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用重氮丝氨酸处理的大鼠中的胰腺癌:诱发、分类及发病率的饮食调节

Pancreatic carcinoma in azaserine-treated rats: induction, classification and dietary modulation of incidence.

作者信息

Longnecker D S, Roebuck B D, Yager J D, Lilja H S, Siegmund B

出版信息

Cancer. 1981 Mar 15;47(6 Suppl):1562-72. doi: 10.1002/1097-0142(19810315)47:6+<1562::aid-cncr2820471419>3.0.co;2-z.

Abstract

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 phas. Supplementation of diet with 0.025% retinyl acetate during the postinitiation phase also inhibited the progression of azaserine-induced lesions in the pancreas.

摘要

通过注射或口服途径,在5 - 52周的时间内给Wistar和W/LEW大鼠施用总量为150 - 520毫克/千克的偶氮丝氨酸,可诱发胰腺癌。侵袭性癌发生的潜伏期为1 - 2年,但腺泡细胞的局灶性异常出现得更早。癌的发生率随偶氮丝氨酸的总剂量、给药途径和给药方案而变化。癌的组织学模式谱包括高分化和低分化的腺泡细胞癌、导管样癌和未分化癌。喂食纯化饮食的大鼠比喂食商业实验室饲料的大鼠发生更多的胰腺肿瘤。在施用致癌物期间和致癌物治疗完成后选择性喂食这些饲料表明,饲料对胰腺癌发生的抑制作用在启动后阶段发挥。在启动后阶段,饮食中添加0.025%的醋酸视黄酯也抑制了偶氮丝氨酸诱导的胰腺病变的进展。

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