预激方案CAG治疗急性髓细胞白血病的疗效及作用机制

目的观察含粒细胞集落刺激因子(G-CSF)的预激方案在治疗初治急性髓细胞白血病(AML)中的疗效,并进一步研究其作用机制。方法13例初治AML患者予以含G-CSF、低剂量阿糖胞苷(Ara-C)和阿克拉霉素(ACR)的CAG方案。以U937细胞株为体外实验模型,流式细胞仪检测细胞早期凋亡标记Annexin V以及进行细胞周期分析。结果一疗程完全缓解率为46.2%(6/13),部分缓解率为38.5%(5/13),总有效率84.7%(11/13);二疗程完全缓解率为76.9%(10/13)。体外实验中,经CAG处理后,早期凋亡标记Annexin V明显升高(P<0.01)。细胞周期检测显示,CAG处理24 h后,S期细胞比例明显升高(P<0.05)。结论G-CSF可增加化疗药物对AML的疗效,其作用机制主要是通过G-CSF促使G0期白血病细胞进入细胞增殖周期,增加细胞周期特异性化疗药物的细胞毒性,诱导细胞凋亡是主要途径。

Curative Effect of CAG Regimen on Patients with Untreated Acute Myeloid Leukemia and Its Mechanism

Objective To evaluate the efficacy of CAG treatment on patients with untreated acute myeloid leukemia(AML) and study its mechanism. Methods Thirteen patients with AML were treated with CAG regimen consisting of low-dose arabinosylcytosine(Ara-c),aclarubicin and granulocyte colony-stimulating factor(G-CSF).By(using) U937 cell line as a model,apoptotic marker Annexin V and cell cycle were determined by flow cytometry assay.(Results)Six cases achieved complete remission,and five cases,partial remission.The total remission rate was(84.7%) after one course of chemotherapy.The total complete remission rate of 13 patients was(76.9%) after two courses of chemotherapy.In vitro,after incubation with CAG,Annexin V increased(P<0.01).Incubation with CAG for 24 h,the S-phase cells increased(P<0.05). Conclusion G-CSF sensitizes leukemia cells to the effect of Ara-C and aclarubicin then enhances the response.The mechanism is that G-CSF can enhance cytotoxicity to drugs such as Ara-c and aclarubicin by promoting G0phase cells into the reproductive cycle.Apoptosis inducing is the main way.