ABL-BCR expression in BCR-ABL-positive human leukemia cell lines

被引:21
作者
Uphoff, CC
Habig, S
Fombonne, S
Matsuo, Y
Drexler, HG
机构
[1] DSMZ German Collect Microorganisms & Cell Culture, Dept Human & Anim Cell Cultures, D-38124 Braunschweig, Germany
[2] Fujisaki Cell Ctr, Hayashibara Biomed Labs, Okayama, Japan
关键词
Philadelphia chromosome; ABL; m-bcr; M-bcr; mu-bcr; cell lines;
D O I
10.1016/S0145-2126(99)00131-9
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Expression of normal ABL and BCR and of reciprocal fusion genes BCR-ABL and ABL-BCR was examined in a panel of 53 BCR-ABL-positive cell lines by RT-PCR to determine the influence of the various transcripts on leukemogenesis. Seventeen out of 18 lymphoid cell lines expressed ABL1a and/or ABL1b, whereas only 16 out of 35 myeloid cell lines expressed one or both normal ABL transcripts. Normal BCR was expressed in seven lymphoid cell lines; all cell lines from the m-bcr group (n = 9) were BCR-negative. Among the myeloid cell lines, 77% expressed the BCR gene. The M-bcr and m-bcr translocations were equally distributed among cell lines with lymphoid phenotype. The m-bcr translocation was not found in myeloid cell lines. b3-a2 constitutes the predominant form of fusion gene in myeloid cell lines with an incidence of about 68%. One myeloid cell line exhibited the mu-bcr variant. An ABL-BCR transcript of the la splice variant was not detected in any of the cell lines. ABL1b-BCR was expressed in all varieties of cell types and translocation forms: 56 and 66% in the lymphoid and myeloid cell lines, respectively; similar distributions were found for the fusion gene types: 67% among e1-a2, 73% among b2-a2, and 61% among b3-a2 translocations. Except for the lack of expression of normal BCR in m-bcr cell lines and of ABL1a-BCR expression in all cell lines, no consistent correlation of expression or lack of expression of BCR and ABL or of ABL-BCR reciprocal fusion genes could be found with cell lineages and translocation types. Further work is required to determine the exact role of the reciprocal fusion gene transcripts on the pathophysiological mechanisms of leukemogenesis. (C) 1999 Published by Elsevier Science Ltd. All rights reserved.
引用
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页码:1055 / 1060
页数:6
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