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糖皮质激素对B16黑色素瘤生长的抑制并非直接源于受体介导的肿瘤细胞抑制作用。

Inhibition of growth of B16 melanoma by glucocorticoids does not result directly from receptor-mediated inhibition of tumour cells.

作者信息

Crowley P, Lai N Y, De Young N, Pearce P, Funder J W, Gill P G

机构信息

Department of Surgery, University of Adelaide, Australia.

出版信息

Oncology. 1988;45(4):331-5. doi: 10.1159/000226634.

Abstract

The ability of dexamethasone (DM) to slow the growth of B16 melanoma in C57B1 mice was confirmed. Inhibition was dose-related and was demonstrated in the use of established tumours as well as initial transplants. Although glucocorticoid receptors (GR) were present in cultured tumour cells, DM did not reduce growth of B16 in vitro, even at high concentration. This dissociation of effect on growth in vivo and in vitro suggests that DM slows B16 tumour growth in vivo by mechanisms other than GR-mediated inhibition of tumour cells.

摘要

地塞米松(DM)减缓C57B1小鼠中B16黑色素瘤生长的能力得到了证实。抑制作用与剂量相关,在已形成的肿瘤以及初始移植瘤中均得到了证明。尽管培养的肿瘤细胞中存在糖皮质激素受体(GR),但即使在高浓度下,DM在体外也不会降低B16的生长。这种体内和体外对生长影响的分离表明,DM通过GR介导的抑制肿瘤细胞以外的机制减缓了体内B16肿瘤的生长。

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