Lu M, Gong Z Y, Shen W F, Ho A D
Northeastern Ontario Regional Cancer Centre, Sudbury, Ontario, Canada.
EMBO J. 1991 Oct;10(10):2905-10. doi: 10.1002/j.1460-2075.1991.tb07840.x.
The t(10;14)(q24;q11) chromosomal translocation found in malignant cells of 5-10% of patients with T-cell acute lymphoblastic leukemia (T-ALL) involves the T-cell receptor delta chain gene on chromosome 14 and a breakpoint cluster region on chromosome 10. The candidate proto-oncogene tcl-3, thought to be involved in the pathogenesis of t(10;14) T-ALL, was cloned and found to be elevated in expression in leukemic cells harboring the t(10;14) translocation. Sequence analysis revealed that tcl-3 is a new homeobox-containing gene. Comparison of the tcl-3 cDNA and its 5' genomic sequences with DNA sequences from the t(10;14) translocation breakpoints showed that this gene is structurally altered in four patients with t(10;14)(q24;q11) T-ALL. These findings suggest that homeobox-containing genes that normally act as transcription factors may contribute to T-cell leukemogenesis when abnormally expressed.
在5%-10%的T细胞急性淋巴细胞白血病(T-ALL)患者的恶性细胞中发现的t(10;14)(q24;q11)染色体易位涉及14号染色体上的T细胞受体δ链基因和10号染色体上的一个断裂点簇区域。候选原癌基因tcl-3被认为与t(10;14) T-ALL的发病机制有关,已被克隆,并发现其在携带t(10;14)易位的白血病细胞中的表达升高。序列分析显示,tcl-3是一个新的含同源框基因。将tcl-3 cDNA及其5'基因组序列与t(10;14)易位断点处的DNA序列进行比较,结果表明该基因在4例t(10;14)(q24;q11) T-ALL患者中发生了结构改变。这些发现表明,正常情况下作为转录因子的含同源框基因在异常表达时可能会促进T细胞白血病的发生。