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多发性骨髓瘤黏附分子CD11a、CD49d的表达特点及临床意义 被引量:4

Expression of cellular adhesion molecules CD11a and CD49d in patients with mutiple myeloma and clinical implications
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摘要 目的:研究多发性骨髓瘤(MM)患者骨髓单个核细胞黏附分子CD11a、CD49d的表达,并探讨其发病机制。方法:用流式细胞仪检测CD11a、CD49d在MM组及对照组2组骨髓标本单个核细胞表达的平均荧光强度和荧光阳性细胞百分率。结果:MM患者骨髓单个核细胞CD49d的表达荧光强度较对照组增强(P<0.05);CD11a的表达阳性细胞百分率及荧光强度均较对照组增强(P<0.05,P<0.01);进展期表达较平台期明显增强(P<0.05,P<0.01)。结论:MM单个核细胞表面CD49d的表达增强,导致患者骨髓细胞与细胞及细胞与骨髓基质间的黏附异常,可能参与了MM的病理过程,而CD11a在MM的平稳期表达较低,进展期表达明显增强,表明CD11a在MM增殖中起作用。 Objective:To explore the expression of CAMs (CD11a, CD49d) in patients with MM, and their effects on the pathogenesis of MM. Method:The sample of bone marrow were obtained. CD11a and CD49d were examined by four-color flow cytometry. Result:The mean fluorescence intensity in mononuclear cells (MNC) from the MM group was significantly stronger than that of control group (P<0.05) in CD49d, and so was the case for CD11a in MNC from MM group and control group. The percentage of CD11a in MNC from MM group was significantly stronger than that of control group (P<0.05), The mean fluorescence intensity(MFI) and the percentage of CD11a also demonstrate significant stronger in the advanced stage than than of the steady stage (P<0.01). Conclusion:These results suggest that CD49d are involved in cellular interaction in MM, CD49d may participate in the pathogenesis of MM, and that the expression of CD11a varies with disease activity in MM. Adhesion molecules are involved at multiple steps in the pathogenesis of MM, therapeutic studies may target these molecules.
出处 《临床血液学杂志》 CAS 2005年第4期198-199,203,共3页 Journal of Clinical Hematology
关键词 多发性骨髓瘤 细胞黏附分子 流式细胞术 Multiple myeloma Cellular adhesion molecules Flow cytometery
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参考文献3

  • 1Horvathova M, Ferencik M. The role of adhesion molecules in the immune system. Bratisl Lek Listy, 2000,101:138-45.
  • 2Kastrinakis N G. Molecular aspects of multiple myelo ma. Ann Oncol, 2000, 11:1217-1228.
  • 3Ruan C G. Advance of the studies on the adhesion mol ecules of blood cells. Zhongguo Shi Yan Xue Ye Xue Za Zhi, 2004, 12:1-5.

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