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目的：阐明残留白血病形成及抗药再生长的机制。方法：用可移植性白血病模型Ｌ６１５和Ｌ７８１１小鼠骨髓作长期培养，用柔红霉素模拟体内治疗。结果：发现少数粘附于基质滋养层的残留白血病细胞逃避了柔红霉素的杀伤作用，并在药物作用下再生长。粘附的白血病细胞群中含有许多分化程度较低的静止期细胞，表达ｂｃｌ－２基因，有一定抗药能力，是残留白血病细胞的来源。结论：骨髓基质细胞滋养层是残留白血病细胞生存和再生长的微环境，可能通过上调ｂｃｌ－２基因表达增强其抗药能力。
Objective: To elucidate the mechanism of residual leukemia formation and drug re-growth. METHODS: The bone marrow of L615 and L7811 mouse models of transplantable leukemia were used for long-term culture, and daunorubicin was used to simulate in vivo therapy. RESULTS: It was found that a few remaining leukemia cells attached to the stroma of the stroma evaded the killing effect of daunorubicin and regrown under the action of drugs. Adherent leukemia cell population contains many quiescent cells with low degree of differentiation. The expression of bcl-2 gene has certain resistance to drugs and is the source of residual leukemia cells. CONCLUSION: Bone marrow stromal cell trophoblast is a microenvironment for the survival and regrowth of residual leukemia cells. It may enhance its anti-drug ability through up-regulation of bcl-2 gene expression.