Howatson A G, Carter D C
Br J Cancer. 1985 Jan;51(1):107-14. doi: 10.1038/bjc.1985.15.
The role of the pancreaticotrophic hormone cholecystokinin (CCK) in modifying the pancreatic response to carcinogen has been examined in the hamster-nitrosamine pancreatic cancer model. Exogenous CCK, 30 IDU kg-1, stimulated a maximal pancreatic secretory response when given intravenously and caused hypertrophy and hyperplasia of the pancreas when given subcutaneously over a period of 6 weeks (pancreatic wet weight, mg per 100 g body weight, controls 295.6 +/- 61; CCK treated 466.4 +/- 77, P less than 0.001). When the same dose of CCK was given to animals receiving N-nitrosobis (2-oxopropyl)amine (BOP; 5 mg kg-1 weekly) there was a reduction in latency period and increase in induction rate of tumour development (CCK + BOP vs. BOP alone, 12 animals with tumours vs. 2 at 15 weeks; P less than 0.02). These effects are consistent with CCK acting as a co-carcinogen or promoter of pancreatic carcinogenesis in this model.
在仓鼠-亚硝胺胰腺癌模型中，研究了促胰激素胆囊收缩素（CCK）在改变胰腺对致癌物反应方面的作用。静脉注射30 IDU kg-1的外源性CCK可刺激最大的胰腺分泌反应，皮下注射6周可导致胰腺肥大和增生（胰腺湿重，每100 g体重毫克数，对照组295.6±61；CCK处理组466.4±77，P<0.001）。当给接受N-亚硝基双（2-氧代丙基）胺（BOP；每周5 mg kg-1）的动物给予相同剂量的CCK时，肿瘤发生的潜伏期缩短，诱导率增加（CCK+BOP组与单独BOP组相比，15周时肿瘤动物数分别为12只和2只；P<0.02）。在该模型中，这些作用与CCK作为胰腺癌发生的促癌剂或启动子的作用一致。
