急性髓系白血病细胞侵袭能力与粘附分子表达关系探讨  

Study on the relationship between the expression of adhesion molecules and the invasiveness of acute myeloid leukemia cells

作　　者：刘廷析[1] 刘秀芳[1] 向建平[1] 邹萍[1] 周剑锋[1] 陈燕[1] 喻东姣[1] 李崇渔[1] 

机构地区：[1]同济医科大学附属协和医院血液病研究所

出　　处：《中华血液学杂志》1997年第1期29-31,共3页Chinese Journal of Hematology

摘　　要：目的：探讨白血病细胞浸润及转移与粘附分子表达的关系。方法：用免疫组织化学ＡＰＡＡＰ、免疫印迹方法研究５０例急性髓系白血病（ＡＭＬ）骨髓和（或）外周血白血病细胞粘附分子ＶＬＡ４（ＣＤ４９ｄ）、ＬＦＡ１（ＣＤ１１ａ）的表达。结果：发现ＡＭＬ浸润组ＣＤ４９ｄ、ＣＤ１１ａ表达较非浸润组显著增高（Ｐ＜０．００５）。结论：ＡＭＬ白血病细胞可能通过ＣＤ４９ｄ／ＶＣＡＭ－１，ＣＤ１１ａ／ＩＣＡＭ－１粘附机制与血管内皮细胞粘附而浸润组织。外周血白血病细胞与骨髓白血病细胞ＣＤ４９ｄ、ＣＤ１１ａ表达无显著差别，说明骨髓白血病细胞ＣＤ４９ｄ、ＣＤ１１ａ表达高低不是其从骨髓释出的唯一因素。Objective:To study the relationship between the expression of adhesion molecules CD 49d (VLA 4) and CD 11a (LFA 1) and the invasiveness of acute myeloid leukemia(AML) cells.Methods:Peripheral blood and/or bone marrow samples from 50 AML patients were investigated by APAAP and Western blotting method.Results: Extramedullary invasion developed in 32 of 50 patients (64%). The expression of CD 49d and CD 11a in the invasive group was much higher than that in the non invasive group(P<0.005),while the difference between the leukemic cells from bone marrow and peripheral blood for CD 49d /CD 11a expression was not significant.Conclusion: AML cells might adhere to and get through vascular endothelium by CD 49d /VCAM 1 and CD 11a /ICAM 1 adhesion mechanism, and the expressions of CD 49d and CD 11a were not critically responsible for the release of leukemic cells from bone marrow.

关 键 词：急性白血病 髓细胞性 粘附分子 肿瘤浸润 

分 类 号：R733.710.2[医药卫生—肿瘤]