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目的大量研究证实导管样复合体就是胰腺癌的前体病变,因此,本研究旨在探索植入致癌剂后胰腺癌前体病变的产生和发展。方法采用手术方法将致癌剂DMBA植入SD大鼠胰腺,从第1天开始,在不同的时间点获取胰腺进行组织学研究,同时,分别以糜蛋白酶和细胞角蛋白作为胰腺腺泡细胞和导管细胞的标记物,通过免疫组化方法进行定位。结果在包埋致癌剂第2天就可以观察到正常胰腺小叶向导管复合体移型的现象,第4天出现典型的导管复合体,同时,胰岛也参与了这一过程。小叶中的非导管细胞迅速转分化为导管细胞的特征。在1个月时观察到导管腺癌的形成。与对照组相比,腺泡-导管转分化过程在DMBA包埋组持续存在。结论胰腺癌前体病变(导管复合体)除了由已经存在于小叶内的导管细胞组成外,主要通过腺泡细胞转分化形成,同时,胰岛细胞在某种程度上也参与了导管复合体的形成。因此,胰腺腺泡细胞、胰岛细胞和导管细胞共同参与了胰腺导管腺癌前体细胞的起源,转分化可以不需要细胞分裂迅速发生,而恶性转化需要较长的时间。
PURPOSE A large number of studies have demonstrated that a catheter-like complex is a precursor to pancreatic cancer. Therefore, this study aimed to explore the generation and development of pancreatic cancer precursor lesions after implantation of a carcinogen. Methods The carcinogenic agent DMBA was implanted into the pancreas of SD rats by surgery. From day 1, the pancreas were harvested at different time points for histological study. Chymotrypsin and cytokeratin were respectively used as pancreatic acinar cells and catheters Cell markers are targeted by immunohistochemistry. Results On the 2nd day after embedding of carcinogen, the normal pancreatic lobule-to-ductal complex was observed. The typical ductal complex appeared on the 4th day. At the same time, the islets participated in the process. Non-ductal cells in the leaflets rapidly transdifferentiate into ductal cells. The formation of ductal adenocarcinoma was observed at 1 month. Compared with the control group, acinar-ductal transdifferentiation persisted in the DMBA-embedding group. Conclusion The precursor of pancreatic cancer (ductal complex) is mainly formed by transdifferentiation of acinar cells besides the ductal cells already existing in the leaflets. In the meantime, islet cells are also involved in the formation of ductal complex to some extent . Therefore, pancreatic acinar cells, islet cells and ductal cells participate in the origin of pancreatic ductal adenocarcinoma precursor cells. Transdifferentiation can occur rapidly without cell division, whereas malignant transformation requires longer time.