Akao Y, Tsujimoto Y, Finan J, Nowell P C, Croce C M
Fels Institute for Cancer Research and Molecular Biology, Temple University School of Medicine, Philadelphia, Pennsylvania 19140.
Cancer Res. 1990 Aug 15;50(16):4856-9.
We have analyzed the molecular features of a t(11;14)(q23;q32) chromosome translocation of a cell line established from a B-cell lymphoma. Somatic hybrid cells carrying the 11q- and/or 14q+ chromosome(s) were produced in order to map the breakpoints. Southern blot analyses of DNAs from these hybrid cell lines together with various probes from the IGH locus on chromosome 14 and the ETS-1 and CD3 genes on chromosome 11 showed that the breakpoints of the translocation occurred between the constant regions of the C phi gamma and C gamma 2 genes on chromosome 14 and between the CD3 and ETS-1 genes on chromosome 11. The t(11;14)(q23;q32) translocation does not seem to involve the same mechanism that is responsible for translocations occurring at the immunoglobulin heavy chain joining segment (JH).
我们分析了一株源自B细胞淋巴瘤的细胞系中t(11;14)(q23;q32)染色体易位的分子特征。为了定位断点,构建了携带11号染色体长臂缺失和/或14号染色体长臂增加的体细胞杂种细胞。对这些杂种细胞系的DNA进行Southern印迹分析,并结合来自14号染色体上IGH基因座以及11号染色体上ETS-1和CD3基因的各种探针,结果显示该易位的断点分别位于14号染色体上C phi gamma和C gamma 2基因的恒定区之间,以及11号染色体上CD3和ETS-1基因之间。t(11;14)(q23;q32)易位似乎并不涉及与免疫球蛋白重链连接段(JH)处发生的易位相同的机制。