The t(10;14)(q24;q11) of T-cell acute lymphoblastic leukemia juxtaposes the delta T-cell receptor with TCL3, a conserved and activated locus at 10q24.
The t(10;14)(q24;q11) of T-cell acute lymphoblastic leukemia juxtaposes the delta T-cell receptor with TCL3, a conserved and activated locus at 10q24.
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T 细胞急性淋巴细胞白血病的 t(10;14)(q24;q11) 将 delta T 细胞受体与 TCL3（10q24 上的保守且激活的位点）并置。
DOI：
10.1073/pnas.87.8.3161
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发表时间：
1990
影响因子：
11.1
通讯作者：
Korsmeyer,SJ
中科院分区：
文献类型：
--
作者：
Zutter,M;Hockett,RD;Roberts,CW;McGuire,EA;Bloomstone,J;Morton,CC;Deaven,LL;Crist,WM;Carroll,AJ;Korsmeyer,SJ
我们从CD3阴性的T细胞急性淋巴细胞白血病细胞中克隆了t(10；14)复发性易位。位于14q11的断裂点涉及DeltaT细胞受体基因座的中间重排，提示易位发生在抗原受体组装时。易位引入了染色体片段10q24，断点衍生的探针与流动分离的染色体和中期染色体的杂交证明了这一点。两个t(10；14)断裂点聚集在10q24的600个碱基对区域内，但在断裂点没有发现类似T细胞受体/免疫球蛋白重排信号的七聚体-间隔物-九聚体基序。在10q24处发现了一个与末端脱氧核苷酸转移酶不同的基因座。对10q24断裂点周围进化保守区域的转录活性进行了检测。10q24断裂点的一个区域端粒，预期易位到der(14)染色体，在t(10；14)T细胞白血病中识别丰富的2.9kb的RNA。该基因座在其他各种正常和肿瘤T细胞中并不活跃，认为它被T细胞受体的引入而解除了调控。该基因是与T细胞瘤相关的原癌基因TCL3的候选基因。
We cloned the t(10;14) recurrent translocation from CD3-negative T-cell acute lymphoblastic leukemia cells. The breakpoint at 14q11 involved an intermediate rearrangement of the delta T-cell receptor locus, suggesting that the translocation arose at the time of antigen receptor assemblage. Translocation introduced chromosome segment 10q24 as proven by hybridization of a breakpoint-derived probe to flow-sorted chromosomes and metaphase chromosomes. Two t(10;14) breakpoints were clustered within a 600-base-pair region of 10q24 but no heptamer-spacer-nonamer motifs resembling T-cell receptor/immunoglobulin rearrangement signals were noted at the breakpoint. A locus distinct from terminal deoxynucleotidyltransferase was found at 10q24. Evolutionarily conserved regions surrounding the 10q24 breakpoint were examined for transcriptional activity. A region telomeric to the 10q24 breakpoint, expected to translocate to the der(14) chromosome, recognized an abundant 2.9-kilobase RNA in a t(10;14) T-cell leukemia. This locus was not active in a variety of other normal and neoplastic T cells, arguing that it was deregulated by the introduction of the T-cell receptor. This locus is a candidate for a putative protooncogene, TCL3, involved in T-cell neoplasia.