Histopathological Studies on the Influence of Mast Cell in the Growth of Rat Mammary Carcinoma 2. Effect of Mast Cell Mediator on the Development of Rat Mammary Carcinoma

Rat mammary carcinoma의 발육(發育)에 있어서 비만세포(肥滿細胞)의 영향(影響)에 관한 병리조직학적(病理組織學的) 연구(硏究) 2. 종양발육(腫瘍發育)에 있어서 mast cell mediator의 영향

  • Kim, Tae-hwan (Laboratory of experiment animal, Korea Cancer Center Hosþital, Korea Atomic Energy Research Institute) ;
  • Lee, Cha-soo (College of Veterinary Medicine, Kyungþook National University)
  • 김태환 (한국원자력연구소 부설 원자력병원 실험동물관리실) ;
  • 이차수 (경북대학교 수의과대학)
  • Received : 1990.08.21
  • Published : 1991.01.31


In order to know the influence of mast cells on the mammary tumor development, the growth of the mammary carcinoma, the numerical changes and the morphological findings of mast cells appeared in the tumor were microscopically observed in the rat treated with DMBA and each chemical of histamine, heparin, pyrilamine or cimetidine. The results observed were summarized as follows: The tumor induction time that represented the number of days elapsing between the 3rd DMBA administration until a first tumor became $10{\times}10mm$ in diameter was $42.5{\pm}4.7$ days, and the mean number of tumor mass per rat was $3.4{\pm}1.2$ in the DMBA-treated group. No significant difference was apparent in the tumor induction time of the histamine-treated group, heparin-treated group or pyrilamine-treated group compared with the control group, but in the cimetidine-treated group the tumor induction time was $61.8{\pm}10.6$ days (p<0.005). The mean number of tumors per rat was $2.1{\pm}0.9$ in the cimetidine-treated group in contrast to $3.4{\pm}1.3$ in the control group (p<0.005). Numerical changes of mast cells were observed according to the development of DMBA induced mammary tumors that were separated into three major classes of tumors. The numbers of mast cells in all the experimental group were inclined to increase significantly according to the mammary tumor development (p<0.005), and the histamine-treated group, heparin-treated group, or pyrilamine-treated group were nearly similar to the control group. But the mast cells in the each stage of tumor development were more numerous in the cimetidine-treated group than in the control group (p<0.005). There were not significant in the numerical changes of mast cells among the experimental groups on each stage of carcinomas separated by early stage, middle stage and late stage. In the morphological characteristics of mast cells, the degranulation was not detectable from the hyperplasia stages to the early stage of carcinoma, but its degranulation was observed at the middle stage of carcinoma. Most mast cells were nearly degranulated at the late stage of carcinoma. The histamine treated group, pyrilamine-treated group and cimetidine treated group did not differ from the control group in morphological changes of mast cells, but the degranulation was shown mild in the heparin-treated group. And the degranulation gave rise to the depletion of intercellular matrix via exocytosis all the experimental group. From above results, it is supposed that mast cells inhibit the tumor development and that the inhibition is not caused by a single-factor, but by a complex activities of mast cell mediators.