Himmele J C, Rabenhorst B, Werner D
J Cancer Res Clin Oncol. 1986;111(2):160-5. doi: 10.1007/BF00400757.
A double tumor model (3LL and EAT) was established in C57BL/6 mice. The primary 3LL tumor was growth-inhibited by EAT inoculated into the same host. Growth inhibition of the 3LL primary tumor depended on the number of EAT cells injected. Inhibition of the growth of the primary 3LL tumor was also observed after injection of the optimal number (10(7)) of EAT cells 24 h to 7 days before or after inoculation of 3LL cells. In contrast, metastasis of the 3LL tumor was only inhibited after simultaneous inoculation of 3LL and ETA cells. Moreover, EAT cells inhibited the growth of preformed 3LL-derived metastases after resection of the primary 3LL tumor. Although the EAT-induced stimulation of a host defense system is not excluded, the results are consisted with the continued release of growth inhibition factors from EAT cells acting on 3LL cells in the primary tumor and in lung metastases.
在C57BL/6小鼠中建立了双肿瘤模型(3LL和EAT)。接种到同一宿主中的EAT抑制了原发性3LL肿瘤的生长。3LL原发性肿瘤的生长抑制取决于注射的EAT细胞数量。在接种3LL细胞前24小时至7天或接种后注射最佳数量(10(7))的EAT细胞后,也观察到原发性3LL肿瘤的生长受到抑制。相比之下,只有在同时接种3LL和ETA细胞后,3LL肿瘤的转移才受到抑制。此外,在切除原发性3LL肿瘤后,EAT细胞抑制了预先形成的3LL来源转移灶的生长。尽管不排除EAT诱导宿主防御系统的刺激,但结果与EAT细胞持续释放作用于原发性肿瘤和肺转移灶中3LL细胞的生长抑制因子一致。