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人脑星形细胞肿瘤组织中凋亡细胞密度和bcl-2基因的表达

Expression of bcl-2 gene and apoptotic cell density in tissues of human astrocytic tumor
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摘要 目的 :探讨人脑星形细胞肿瘤组织中bcl 2基因表达情况及其与肿瘤细胞凋亡的相关关系。方法 :采用免疫组织化学SABC法和原位末端标记的TUNEL技术分别检测了 6 0例星形细胞肿瘤组织中bcl 2基因的表达和凋亡细胞密度。结果 :6 0例患者的星形细胞肿瘤组织中bcl 2基因表达阳性率为 5 0 % ,不同恶性级别的肿瘤之间差异无显著性 (P >0 .0 5 ) ,但其表达强度在不同级别肿瘤之间差异有显著性 (P <0 .0 5 ) ,高度恶性肿瘤bcl 2基因表达较强 ;随着星形细胞肿瘤恶性程度的升高 ,凋亡细胞密度呈逐渐降低之趋势 ,其中星形细胞肿瘤组织中凋亡细胞密度显著高于胶质母细胞瘤 (P <0 .0 1) ,并且凋亡细胞密度与bcl 2基因表达强度呈显著负相关 (r=- 0 .992 ,P <0 .0 1)。结论 :星形细胞肿瘤组织中bcl 2基因高度表达可能是细胞凋亡受抑的重要原因 ,bcl 2基因表达上调可能对肿瘤的生长及进一步间变起着关键作用。 Aim:To study the expression of bcl 2 gene and its correlation with cell apoptosis in human astrocytic tumor tissues. Methods: Apoptotic cell density (AD) and the expression of bcl 2 gene were determined by using TUNEL and immunohistochemical SABC methods in tumor tissues from 60 cases of astrocytic tumor respectively. Results: The positivity rate of bcl 2 expression was 50%. No significance was found among different grades ( P >0.05),but the degree of bcl 2 expression had significant differences among different grades ( P <0.05). Astrocytic tumors for high malignant grade had a strong expression of bcl 2 gene. Meanwhile,AD decreased gradually with the increase of malignant grade of astrocytic tumor. AD in tissues of astrocytic tumor was significanly higher than that in gliocytoma( P <0.01).AD was negatively correlated to the degree of bcl 2 gene expression in human astrocytic tumor tissues. Conclusions: The high expression of bcl 2 gene might be an important cause for the inhibition of cell apoptosis in human astrocytic tumor tissues. The expression of bcl 2 gene being regulated up might plays a key role in tumor growth and its further anaplasia.
出处 《郑州大学学报(医学版)》 CAS 北大核心 2002年第2期176-179,共4页 Journal of Zhengzhou University(Medical Sciences)
关键词 星形细胞肿瘤 BCL-2基因 细胞凋亡 脑肿瘤 细胞密度 基因表达 astrocyte neoplasm bcl 2 gene cell apoptosis
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参考文献1

  • 1M. Deckert-Schlüter,Andrea Rang,Otmar D. Wiestler. Apoptosis and apoptosis-related gene products in primary non-Hodgkin’s lymphoma of the central nervous system[J] 1998,Acta Neuropathologica(2):157~162

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