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目的 :探讨IFN α及IFN α联合GM CSF调节慢性期慢性粒细胞白血病 (CML CP)患者骨髓单个核细胞(MNCs) bcr abl,bcl 2 和 c myc基因表达的影响。方法 :淋巴细胞分离液离心富集 14例CML CP患者骨髓MNCs,经干扰素 α(IFN α)及IFN α联合粒细胞 -巨噬细胞集落刺激因子 (GM CSF)培养 2 4h后 ,采用相对定量逆转录 -聚合酶链反应 (RT PCR)及扩增片段光密度扫描分析bcr abl,bcl 2 ,c myc及β actin 基因表达水平 ,配对t检验统计分析组间差异。结果 :IFN α(2 0 0U·ml-1)及IFN α(2 0 0U·ml-1)联合GM CSF(10ng·ml-1)均显著抑制bcr abl基因表达 ;IFN α部分抑制 c myc及 bcl 2 基因表达 ;GM CSF在IFN α作用的基础上部分促进 bcr abl及 c myc基因表达和显著抑制 bcl 2 基因表达。结论 :IFN α及IFN α联合GM CSF均可抑制抗凋亡基因bcr abl和bcl 2基因表达 ,并调节c myc基因表达水平。通过促进细胞凋亡而抑制恶性克隆增长是IFN α或IFN α联合GM CSF治疗CML的可能作用机制。
AIM: To investigate the effects of IFNα and IFNα combined with GM CSF on the expression of bcr abl, bcl 2 and c myc in bone marrow mononuclear cells (MNCs) of patients with chronic myeloid leukemia (CML CP). METHODS: Bone marrow MNCs from 14 patients with CML CP were enriched by centrifugation in lymphocytes. The cells were cultured for 24 hours with interferon α (IFN α) and IFN α (GM-CSF) for 24 h. The relative quantification The expression of bcr abl, bcl 2, c myc and β actin were detected by reverse transcriptase-polymerase chain reaction (RT PCR) and optical density scanning (FTIR). The difference between groups was statistically analyzed by paired t-test. Results: IFNα (200U · ml-1) and IFNα (200U · ml-1) combined with GM CSF (10ng · ml-1) significantly inhibited bcr abl gene expression; IFNα partially inhibited c myc and bcl 2 gene expression; GM CSF partially promote the expression of bcr abl and c myc genes and significantly inhibit bcl 2 gene expression on the basis of IFN α. CONCLUSION: Both IFNα and IFNα combined with GM-CSF can inhibit the expression of anti-apoptotic genes bcr abl and bcl 2 and regulate the expression of c-myc gene. Inhibition of malignant clonal growth by promoting apoptosis is a potential mechanism of action of IFNα or IFNα in combination with GM CSF in the treatment of CML.