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P27kip1与细胞周期素D3在非霍奇金淋巴瘤中的表达、定位及相互关系
引用本文:张冬梅,陆建新,沈爱国,陈莉,何松,邵晓轶,刘海鸥,程纯. P27kip1与细胞周期素D3在非霍奇金淋巴瘤中的表达、定位及相互关系[J]. 中华血液学杂志, 2005, 26(12): 723-727
作者姓名:张冬梅  陆建新  沈爱国  陈莉  何松  邵晓轶  刘海鸥  程纯
作者单位:1. 226001,南通大学微生物与免疫学教研室
2. 226001,南通大学病理教研室
3. 南通市肿瘤医院病理科
基金项目:江苏省高校自然科学研究基金资助项目(04KJB320114);江苏省高校研究生创新计划资助项目(xm04-66)
摘    要:目的探讨P27^kip1和细胞周期素(cyclin)D3在非霍奇金淋巴瘤(NHL)中的表达、定位、相互关系及意义.方法采用免疫组织化学方法检测100例NHL患者病理标本及20例反应性增生淋巴结标本中P27^kip1、cyclin D3及细胞增殖指标Ki-67的表达.采用Western blot、免疫荧光双标法和激光共聚焦技术检测3种淋巴瘤细胞系细胞内P27^kip1和cyclin D3的表达、定位.结果 P27^kip1在NHL组织中的阳性率低于反应性增生淋巴结,且与肿瘤侵袭性以及增殖活性(Ki-67指数,Ki-67 LI)呈负相关;cyclin D3在NHL组织中的阳性率高于反应性增生淋巴结,且与肿瘤侵袭性以及增殖活性呈正相关;P27^kip1与cyclin D3呈负相关.但在少数病例出现P27^kip1的异常高表达并伴有cyclin D3和Ki-67的高表达.P27^kip1与cyclin D3在3种淋巴瘤细胞系的表达水平不一,在Raji细胞中P27^kip1与cyclin D3共同高表达并且共定位.结论 P27^kip1的低表达,cyclin D3的高表达与多数NHL的发生发展有关;部分病例或细胞系中P27^kip1的异常高表达及其与cyclin D3相互作用可能是NHL发生的另一机制.

关 键 词:细胞周期蛋白质类 淋巴瘤  非霍奇金氏 免疫组织化学
收稿时间:2005-03-21
修稿时间:2005-03-21

Expression, localization and interrelationship of P27kip1 and cyclin D3 in non-Hodgkin'''' s lymphoma
ZHANG Dong-mei,LU Jian-xin,SHEN Ai-guo,CHEN Li,HE Song,SHAO Xiao-yi,LIU Hai-ou,CHENG Chun. Expression, localization and interrelationship of P27kip1 and cyclin D3 in non-Hodgkin'''' s lymphoma[J]. Chinese Journal of Hematology, 2005, 26(12): 723-727
Authors:ZHANG Dong-mei  LU Jian-xin  SHEN Ai-guo  CHEN Li  HE Song  SHAO Xiao-yi  LIU Hai-ou  CHENG Chun
Affiliation:Department of Microbiology and Immunology, Nantong University, Nantong 226001, China
Abstract:OBJECTIVE: To investigate the expression, localization and interrelationship of P27(kip1) and cyclin D3 in non-Hodgkin's lymphoma (NHL). METHODS: The expressions of P27(kip1), cyclin D3 and index Ki-67 was detected in 100 NHL and 20 reactive lymph nodes by immunohistochemical technique. The expression and localization of P27(kip1) and cyclin D3 in 3 NHL cell lines were detected by Western blot, double immunolabelling and laser scanning confocal microscopy, respectively. RESULTS: In general the expression of P27(kip1) in NHL was lower than in control group, and was negatively related to the tumor aggressiveness and proliferating activity; the expression of cyclin D3 in NHL was higher than in control group, and was positively related to the tumor aggressiveness and proliferating activity. There was a negative correlation between P27(kip1) and cyclin D3. Nevertheless, anomalous high P27(kip1) expression was found in a few NHL tissues with high expression of cyclin D3 and Ki-67. Overexpression and colocalization of P27(kip1) and cyclin D3 was found in Raji cell line. CONCLUSIONS: Under expression of P27(kip1) and overexpression of cyclin D3 may play a role in the occurrence and development of NHL. Anomalous high P27(kip1) expression and its interaction with cyclin D3 may be another mechanism for tumorogenesis of NHL.
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