Rubio C A, Nylander G, Wahlin B, Sveander M, Duvander A, Alun M L
J Surg Oncol. 1986 Mar;31(3):225-8. doi: 10.1002/jso.2930310319.
A total of 306 male Sprague-Dawley rats, injected with dimethylhydrazine (DMH), dose 21 mg/kg body weight s.c., were investigated. Of the 109 rats receiving the dose once only, seven colonic adenocarcinomas developed; all seven (100%) were seen to originate in discrete lymphoid patches. Of the 97 rats treated with one dose/week for 3 months, only 6% of the 50 adenocarcinomas developed in discrete lymphoid patches, while 46% were seen to originate in a pre-existing adenoma. Of the remaining 100 rats, receiving one dose/week for 6 months, only 3.5% of the 57 adenocarcinomas arose from discrete lymphoid patches; 43.9% arose from a pre-existing adenoma. Thus, the histogenesis of adenocarcinomas at our laboratory appears to be dose-dependent. Experiments are therefore being designed to monitor in detail the events of these two histogenetically different adenocarcinomas in the colonic mucosa in our animal model.
共对306只雄性斯普拉格-道利大鼠进行了研究,这些大鼠皮下注射了剂量为21毫克/千克体重的二甲基肼(DMH)。在仅接受一次该剂量的109只大鼠中,出现了7例结肠腺癌;所有7例(100%)均起源于离散的淋巴滤泡。在每周接受一次剂量、持续3个月的97只大鼠中,50例腺癌中只有6%起源于离散的淋巴滤泡,而46%起源于先前存在的腺瘤。在其余每周接受一次剂量、持续6个月的100只大鼠中,57例腺癌中只有3.5%起源于离散的淋巴滤泡;43.9%起源于先前存在的腺瘤。因此,在我们实验室中,腺癌的组织发生似乎是剂量依赖性的。因此,正在设计实验以详细监测我们动物模型中结肠黏膜这两种组织发生不同的腺癌的发生过程。