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T细胞急性淋巴细胞白血病患者中因t(1;5)(p32;31)导致TAL1基因表达失调。

Deregulated expression of the TAL1 gene by t(1;5)(p32;31) in patient with T-cell acute lymphoblastic leukemia.

作者信息

François S, Delabesse E, Baranger L, Dautel M, Foussard C, Boasson M, Blanchet O, Bernard O, Macintyre E A, Ifrah N

机构信息

Department of Clinical Hematology, Hôtel Dieu Hospital, Angers, France.

出版信息

Genes Chromosomes Cancer. 1998 Sep;23(1):36-43. doi: 10.1002/(sici)1098-2264(199809)23:1<36::aid-gcc6>3.0.co;2-7.

Abstract

TAL1 gene deregulation is frequent in T-cell acute lymphoblastic leukemia (T-ALL) and can result from translocations involving 1p32 or, more frequently, from a cytogenetically undetectable interstitial deletion of chromosome 1. This study presents a case of T-ALL with a t(1;5)(p32;q31) involving TAL1, in which the breakpoint occurs approximately 10kbp 5' to the gene and leads to transcriptional activation and synthesis of a TAL1 protein, and extends the spectrum of recognized TAL1 gene translocations associated with T-ALL.

摘要

TAL1基因失调在T细胞急性淋巴细胞白血病(T-ALL)中很常见,可能由涉及1p32的易位引起,或者更常见的是由细胞遗传学检测不到的1号染色体间质性缺失导致。本研究报告了一例T-ALL病例,其发生了涉及TAL1的t(1;5)(p32;q31),其中断点出现在该基因5'端约10kbp处,导致TAL1蛋白的转录激活和合成,并扩展了与T-ALL相关的已识别TAL1基因易位的范围。

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