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目的:探讨凋亡及EB病毒与经典型Hodgkin淋巴瘤的关系。方法:应用组织芯片、免疫组化双标记和原位杂交技术检测bcl蛳2、LMP1、EBER、TUNEL(TdT蛳mediated dUTP nick end蛳labeling)显示的凋亡在62 例经典型Hodgkin淋巴瘤H/RS细胞的表达。结果:62 例经典型Hodgkin淋巴瘤中35例表达bcl蛳2,37例表达LMP1/ EBER,62例的背景细胞均可见TUNEL显示的凋亡,但仅有10例CD+30的H/RS细胞出现凋亡。经χ2检验,bcl蛳2、LMP1/ EBER、TUNEL显示的凋亡与分期、分型均无相关性(P>0.05);EBV与bcl蛳2 、凋亡也无相关性(P>0.05);bcl蛳2与凋亡之间呈负相关(P<0.05)。结论:凋亡是CHL的一个发病因素。bcl蛳2的过表达可阻断细胞的凋亡,促进肿瘤的生长。但凋亡与临床分期及分型均无相关性;一半以上的经典型Hodgkin淋巴瘤是EBV相关性的,但EBV与临床分期、分型及凋亡均无相关性,其发病机制尚不清楚。
Objective: To investigate the relationship between apoptosis and Epstein-Barr virus (EBV) and classical Hodgkin’s lymphoma. Methods: Tissue microarray, immunohistochemistry and in situ hybridization were used to detect the apoptosis of bcl-2, LMP1, EBER and TUNEL (TdT-mediated dUTP nick end labeling) in 62 cases of Hodgkin’s lymphoma H / RS cells. RESULTS: Of the 62 Hodgkin’s lymphoma cases, 35 showed bcl 蛳 and 2,37 had LMP1 / EBER. TUNEL showed apoptotic cells in all 62 background cells, but only 10 H / RS cells with CD + 30 Apoptosis occurs. There was no correlation between the apoptosis of bcl-2, LMP1 / EBER and TUNEL (P> 0.05) and the apoptosis of EBV and bcl-2 (P> 0.05) by χ2 test. There was a negative correlation between bcl 蛳 2 and apoptosis (P <0.05). Conclusion: Apoptosis is a risk factor for CHL. Overexpression of bcl? 2 can block cell apoptosis and promote tumor growth. However, there was no correlation between apoptosis and clinical staging and typing. More than half of the classic Hodgkin’s lymphoma was EBV-related, but EBV was not associated with clinical stage, classification and apoptosis, and its pathogenesis was not clear .