摘要
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 mechanisms of residual leukemia and its drug resistant regrowth.Methods:Bone marrow cells from transplantable mouse leukemia models L615 and L7811 were cultivated in long term culture system respectively .Daunorubicin(DNR) was added to the systems to mimick in vivo chemotherapy.Results:Residual leukemic cells on stromal layers escaped DNR killing.They derived from the adherent leukemic cell population,which was heterogeneous with many undifferentiated and dormant cells.They were drug resistant and expressed bcl 2 gene .Conclusion:Bone marrow stromal layer was the vital microenvironment for the residual leukemic cells to survive and regrow,and might increase the drug resistance by up regulating bcl 2 gene expression.
出处
《中华血液学杂志》
CAS
CSCD
北大核心
1997年第5期231-233,共3页
Chinese Journal of Hematology
关键词
残留白血病细胞
骨髓基质
抗药性
Residual leukemic cell Bone marrow stromal layer Drug resistant regrowth
