Sandgren E P, Quaife C J, Paulovich A G, Palmiter R D, Brinster R L
Laboratory of Reproductive Physiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia 19104.
Proc Natl Acad Sci U S A. 1991 Jan 1;88(1):93-7. doi: 10.1073/pnas.88.1.93.
Transgenic mice in which c-myc expression is targeted to pancreatic acinar cells develop mixed acinar/ductal pancreatic adenocarcinomas between 2 and 7 months of age. This contrasts with the effect on pancreas of the simian virus 40 tumor antigen or activated ras, which in adult mice causes lesions composed exclusively of acinar-like cells. Furthermore, during an early stage of myc-induced pathology, transformed acinar-derived cells appear within islets, suggesting that islet hormones may influence the progression of these exocrine pancreatic tumors. These findings demonstrate that the initial oncogenic alteration can influence the pattern of subsequent tumor pathogenesis and, given that human exocrine pancreatic tumors are predominantly ductal adenocarcinomas, support the suggestion that transformed acinar cells may contribute to the genesis of this serious disease in man.
c - myc 表达靶向于胰腺腺泡细胞的转基因小鼠在2至7月龄时会发生混合性腺泡/导管胰腺腺癌。这与猿猴病毒40肿瘤抗原或激活的ras对胰腺的影响形成对比，后者在成年小鼠中会导致仅由腺泡样细胞组成的病变。此外，在 myc 诱导的病理学早期阶段，转化的腺泡来源细胞出现在胰岛内，这表明胰岛激素可能影响这些外分泌性胰腺肿瘤的进展。这些发现表明，最初的致癌改变可影响后续肿瘤发病机制的模式，而且鉴于人类外分泌性胰腺肿瘤主要是导管腺癌，这支持了转化的腺泡细胞可能促成人类这种严重疾病发生的观点。
