Conley F K
Cancer Res. 1979 Mar;39(3):1001-7.
This study reports an easily accomplished and reliable model of metastatic tumor in the brains of mice. Five experimental groups of female C3H/Bi mice received left intracardiac injections of a syngeneic KHT sarcoma cell suspension (1 X 10(5) cells) and were followed until death. Two groups of mice also received 3,000 rads of radiation to a limited cardiac port 24 hr after tumor injections. All mice were completely autopsied, and the brains were examined both grossly and microscopically. Metastatic brain tumor developed in 60 to 70% of mice; the tumor foci were parenchymal, usually multifocal, and had wide distribution throughout the cerebrum, brainstem, and cerebellum. There was occasional meningeal tumor, but tumor never involved the skull, choroid plexus, pituitary gland, or local extracranial structures. Cardiac irradiation did not increase the number of the mean survival of mice with metastatic brain tumor but did decrease the total tumor burden of individual animals by markedly reducing the incidence of metastatic lung tumor and totally preventing tumor infiltration of the heart. This demonstration of consistently produced blood-borne metastatic brain tumor in mice should provide a valuable research model which will allow the central nervous system to be studied for internal mechanisms and/or external factors which influence the arrest and growth of embolic tumor cells in the brain.
本研究报告了一种在小鼠脑内易于建立且可靠的转移性肿瘤模型。五组雌性C3H/Bi小鼠经左心内注射同基因KHT肉瘤细胞悬液(1×10⁵个细胞),并追踪至死亡。两组小鼠在肿瘤注射后24小时还接受了对有限心脏区域的3000拉德辐射。所有小鼠均进行了完整的尸检,并对脑进行了大体和显微镜检查。60%至70%的小鼠发生了转移性脑肿瘤;肿瘤灶位于实质内,通常为多灶性,广泛分布于大脑、脑干和小脑。偶尔有脑膜肿瘤,但肿瘤从未累及颅骨、脉络丛、垂体或局部颅外结构。心脏照射并未增加患有转移性脑肿瘤小鼠的平均存活天数,但通过显著降低转移性肺肿瘤的发生率并完全防止肿瘤浸润心脏,确实降低了个体动物的总肿瘤负荷。在小鼠中持续产生血源性转移性脑肿瘤的这一现象应提供一个有价值的研究模型,这将使人们能够研究影响脑内栓塞性肿瘤细胞停滞和生长的内部机制和/或外部因素。