急性髓系白血病自体免疫的产生和干扰素治疗后完全缓解的维持。

M W Lowdell, R Craston, H G Prentice
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引用次数: 0

摘要

干扰素- α (ifn - α)已被确定为慢性髓性白血病治疗的一部分,尽管其确切的作用方式在很大程度上仍不清楚。它在急性髓性白血病(AML)中的应用受到限制。我们之前已经记录了自体骨髓移植后患者对AML原细胞的自体细胞溶解活性。在这里,我们提出了一个低风险AML患者,首次完全缓解(CR)复发,不愿意接受大剂量化疗和干细胞救援。在第二次化疗诱导的CR中,患者在体外试验中没有抗白血病溶细胞活性的证据,她开始使用ifn - α (Roferon)。她随后出现了高水平的白血病特异性细胞毒性,并在第二CR中停留了两年。这些发现支持在低风险AML患者中使用ifn - α,并提示其中一种作用机制可能是免疫学的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Generation of autologous immunity to acute myeloid leukaemia and maintenance of complete remission following interferon-alpha treatment.

Interferon-alpha (IFN-alpha) is established as part of the treatment for chronic myeloid leukaemia, although its precise mode of action remains largely unknown. Its use in acute myeloid leukaemia (AML) has been limited. We have previously documented autologous cytolytic activity against AML blasts in patients after autologous bone marrow transplantation. Here we present a patient with poor-risk AML who relapsed from first complete remission (CR) and was unwilling to undergo high-dose chemotherapy with stem cell rescue. In second chemotherapy-induced CR, the patient had no evidence of antileukaemia cytolytic activity in an in vitro assay, and she commenced IFN-alpha (Roferon). She subsequently developed high levels of leukaemia-specific cytotoxicity, and has remained in second CR for two years. These findings support the use of IFN-alpha in patients with poor-risk AML, and suggest that one mechanism of action may be immunological.

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