Taub R, Moulding C, Battey J, Murphy W, Vasicek T, Lenoir G M, Leder P
Cell. 1984 Feb;36(2):339-48. doi: 10.1016/0092-8674(84)90227-7.
In contrast to other human tumors in which the c-myc gene and its transcript are greatly amplified, careful analysis of t(8;14) Burkitt cell lines indicates that the c-myc transcript is marginally, and in some cases not at all, increased by comparison to control lymphoblastoid cell lines. Instead, there is a more subtle alteration in the expression of the translocated c-myc gene characterized by a shift in promoter utilization and an apparent insensitivity to the regulation that inactivates the normal c-myc allele within these same cells. In some Burkitt cell lines, such deregulation might be because of the loss of a putative control region through removal of the large dual promoter/leader segment of the c-myc gene. In other cell lines, however, this deregulation may be explained by somatic mutations that occur within the putative control region even though it is located many hundreds of bases from the translocation breakpoint.
与其他c-myc基因及其转录本大量扩增的人类肿瘤不同,对t(8;14)伯基特细胞系的仔细分析表明,与对照淋巴母细胞系相比,c-myc转录本只是略有增加,在某些情况下根本没有增加。相反,易位的c-myc基因的表达存在更细微的改变,其特征是启动子利用发生改变,并且对使这些相同细胞内正常c-myc等位基因失活的调控明显不敏感。在一些伯基特细胞系中,这种失调可能是由于c-myc基因的大型双启动子/前导序列被去除,从而导致一个假定的控制区域丢失。然而,在其他细胞系中,这种失调可能是由假定控制区域内发生的体细胞突变所解释的,尽管该区域距离易位断点有数百个碱基。