Pancreatic carcinoma in azaserine‐treated rats: Induction, classification and dietary modulation of incidence
Pancreatic carcinoma in azaserine‐treated rats: Induction, classification and dietary modulation of incidence
复制标题
重氮丝氨酸治疗大鼠的胰腺癌：发病率的诱导、分类和饮食调节
作者：
D. Longnecker;B. Roebuck;J. Yager;H. Lilja;Brad Siegmund
在Wistar和W/LEW大鼠中，通过注射或口服总剂量为150-520 mg/kg的氮扎塞林诱导胰腺癌，持续5-52周。浸润性癌的潜伏期为1-2年，但腺泡细胞的局灶性异常出现得更早。癌症的发生率随阿扎塞林给药的总剂量、途径和计划而变化。肿瘤的组织学类型包括高分化和低分化的腺泡细胞癌、导管样癌和未分化癌。喂食纯饲料的大鼠比喂食商业实验室饲料的大鼠患胰腺肿瘤的几率更高。在致癌物治疗期间和完成致癌物治疗后对这些饲料的选择性喂养表明，在启动后阶段，chow对胰腺癌的抑制作用发挥作用。在起始后阶段，添加0.025%视黄醇醋酸酯的饮食也抑制了azaserine诱导的胰腺病变的进展。
Pancreatic carcinomas have been induced in Wistar and W/LEW rats by administration of total azaserine doses of 150–520 mg/kg by injection or oral routes over periods of 5–52 weeks. The latent period for development of invasive carcinomas was 1–2 years, but focal abnormalities in acinar cells appear earlier. The incidence of carcinomas varied with total dose, route, and schedule of azaserine administration. The spectrum of histologic patterns of the carcinomas included well and poorly differentiated acinar cell, ductlike, and undifferentiated carcinomas. Rats fed a purified diet developed more pancreatic neoplasms than rats fed a commercial laboratory chow. Selective feeding of these diets during the administration of carcinogen and following completion of carcinogen treatment indicated that the inhibitory effect of chow on pancreatic carcinogenesis was exerted during the postinitiation phase. Supplementation of diet with 0.025% retinyl acetate during the postinitiation phase also inhibited the progression of azaserine‐induced lesions in the pancreas.