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Diethylnitrosamine으로 유발된 흰쥐 간암 발생 및 진행 과정에서 VEGF와 Factor Ⅷ R-Ag의 발현
김형준,기승석,박용진,김남돈,견종만,박언섭 중앙대학교 의과대학 의과학연구소 2003 中央醫大誌 Vol.28 No.2-3
It is widely believed that chemical carcinogenesis is a multistage process, so-called initiation, promotion and propagation. Diethylnitrosamine (DEN) has been proved to have carcinogenic potential either at initiation or at promotion stage, resulting hepatocellular carcinomas in rat liver. In addition, neoplastic and metastatic propagation of transformed cells exclusively need a plenty of vascular supply for their metabolic requirement. To elucidate the tumor angiogenesis during the chemically induced carcinogenesis in rat liver, analysis of histopathology and the expression of vascular endothelial growth factor (VEGF) and Factor VⅢ related antigen were examined by immunohistochemical study using avidine-biotin complex. The hyperplastic nodules appeared at 3 weeks, the hepatocellular carcinomas were 15 weeks, and the pulmonary metastatic foci were developed at 18 weeks after oral administration of 120 ppm DEN to the rat. The VEGF expression appeared at 3 weeks and continuously increased with weeks. The staining of Factor VⅢ R-Ag was negative in any sinusoids in normal control livers, focal or scattered expressed in hyperplastic nodules, and diffusely expressed in hepatocellular carcinomas. As above results, it could be suggested that VEGF expression plays an important role from early period of DEN-induced hepatocarcinogenesis. Also, the expression of VEGF is likely to be associated with phenotypic changes of the sinusoidal endothelium presenting Factor VⅢ expression. However, there was no correlation between the expression pattern of VEGF and the state of metastasis.
Urethane으로 유발된 생쥐 페샘암종 발생과정에서 세포주기 관련인자(Cyclin D1, p21, and p27)에 대한 비소의 효과
임성혁(Sung Hyuk Yim),정지훈(Ji Hoon Jeong),견종만(Jong Man Gyeon),박언섭(Eon Sub Park) 대한약학회 2006 약학회지 Vol.50 No.2
The present study investigated an effect of arsenic trioxide on the urethane-induced lung carcinogenesis in mice. To understand its carcinogenesis, we examined proliferating cell nuclear antigen (PCNA), apoptotic index as well as cell cycle-related proteins (cyclin D l, p21, and p27). Urethane was injected intraperitoneally in ICR mice, and then they were sacrificed at 5, 15, or 25 weeks following treatment of arsenic trioxide. Arsenic trioxide was given with tap water at a concentration of 1 mg/l (low-dose) and 5 mg/l (high-dose) for 25 weeks. During the carcinogenesis, sequential histological changes from hyperplasia to adenomas, and ultimately to overt carcinomas were noted. The development of hyperplasias, adenomas, and carcinomas in the lung were slightly increased by the treatment of low-dose arsenic trioxide. However, there is no correlation between dose and tumor multiplicity. The administration of low-dose arsenic trioxide, significantly increased the tumor size. The proliferative index observed on 5 weeks after significantly increased. Cyclin D1 and p21 protein, cell cycle related proteins, were more significantly increased in hyperplasia and adenoma in low dose arsenic treated group than urethane alone group. The p27 protein expression did not show any significantly changes with arsenic treated or untreated group. Low dose exposure to arsenic trioxide resulted in increased expression of cyclin D1 and p21 protein. The present results indicate that low-dose treatment of arsenic trioxide, but not high dose of it, partly modulate the cellular proliferation, cyclin D1, and p21 protein expression, and that this effect may contribute to accelerated development of lung adenocarcinomas in urethane-induced mice.