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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 investigate the relationship between leukemia cell infiltration and metastasis and expression of adhesion molecules. METHODS: The expression of adhesion molecules VLA4 (CD49d) and LFA1 (CD11a) in 50 cases of acute myeloid leukemia (AML) bone marrow and/or peripheral blood were studied by immunohistochemical APAAP and Western blot. RESULTS: The expression of CD49d and CD11a in the AML infiltrating group was significantly higher than that in the non-infiltrating group (P<0.005). Conclusion: AML leukemia cells may infiltrate tissues through adhesion mechanism of CD49d/VCAM-1 and CD11a/ICAM-1 with vascular endothelial cells. There was no significant difference in the expression of CD49d and CD11a between peripheral blood leukemia cells and myeloid leukemia cells, indicating that the level of CD49d and CD11a expression in myeloid leukemia cells was not the only factor for their release from bone marrow.