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米非司酮抑制人脑膜瘤生长作用机制的体内实验研究

THE MECHANISMS OF MIFEPRISTONE′S ANTITUMOR EFFECTS ON HUMAN MENINGIOMA CELLS IN VIVO
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摘要 目的 探索米非司酮抑制人脑膜瘤生长的作用机制。方法 应用裸鼠肾包膜下法建立人脑膜瘤动物模型。采用实验剂量的米非司酮皮下用药 ,而对照组只注射溶剂 ,2 8d后将肿瘤生长率作统计学分析。原始标本用免疫组化SP法检测孕激素受体 (PR) ;增殖细胞核抗原 (PCNA)免疫组化法检测细胞增殖情况 ;电镜观察用药前后的肿瘤细胞超微结构改变。结果 实验组与对照组之间有显著性差异 (P <0 0 1) ,免疫组化、PCNA免疫组化以及电镜的结果表明米非司酮可明显抑制脑膜瘤细胞的增殖。结论 米非司酮可能是通过阻断PR/糖皮质激素受体 (GR) Objective: To explore the mechanisms of mifepristone′s antitumor effects on human meningioma through morphology changes. Methods: Meningioma tissues from 7 patients were implanted into the subrenal capsules of nude mice. The effective doses of mifepristone were given to experiment group for 28 days, and the second group was given sesame oil alone as control. All meningioma tissues were examined for the PR by the immunohistochemitry method; meningioma tissues, including original tissue and the one after mifepristone treatment, were examined with PCNA immunohistochemitry methods. To investigate the changes of histology, electro-microscope examination was applied. Results: Antiprogesterone treatment results in a marked reduction of the tumor volume in experiment group. PR positive was found in four meningioma tissues of 7 patients. PCNA and electromicroscope results suggested that mifepristone could inhibit the reproduction of meningioma cells. Conclusion: This study suggests that mifepristone has an antitumor effect against meningioma cells via the PR and/or other receptor, which perhaps mediates the glucocorticoid receptor.
出处 《实用临床医药杂志》 CAS 2003年第3期246-248,共3页 Journal of Clinical Medicine in Practice
基金 国家铁道部青年科技基金资助 (课题号 98 J 2 7)
关键词 裸鼠 脑膜瘤 异体移植 米非司酮 孕激素受体 nude mouse meningioma xenograft mifepristone progesterone receptor
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  • 1Scoles DR, Huynh DP, Morcos PA, et al. Neurofibromatosis 2 tumour suppressor schwannomin interacts with beta Ⅱ - spectrim. Nat Genet,1998; 18(4) :354- 359
  • 2Sherman L, Xu HM, Geist RT, et al. Interdomain binding mediates tumor growth suppression by the NF2 gene product. Oncogene, 1997; 15(20):2505-2509
  • 3James J, Evans, Sin - Soo Jeun, et al. Molecular alterations in the neurofibromatosis type 2 gene and its protein rarely occurring in meningothelial meningiomas. J Neurosurg, 2000;94:111 - 117
  • 4Lekanne Depez RH, Riegman PH, Groen NA, et al. Cloning and characterization of MN1 , a gene from chromosome 22q11, Which is disrupted by a balanced translocation in a meningioma. Oncogene,1995; 10(8): 1521 - 1528
  • 5Simon M, yon Deimling A, Larson JJ,et al. Allelic losses on chomosome 14, 10 and 1 in atypical and malignant meningiomas: a genetic model of meningioma progression. Cancer Res, 1995; 55(20):4696-4701
  • 6Weber RG, Bostrom J, Wolter M, et al. Analysis of genomic alteration in benign,atypical ,and anaplastic meningiomas:toward a genetic model of meningioma progression. Proc Natl Acad Sci U.S.A, 1997; 94(26):14719 - 14724
  • 7Schoenberg BS, Christine BW, Whisnant JF, et al. Nervous system neoplasms and the primary malignancies of other site. The unique association between meningiomas and breast cancer. Neurology, 1975;25(8) :705 - 712
  • 8Hsu DW, Efird JT, Hedley - Whyte ET. Progesterone and oestrogen receptors in meningiomas: prognostic considerations. J Neurosurg,1997; 86(1):113 - 120
  • 9Carroll RS, Zhang J, Dashner K, et al. Progesterone and glucocorticoid receptor activation in meningiomas. Neurosurgery, 1995;37(1) :92 - 97
  • 10Tonn JC, Ott MM, Bouterfa H, Kerkaau S, et al. Inverse correlation of cell proliferation and expression of progesterone receptors in tumor spheroids and monolayer cultures of human meningiomas. Neurosurgery,1997; 41(5): 1152 - 1159

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