa S. Ogawa Third Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan. Search for more papers by this author T. Tanaka T. Tanaka Third Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan. Search for more papers by this author H. Miyoshi H. Miyoshi Third Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan. Search for more papers by this author M. Kurokawa M. Kurokawa Third Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan. Search for more papers by this author H. Mano H. Mano Third Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan. Search for more papers by this author Y. Yazaki Y. Yazaki Third Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan. Search for more papers by this author M. Ohki M. Ohki Third Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan. Search for more papers by this author H. Hirai H. Hirai Third Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan. Search for more papers by this author K. Mitani K. Mitani Third Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan. Search for more papers by this author S. Ogawa S. Ogawa Third Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan. Search for more papers by this author T. Tanaka T. Tanaka Third Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan. Search for more papers by this author H. Miyoshi H. Miyoshi Third Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan. Search for more papers by this author M. Kurokawa M. Kurokawa Third Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan. Search for more papers by this author H. Mano H. Mano Third Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan. Search for more papers by this author Y. Yazaki Y. Yazaki Third Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan. Search for more papers by this author M. Ohki M. Ohki Third Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan. Search for more papers by this author H. Hirai H. Hirai Third Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan. Search for more papers by this author Author Information K. Mitani1, S. Ogawa1, T. Tanaka1, H. Miyoshi1, M. Kurokawa1, H. Mano1, Y. Yazaki1, M. Ohki1 and H. Hirai1 1Third Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan. The EMBO Journal (1994)13:504-510https://doi.org/10.1002/j.1460-2075.1994.tb06288.x PDFDownload PDF of article text and main figures. ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinked InMendeleyWechatReddit Figures & Info The t(3;21)(q26;q22) translocation, which is one of the consistent chromosomal abnormalities found in blastic crisis of chronic myelocytic leukemia (CML), is thought to play an important role in the leukemic progression of CML to an acute blastic crisis phase. The AML1 gene, which is located at the translocation breakpoint of the t(8;21)(q22;q22) translocation found in acute myelocytic leukemia, was also rearranged by the t(3;21)(q26;q22) translocation. Screening of a cDNA library of the t(3;21)-carrying leukemic cell line cells (SKH1) resulted in the isolation of two potentially complete AML1-EVI-1 chimeric cDNAs of 6 kb. Two species of AML1-EVI-1 fusion transcripts of 8.2 and 7.0 kb were detected in SKH1 cells. These cells expressed the 180 kDa AML1-EVI-1 fusion protein containing an N-terminal half of AML1 including a runt homology domain which is fused to the entire zinc finger EVI-1 protein. The AML1-EVI-1 fusion transcript was consistent in all three cases of the t(3;21)-carrying leukemia examined by RNA-based PCR. These findings strongly suggest that the t(3;21) translocation results in the formation of a new class of chimeric transcription factor which could contribute to the leukemic progression of CML through interference with cell growth and differentiation. Previous ArticleNext Article Volume 13Issue 31 February 1994In this issue RelatedDetailsLoading ...