Quaife C J, Pinkert C A, Ornitz D M, Palmiter R D, Brinster R L
Cell. 1987 Mar 27;48(6):1023-34. doi: 10.1016/0092-8674(87)90710-0.
Expression of an activated human c-H-ras oncogene under control of rat elastase I regulating elements leads to neoplasia of the fetal exocrine pancreas. In most transgenic mice bearing this gene construct, massive tumors involving all the pancreatic acinar cells develop within a few days of pancreatic differentiation. Expression of the normal c-H-ras proto-oncogene in acinar cells leads to more subtle anomalies, but no tumors develop. Thus modest amounts of the mutant ras proteins are sufficient, in an otherwise normal genetic background, to lead to neoplastic transformation of differentiating pancreatic acinar cells. In contrast, a comparable elastase-myc construct produces no pancreatic tumors in transgenic mice.
在大鼠弹性蛋白酶I调控元件的控制下，活化的人类c-H-ras癌基因的表达会导致胎儿外分泌胰腺发生肿瘤形成。在大多数携带这种基因构建体的转基因小鼠中，在胰腺分化后的几天内就会出现涉及所有胰腺腺泡细胞的大量肿瘤。在腺泡细胞中正常c-H-ras原癌基因的表达会导致更细微的异常，但不会形成肿瘤。因此，在其他方面正常的遗传背景下，适量的突变型ras蛋白就足以导致分化中的胰腺腺泡细胞发生肿瘤转化。相比之下，类似的弹性蛋白酶-myc构建体在转基因小鼠中不会产生胰腺肿瘤。
