Activation of evi1 transcripts with chromosomal translocation joining the tcrvβ 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)


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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 Vβ region from T cell receptor beta (TCRβ) at 7q35 was translocated to the upstream of _EVI1_. A 1.0 kb _TCR_β transcript was expressed in the Kasumi-3


cells, suggesting that _TCR_β rearrangement occurred as Dβ–Jβ joining events. Fluorescence _in situ_ hybridization analysis revealed that the inverted chromosome 7q22-q35 segment between


_TCR_β 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 _TCR_β 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. Access through your institution Buy or subscribe This is a preview of subscription


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29 November 2022 AUTHOR INFORMATION AUTHORS AND AFFILIATIONS * Biology Division, National Cancer Center Research Institute, Tokyo, Japan K Suzukawa, T Kodera, S Shimizu, J Yokota & K


Morishita * Division of Hematology, Institute of Clinical Medicine, University of Tsukuba, Ibaraki, Japan K Suzukawa & T Nagasawa * Department of Cancer Cytogenetics, Research Institute


for Radiation Biology and Medicine, Hiroshima University, Hiroshima, Japan H Asou & N Kamada * Third Department of Internal Medicine, Kyoto Prefectural University of Medicine, Kyoto,


Japan M Taniwaki Authors * K Suzukawa View author publications You can also search for this author inPubMed Google Scholar * T Kodera View author publications You can also search for this


author inPubMed Google Scholar * S Shimizu View author publications You can also search for this author inPubMed Google Scholar * T Nagasawa View author publications You can also search for


this author inPubMed Google Scholar * H Asou View author publications You can also search for this author inPubMed Google Scholar * N Kamada View author publications You can also search for


this author inPubMed Google Scholar * M Taniwaki View author publications You can also search for this author inPubMed Google Scholar * J Yokota View author publications You can also search


for this author inPubMed Google Scholar * K Morishita View author publications You can also search for this author inPubMed Google Scholar RIGHTS AND PERMISSIONS Reprints and permissions


ABOUT THIS ARTICLE CITE THIS ARTICLE Suzukawa, K., Kodera, T., Shimizu, S. _et al._ Activation of _EVI1_ transcripts with chromosomal translocation joining the _TCRVβ_ 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). _Leukemia_ 13, 1359–1366 (1999). https://doi.org/10.1038/sj.leu.2401483


Download citation * Received: 12 November 1998 * Accepted: 23 April 1999 * Published: 09 September 1999 * Issue Date: 01 September 1999 * DOI: https://doi.org/10.1038/sj.leu.2401483 SHARE


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clipboard Provided by the Springer Nature SharedIt content-sharing initiative KEYWORDS * _EVI1_ * _TCRβ_ * Kasumi-3 * chromosomal breakpoint * AML (FAB-M0)