Narducci M G, Virgilio L, Isobe M, Stoppacciaro A, Elli R, Fiorilli M, Carbonari M, Antonelli A, Chessa L, Croce C M, Russo G
Laboratory of Molecular Genetics, Raggio-Italgene, Pomezia, Rome, Italy.
Blood. 1995 Sep 15;86(6):2358-64.
The TCL1 oncogene on human chromosome 14q32.1 is involved in chromosome translocations [t(14;14)(q11;q32.1) and t(7;14)(q35;q32.1)] and inversions [inv14(q11;q32.1)] with TCR alpha/beta loci in T-cell leukemias, such as T-prolymphocytic (T-PLL). It is also involved in T-acute and -chronic leukemias arising in cases of ataxia-telangiectasia (AT), an immunodeficiency syndrome. Similar chromosomal rearrangements occur also in the clonally expanded T cells in AT patients before the appearance of the overt leukemia. We have analyzed the expression of TCL1 mRNA and protein in peripheral blood lymphocytes (PBLs) from four AT cases and from healthy controls. We found that the TCL1 gene was overexpressed in the PBLs of an AT patient with a large clonal T-cell population exhibiting the t(14;14) translocation but not in the lymphocytes of the other cases. Fluorescence in situ hybridization of the TCL1 genomic locus to lymphocyte metaphases from the AT patient with the T-cell clonal expansion showed that the breakpoint of the t(14;14) translocation lies within the TCL1 locus and is accompanied by an inverted duplication of the distal part of chromosome 14. These data indicate that TCL1 is activated in preleukemic clonal cells as a consequence of chromosome translocation involving sequences from the TCR locus at 14q11. Deregulation of TCL1 is the first event in the initiation of malignancy in these types of leukemias and represents a potential tool for clinical evaluation.
人类染色体14q32.1上的TCL1癌基因参与了T细胞白血病(如T - 前淋巴细胞白血病,T - PLL)中与TCRα/β基因座的染色体易位[t(14;14)(q11;q32.1)和t(7;14)(q35;q32.1)]及倒位[inv14(q11;q32.1)]。它也与共济失调毛细血管扩张症(AT,一种免疫缺陷综合征)患者发生的T急性和慢性白血病有关。在明显白血病出现之前,AT患者克隆性扩增的T细胞中也会发生类似的染色体重排。我们分析了4例AT患者和健康对照外周血淋巴细胞(PBL)中TCL1 mRNA和蛋白的表达。我们发现,在一名具有大量表现出t(14;14)易位的克隆性T细胞群体的AT患者的PBL中,TCL1基因过表达,而在其他病例的淋巴细胞中未过表达。对具有T细胞克隆扩增的AT患者淋巴细胞中期进行TCL1基因组位点的荧光原位杂交显示,t(14;14)易位的断点位于TCL1基因座内,并伴有14号染色体远端部分的反向重复。这些数据表明,由于涉及14q11处TCR基因座序列的染色体易位,TCL1在白血病前期克隆细胞中被激活。TCL1的失调是这些类型白血病发生恶性肿瘤的首个事件,代表了一种潜在的临床评估工具。