Axelson H, Panda C K, Silva S, Sugiyama H, Wiener F, Klein G, Sumegi J
Department of Tumor Biology, Karolinska Institute, Stockholm, Sweden.
Oncogene. 1991 Dec;6(12):2263-70.
Mouse plasmacytomas (MPCs) induced by pristane oil, or by a combination of pristane oil and Abelson virus, carry one of two chromosomal translocations. The typical 12; 15 translocation leads to the juxtaposition of c-myc and immunoglobulin heavy-chain sequences, whereas the 6; 15 translocation links the kappa light-chain locus with the pvt-1 (plasmacytoma variant translocation) locus, located at least 75kb 3' of c-myc [Cory, S., Graham, M., Webb, E., Corcoran, L. & Adams, J. (1985). EMBO J., 4, 675-681]. Unlike the human Burkitt's lymphoma-associated translocation, the lambda/myc juxtaposed variant translocation has not been found previously in MPCs. Using unconventional MPC induction systems in which the tumor precursor cell was induced to proliferate in a secondary host, we have recently identified a 15; 16 translocation in six of the derived MPCs [Wiener, F., Silva, S., Sugiyama, H., Babonits, M. & Klein, G. (1990). Genes Chromosomes Cancer, 2, 36-43]. Chromosome 16 harbors the lambda light-chain gene. To explore whether the 15; 16 translocation represents the lambda/myc juxtaposition, we have mapped the breakpoints on chromosomes 15 and 16 by pulsed-field gel electrophoresis (PFGE). The pvt-1 region was mapped to approximately 220 kb 3' of c-myc. The breakpoint on chromosome 15 in ABPC-Ch-163-10, one of the six 15; 16 translocation-carrying MPCs, was situated approximately 80 kb 3' of c-myc and 140 kb 5' of pvt-1b, the major breakpoint cluster region of the previously analysed 6; 15 variant MPCs. The breakpoint on chromosome 16 was found to cut between the V1 and C3 regions of the lambda locus. Co-migration experiments showed that the C3 and the myc gene were juxtaposed head to tail on the 15; 16 translocation chromosome. On the reciprocal product V1 was juxtaposed to pvt-1.
由 pristane 油或 pristane 油与 Abelson 病毒联合诱导产生的小鼠浆细胞瘤(MPC)携带两种染色体易位之一。典型的 12; 15 易位导致 c-myc 与免疫球蛋白重链序列并列,而 6; 15 易位则将κ轻链基因座与位于 c-myc 下游至少 75kb 的 pvt-1(浆细胞瘤变异易位)基因座相连[Cory, S., Graham, M., Webb, E., Corcoran, L. & Adams, J. (1985). EMBO J., 4, 675 - 681]。与人类伯基特淋巴瘤相关的易位不同,λ/myc 并列变异易位此前在 MPC 中尚未被发现。利用非常规的 MPC 诱导系统,其中肿瘤前体细胞在二级宿主中被诱导增殖,我们最近在六个衍生的 MPC 中鉴定出了 15; 16 易位[Wiener, F., Silva, S., Sugiyama, H., Babonits, M. & Klein, G. (1990). Genes Chromosomes Cancer, 2, 36 - 43]。16 号染色体包含λ轻链基因。为了探究 15; 16 易位是否代表λ/myc 并列,我们通过脉冲场凝胶电泳(PFGE)绘制了 15 号和 16 号染色体上的断点。pvt-1 区域被定位到 c-myc 下游约 220kb 处。在六个携带 15; 16 易位的 MPC 之一 ABPC-Ch-163-10 中,15 号染色体上的断点位于 c-myc 下游约 80kb 处,且在 pvt-1b(先前分析的 6; 15 变异 MPC 的主要断点簇区域)上游 140kb 处。发现 16 号染色体上的断点在λ基因座的 V1 和 C3 区域之间切断。共迁移实验表明,在 15; 16 易位染色体上,C3 和 myc 基因头对尾并列。在相互产物上,V1 与 pvt-1 并列。