Stanton L W, Fahrlander P D, Tesser P M, Marcu K B
Nature. 1984;310(5976):423-5. doi: 10.1038/310423a0.
Plasmacytoid tumours in mice and Burkitt's lymphomas in humans display characteristic chromosomal translocations involving the c-myc proto-oncogene. Models to explain quantitative changes in c-myc expression have been proposed based on the loss of normal promoters as a result of translocation. However, alternative explanations, such as somatic mutation are needed to explain altered c-myc expression in the absence of gene breakage. We present here the nucleotide sequence of the normal murine c-myc gene. Comparison of this sequence with that of a translocated c-myc gene from a murine plasmacytoma reveals complete identity of coding sequence. One nucleotide difference was found in the non-coding first exon. This shows that qualitative changes of the c-myc gene product are not required for oncogenesis in murine plasmacytomas. In contrast, mutations are found in coding and non-coding regions of translocated c-myc genes from Burkitt's lymphomas, suggesting that the mechanisms by which c-myc is activated in plasmacytomas and Burkitt's lymphomas are different.
小鼠中的浆细胞样肿瘤和人类中的伯基特淋巴瘤表现出涉及c-myc原癌基因的特征性染色体易位。基于易位导致正常启动子缺失,已提出了解释c-myc表达定量变化的模型。然而,在没有基因断裂的情况下,需要诸如体细胞突变等其他解释来解释c-myc表达的改变。我们在此展示正常小鼠c-myc基因的核苷酸序列。将该序列与来自小鼠浆细胞瘤的易位c-myc基因的序列进行比较,发现编码序列完全相同。在非编码的第一外显子中发现了一个核苷酸差异。这表明在小鼠浆细胞瘤的肿瘤发生过程中,c-myc基因产物的定性变化并非必需。相比之下,在来自伯基特淋巴瘤的易位c-myc基因的编码区和非编码区发现了突变,这表明c-myc在浆细胞瘤和伯基特淋巴瘤中被激活的机制是不同的。