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September 1999, Volume 13, Number 9, Pages 1359-1366
Table of contents    Previous  Abstract  Next   Article  PDF
Original manuscript
Activation of EVI1 transcripts with chromosomal translocation joining the TCRVbold italic beta locus and the EVI1 gene in human acute undifferentiated leukemia cell line (Kasumi-3) with a complex translocation of der(3)t(3;7;8)
K Suzukawa1,2, T Kodera1, S Shimizu1, T Nagasawa2, H Asou3, N Kamada3, M Taniwaki4, J Yokota1 and K Morishita1

1Biology Division, National Cancer Center Research Institute, Tokyo, Japan

2Division of Hematology, Institute of Clinical Medicine, University of Tsukuba, Ibaraki, Japan

3Department of Cancer Cytogenetics, Research Institute for Radiation Biology and Medicine, Hiroshima University, Hiroshima, Japan

4Third Department of Internal Medicine, Kyoto Prefectural University of Medicine, Kyoto, Japan

Correspondence to: K Morishita, Biology Division, National Cancer Center Research Institute, 1-1, Tsukiji 5-chome, Chuo-ku, Tokyo 104, Japan; Fax: 81 3 3542 0807

Abstract

A cell line (Kasumi-3) established from acute myeloid leukemia (AML-M0) had unique phenotypes of undifferentiated leukemia cells with expression of both T cell and myeloid antigens. Kasumi-3 cells with t(3;7)(q26;q22) highly expressed a 6 kb transcript of EVI1, which is located on chromosome 3q26. Therefore, we further characterized the chromosomal breakpoint by pulsed-field gel electrophoresis near EVI1. We identified and isolated the chromosomal breakpoint at approximately 80 kb upstream from the 5' end of EVI1. Sequence analysis of the breakpoint revealed that the whole Vbeta region from T cell receptor beta (TCRbeta) at 7q35 was translocated to the upstream of EVI1. A 1.0 kb TCRbeta transcript was expressed in the Kasumi-3 cells, suggesting that TCRbeta rearrangement occurred as Dbeta-Jbeta joining events. Fluorescence in situ hybridization analysis revealed that the inverted chromosome 7q22-q35 segment between TCRbeta and the region proximal to the erythropoietin gene at 7q22 was translocated to the region distal to EVI1 in der(3). Since the telomeric region of chromosome 8 q was also translocated to the inverted chromosome 7q22-q35 segment in der(3), the chromosomal abnormalities of der(3) were defined as being der(3)t(3;7;8)(3pter-3q26::7q35-7q22::8q22-8qter). It is suggested that a translocated enhancer element in the TCRbeta locus and/or loss of a negative regulatory element near EVI1 might function to enhance the EVI1 expression. Therefore, the enhanced EVI1 expression may contribute to the development of a subset of undifferentiated leukemia.

Keywords

EVI1; TCRbeta; Kasumi-3; chromosomal breakpoint; AML (FAB-M0)

Received 12 November 1998; accepted 23 April 1999
September 1999, Volume 13, Number 9, Pages 1359-1366
Table of contents    Previous  Abstract  Next   Article  PDF