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Regulation of Tumor Necrosis Factor-related Apoptosis-inducing Ligand Expression in Primary Acute Leukemic Cells by Chemotherapeutics

机译:化学疗法对肿瘤坏死因子相关凋亡诱导配体在原发急性白血病细胞中表达的调节

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摘要

>Objective: The expression of the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) protein and its regulation by chemotherapeutics were analyzed in primary acute leukemic cells. >Materials and Methods: Peripheral blood was collected from 16 patients with acute leukemia on days 0, 1, 3, and 5 of chemotherapy. The mononuclear cells were separated from the peripheral blood, and TRAIL expression was assessed by flow cytometry. The bone marrow mononuclear cells of patients with acute leukemia were separated before chemotherapy and cultured in vitro with VP-16 and/or interferon (IFN). The TRAIL expression level was detected after the cell culture. Re>sults: TRAIL expression in the mononuclear cells of peripheral blood was significantly upregulated on day 1 (p<0.05) and then significantly decreased on day 5 after chemotherapy (p<0.05). Results from the in vitro culture revealed that VP-16 upregulated TRAIL expression in the bone marrow mononuclear cells of patients with acute leukemia, but the binding of VP-16 to IFN did not enhance TRAIL expression as compared with VP-16 alone (p>0.05). >onclusion: OA single chemotherapy mechanism for leukemia may suffice to induce TRAIL expression and promote the apoptosis of leukemic cells.>Conflict of interest:None declared.
机译:>目的:分析了原发性急性白血病细胞中肿瘤坏死因子相关的凋亡诱导配体(TRAIL)蛋白的表达及其化学疗法的调控作用。 >材料和方法:在化疗的第0、1、3和5天从16例急性白血病患者中收集外周血。从外周血中分离单核细胞,并通过流式细胞术评估TRAIL表达。化疗前分离出急性白血病患者的骨髓单个核细胞,并在体外用VP-16和/或干扰素(IFN)培养。细胞培养后检测TRAIL表达水平。 >结果:化疗后第1天,外周血单核细胞中TRAIL表达显着上调(p <0.05),然后在第5天显着降低(p <0.05)。体外培养的结果表明,VP-16上调了急性白血病患者骨髓单个核细胞中的TRAIL表达,但与单独的VP-16相比,VP-16与IFN的结合并未增强TRAIL的表达(p> 0.05)。 >纳入: OA单一白血病化疗机制可能足以诱导TRAIL表达并促进白血病细胞凋亡。>利益冲突:尚无明确声明。

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