Povoski S P, Zhou W, Longnecker D S, Bell R H
Department of Surgery, University of Cincinnati College of Medicine, OH 45267.
Pancreas. 1993 Sep;8(5):615-21. doi: 10.1097/00006676-199309000-00014.
Cholecystokinin (CCK-A) and gastrin (CCK-B) receptors have been demonstrated in the azaserine-induced rat pancreatic carcinoma DSL-6. In order to determine at what stage in azaserine-induced pancreatic carcinogenesis gastrin (CCK-B) receptors are first expressed, we examined the binding of [125I]gastrin-I to normal rat pancreas, azaserine-induced premalignant pancreatic nodules, grossly normal internodular pancreas, and DSL-6 carcinoma. We observed that specific gastrin binding was absent in normal pancreas, premalignant nodules, and internodular pancreas, and also reconfirmed our previous report of marked overexpression of gastrin (CCK-B) receptors in the DSL-6 carcinoma. Specific cholecystokinin (CCK) binding was present in all pancreatic tissue types tested. Therefore, we conclude that the presence of gastrin (CCK-B) receptors in the azaserine-induced pancreatic carcinoma DSL-6, in contrast to their absence in premalignant nodules, suggests that the expression of the gastrin (CCK-B) receptor may be important in the transformation from premalignant nodules to pancreatic cancer.
在氮杂丝氨酸诱导的大鼠胰腺癌DSL-6中已证实存在胆囊收缩素（CCK-A）和胃泌素（CCK-B）受体。为了确定在氮杂丝氨酸诱导的胰腺癌发生过程中胃泌素（CCK-B）受体首次表达的阶段，我们检测了[125I]胃泌素-I与正常大鼠胰腺、氮杂丝氨酸诱导的癌前胰腺结节、大体正常的结节间胰腺以及DSL-6癌的结合情况。我们观察到正常胰腺、癌前结节和结节间胰腺中不存在特异性胃泌素结合，并且再次证实了我们之前关于DSL-6癌中胃泌素（CCK-B）受体明显过度表达的报道。在所有检测的胰腺组织类型中均存在特异性胆囊收缩素（CCK）结合。因此，我们得出结论，与癌前结节中不存在胃泌素（CCK-B）受体相反，氮杂丝氨酸诱导的胰腺癌DSL-6中存在该受体，这表明胃泌素（CCK-B）受体的表达可能在从癌前结节向胰腺癌的转变中起重要作用。
