Kaneko Y, Maseki N, Homma C, Sakurai M, Mizutani S, Takeda T, Shikano T, Fujimoto T, Yaoi K, Shimokawa T
Department of Laboratory Medicine, Saitama Cancer Center, Japan.
Blood. 1988 Aug;72(2):534-8.
In a chromosome study in childhood T-cell leukemia/lymphoma, we found t(7;11)(q35;p13) in 2 patients, t(7;14) (q35;q11) in one patient, and t(7;14)(p15;q32) in 1 patient. Southern blotting and in situ chromosomal hybridization studies in one patient with the t(7;11) demonstrated that both alleles of the T-cell antigen receptor beta-subunit gene (TCRB) were rearranged, and that one TCRB allele had relocated from 7q35 to the fusion point in band p13 of the involved chromosome 11 (11p-). These findings suggest that juxtaposition of TCRB with the putative oncogene tcl-2 located in band 11p13 may be a critical step toward development of this T-cell leukemia/lymphoma. In the other two translocations, all breakpoints were sites for lymphocyte function genes, ie, 7q35 for TCRB, 14q11 for T-cell antigen receptor alpha-subunit gene (TCRA), 7p15 for T-cell antigen receptor alpha-subunit gene (TCRG), and 14q32 for immunoglobulin heavy-chain gene (IGH). Thus, the findings in these cases allow us to expand the above hypothesis and propose that the juxtaposition of TCRB or TCRG with tcl-2, TCRA, or IGH through chromosomal translocation may activate a mechanism for the genesis of T-cell leukemia/lymphoma with these chromosome translocations.
在一项针对儿童T细胞白血病/淋巴瘤的染色体研究中，我们在2例患者中发现了t(7;11)(q35;p13)，在1例患者中发现了t(7;14)(q35;q11)，在1例患者中发现了t(7;14)(p15;q32)。对1例携带t(7;11)的患者进行的Southern印迹法和原位染色体杂交研究表明，T细胞抗原受体β亚基基因（TCRB）的两个等位基因均发生了重排，并且一个TCRB等位基因已从7q35移位至受累染色体11（11p-）带p13的融合点。这些发现表明，TCRB与位于11p13带的假定癌基因tcl-2并列可能是该T细胞白血病/淋巴瘤发生发展的关键步骤。在其他两种易位中，所有断点均为淋巴细胞功能基因的位点，即TCRB的7q35、T细胞抗原受体α亚基基因（TCRA）的14q11、T细胞抗原受体α亚基基因（TCRG）的7p15以及免疫球蛋白重链基因（IGH）的14q32。因此，这些病例中的发现使我们能够扩展上述假设，并提出通过染色体易位使TCRB或TCRG与tcl-2、TCRA或IGH并列可能激活了这些染色体易位所致T细胞白血病/淋巴瘤发生的机制。
