Department of Pathology, Duke University Medical Center, Durham, NC 27710, USA.
Leukemia. 2010 Sep;24(9):1580-7. doi: 10.1038/leu.2010.150. Epub 2010 Jul 8.
B-cell chronic lymphocytic leukemia (CLL) is characterized by slow accumulation of malignant cells, which are supported in the microenvironment by cell-cell interactions and soluble cytokines such as tumor necrosis factor (TNF). We evaluated the effect of the small molecule TNF inhibitor LMP-420 on primary CLL cells. The mean concentration of LMP-420 required to induce 50% cytotoxicity (ED50) at 72 h was 245 n. LMP-420-induced time- and dose-dependent apoptosis, as shown by annexin V staining, caspase activation and DNA fragmentation. These changes were associated with decreased expression of anti-apoptotic proteins Mcl-1, Bcl-xL and Bcl-2. CLL cells from patients with poor prognostic indicators showed LMP-420 sensitivity equal to that for cells from patients with favorable characteristics. In addition, LMP-420 potentiated the cytotoxic effect of fludarabine and inhibited in vitro proliferation of stimulated CLL cells. Gene expression profiling indicated that the mechanism of action of LMP-420 may involve suppression of nuclear factor-kappaB and immune response pathways in CLL cells. LMP-420 had minimal effects on normal peripheral blood mononuclear cell, B- and T-cell function, and hematopoietic colony formation. Our data suggest that LMP-420 may be a useful treatment for CLL with negligible hematologic toxicities.
B 细胞慢性淋巴细胞白血病(CLL)的特征是恶性细胞缓慢积累,这些细胞在细胞间相互作用和肿瘤坏死因子(TNF)等可溶性细胞因子的支持下,在微环境中生存。我们评估了小分子 TNF 抑制剂 LMP-420 对原代 CLL 细胞的影响。在 72 小时内诱导 50%细胞毒性(ED50)所需的 LMP-420 平均浓度为 245n。LMP-420 诱导的时间和剂量依赖性细胞凋亡,如 Annexin V 染色、半胱天冬酶激活和 DNA 片段化所示。这些变化与抗凋亡蛋白 Mcl-1、Bcl-xL 和 Bcl-2 的表达减少有关。来自预后不良指标患者的 CLL 细胞与来自特征良好患者的细胞表现出相同的 LMP-420 敏感性。此外,LMP-420 增强了氟达拉滨的细胞毒性作用,并抑制了刺激的 CLL 细胞的体外增殖。基因表达谱分析表明,LMP-420 的作用机制可能涉及抑制 CLL 细胞中的核因子-κB 和免疫反应途径。LMP-420 对正常外周血单个核细胞、B 细胞和 T 细胞功能以及造血集落形成的影响最小。我们的数据表明,LMP-420 可能是一种有用的 CLL 治疗方法,具有可忽略的血液学毒性。