Potter M, Mushinski J F, Mushinski E B, Brust S, Wax J S, Wiener F, Babonits M, Rapp U R, Morse H C
Science. 1987 Feb 13;235(4790):787-9. doi: 10.1126/science.3810165.
Deregulation of c-myc expression in association with chromosomal translocations occurs in over 95% of murine plasmacytomas, rat immunocytomas, and human Burkitt lymphomas. Infection with a murine retrovirus (J-3) containing an avian v-myc rapidly induced plasmacytomas in pristane-primed BALB/cAn mice. Only 17% of the induced plasmacytomas that were karyotyped showed the characteristic chromosomal translocations involving the c-myc locus. Instead, all of the translocation-negative tumors demonstrated characteristic J-3 virus integration sites that were actively transcribed. Thus, the high levels of v-myc expression have replaced the requirement for chromosomal translocation in plasmacytomagenesis and accelerated the process of transformation.
超过95%的鼠浆细胞瘤、大鼠免疫细胞瘤和人类伯基特淋巴瘤中,c-myc表达失调与染色体易位相关。用含有禽v-myc的鼠逆转录病毒(J-3)感染在 pristane 预处理的 BALB/cAn 小鼠中可迅速诱发浆细胞瘤。在进行核型分析的诱导浆细胞瘤中,只有17%显示出涉及c-myc基因座的特征性染色体易位。相反,所有易位阴性肿瘤都显示出活跃转录的特征性J-3病毒整合位点。因此,高水平的v-myc表达取代了浆细胞瘤发生过程中对染色体易位的需求,并加速了转化过程。