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建立一种新的前体B细胞急性淋巴细胞白血病细胞系(TS-2),其具有不涉及E2A基因的t(1;19)。

Establishment of a novel cell line (TS-2) of pre-B acute lymphoblastic leukemia with a t(1;19) not involving the E2A gene.

作者信息

Yoshinari M, Imaizumi M, Eguchi M, Ogasawara M, Saito T, Suzuki H, Koizumi Y, Cui Y, Sato A, Saisho T, Ichinohasama R, Matsubara Y, Kamada N, Iinuma K

机构信息

Department of Pediatrics, Tohoku University School of Medicine, Sendai, Japan.

出版信息

Cancer Genet Cytogenet. 1998 Mar;101(2):95-102. doi: 10.1016/s0165-4608(97)00260-4.

Abstract

The t(1;19)(q23;p13) translocation involving the E2A gene on chromosome 19p13.3 is a nonrandom translocation that is often seen in childhood pre-B-cell acute lymphoblastic leukemia (ALL). However, recent studies have demonstrated the presence of immunophenotypic and molecular heterogeneity among patients with the cytogenetically identical chromosome translocation. Here we report a novel pre-B ALL cell line, TS-2, with t(1;19) translocation not involving the E2A gene. The breakpoint of t(1;19) in TS-2 was demonstrated to be at 19p13.3, a region indistinguishable from the locus of the E2A gene, by cytogenetic study and fluorescence in situ hybridization. However, rearrangement of the E2A gene was not detected in TS-2 by Southern blot analysis. Moreover, the expressions of PBX1 or E2A/PBX1 fusion genes were not detected by an extensive study with Northern blot analysis and reverse transcription-polymerase chain reaction. These findings suggest that TS-2 may have a genetic abnormality involving uncharacterized gene(s) at 19p13.3 distinct from the E2A gene and, therefore, may be useful for investigating the heterogeneity of molecular pathogenesis in leukemias with t(1;19)(q23;p13) translocation.

摘要

涉及19号染色体p13.3上E2A基因的t(1;19)(q23;p13)易位是一种非随机易位,常见于儿童前B细胞急性淋巴细胞白血病(ALL)。然而,最近的研究表明,在细胞遗传学上具有相同染色体易位的患者中存在免疫表型和分子异质性。在此,我们报告了一种新的前B ALL细胞系TS-2,其具有不涉及E2A基因的t(1;19)易位。通过细胞遗传学研究和荧光原位杂交证实,TS-2中t(1;19)的断点位于19p13.3,该区域与E2A基因座无法区分。然而,通过Southern印迹分析在TS-2中未检测到E2A基因重排。此外,通过Northern印迹分析和逆转录-聚合酶链反应的广泛研究未检测到PBX1或E2A/PBX1融合基因的表达。这些发现表明,TS-2可能具有涉及19p13.3上不同于E2A基因的未表征基因的遗传异常,因此可能有助于研究具有t(1;19)(q23;p13)易位的白血病分子发病机制的异质性。

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