Stewart T A, Pattengale P K, Leder P
Cell. 1984 Oct;38(3):627-37. doi: 10.1016/0092-8674(84)90257-5.
We have produced 13 strains of transgenic mice that carry an otherwise normal mouse myc gene in which increasingly larger portions of the myc promoter region have been replaced by a hormonally inducible mouse mammary tumor virus promoter. Although expression of the fusion genes varies among these animals, the female founders of two of these transgenic strains spontaneously developed mammary adenocarcinomas during one of their early pregnancies. Both the tumors and the breast tissue of these founder animals expressed RNA transcripts corresponding to the fusion gene. Furthermore, in the best studied strain, all the available F1 female progeny that inherited the MTV/myc gene also developed mammary adenocarcinomas during their second or third pregnancies. Thus, although it has no obvious effect on the early development of these mice, the constitutionally deregulated myc gene appears to act as a heritable, predisposing factor favoring the accelerated development of a tissue-specific adenocarcinoma.
我们已经培育出13株转基因小鼠，它们携带一个原本正常的小鼠myc基因，其中越来越大的myc启动子区域已被激素诱导型小鼠乳腺肿瘤病毒启动子所取代。尽管这些动物中融合基因的表达各不相同，但其中两个转基因品系的雌性奠基者在其早期怀孕的某一阶段自发地发展出了乳腺腺癌。这些奠基动物的肿瘤和乳腺组织都表达了与融合基因相对应的RNA转录本。此外，在研究最深入的品系中，所有继承了MTV/myc基因的F1雌性后代在其第二次或第三次怀孕期间也都发展出了乳腺腺癌。因此，尽管它对这些小鼠的早期发育没有明显影响，但组成型失调的myc基因似乎作为一种可遗传的易感因素，有利于组织特异性腺癌的加速发展。
