Grigorieva I, Thomas X, Epstein J
The Arkansas Cancer Research Center, Department of Medicine, University of Arkansas for Medical Sciences, Little Rock 72205, USA.
Exp Hematol. 1998 Jul;26(7):597-603.
Dexamethasone (Dex), which is often used for the treatment of multiple myeloma, produces rapid reductions in tumor mass and improvement in disease symptoms; however, it is not curative, and drug-resistant cells eventually emerge. To elucidate this apparent paradox, we tested the effect of the bone marrow environment on myeloma cell response to this drug. To determine whether bone marrow stroma provides sufficient amounts of interleukin (IL)-6 to protect myeloma cells against the effects of Dex, we compared the production of IL-6 by marrow stromal cells from four myeloma patients before, during, and after exposure to 10(-7) M Dex, and found that even in the presence of this drug, stromal cells continued to produce IL-6, albeit in reduced concentrations. We tested the ability of stromal cells to protect myeloma cells, purified from the bone marrow of seven patients by cell sorting on the basis of CD38 and CD45 expression, and two light-scatter parameters, from Dex-induced apoptosis. In contrast to mature CD38+CD45- cells, which were not protected, coculture with stroma very effectively protected immature CD38+CD45+ myeloma cells from Dex. These data may explain the palliative efficacy of Dex treatment and provide a rationale for combining IL-6 antagonists with Dex to overcome the IL-6-mediated resistance of immature tumor cells.
地塞米松(Dex)常用于治疗多发性骨髓瘤,可使肿瘤体积迅速缩小并改善疾病症状;然而,它无法治愈疾病,最终会出现耐药细胞。为阐明这一明显的矛盾现象,我们测试了骨髓环境对骨髓瘤细胞对该药物反应的影响。为确定骨髓基质是否能提供足够量的白细胞介素(IL)-6来保护骨髓瘤细胞免受Dex的影响,我们比较了4例骨髓瘤患者的骨髓基质细胞在暴露于10⁻⁷M Dex之前、期间和之后IL-6的产生情况,发现即使在该药物存在的情况下,基质细胞仍继续产生IL-6,尽管浓度有所降低。我们测试了基质细胞保护骨髓瘤细胞的能力,这些骨髓瘤细胞是通过基于CD38和CD45表达以及两个光散射参数的细胞分选从7例患者的骨髓中纯化得到的,使其免受Dex诱导的凋亡。与未受保护的成熟CD38⁺CD45⁻细胞不同,与基质细胞共培养能非常有效地保护未成熟的CD38⁺CD45⁺骨髓瘤细胞免受Dex的影响。这些数据可能解释了Dex治疗的姑息疗效,并为将IL-6拮抗剂与Dex联合使用以克服未成熟肿瘤细胞的IL-6介导的耐药性提供了理论依据。