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慢性髓性白血病患者无治疗缓解的替代标志物。

Surrogate Markers for Treatment-Free Remission in Patients With Chronic Myeloid Leukemia.

机构信息

Division of Hematology, Respiratory Medicine and Oncology, Department of Internal Medicine, Faculty of Medicine, Saga University, Saga, Japan; Department of Drug Discovery and Biomedical Sciences, Faculty of Medicine, Saga University, Saga, Japan.

Division of Hematology, Respiratory Medicine and Oncology, Department of Internal Medicine, Faculty of Medicine, Saga University, Saga, Japan; Department of Drug Discovery and Biomedical Sciences, Faculty of Medicine, Saga University, Saga, Japan.

出版信息

Clin Lymphoma Myeloma Leuk. 2020 Dec;20(12):785-790. doi: 10.1016/j.clml.2020.07.004. Epub 2020 Jul 16.

Abstract

BCR-ABL1 tyrosine kinase inhibitors (TKIs) improve long-term survival of patients with chronic-phase (CP) chronic myeloid leukemia (CML). Recently, the treatment goal for patients with CML-CP became safe discontinuation of TKIs. Several clinical trials have shown that approximately half of patients who experience a durable deep molecular response during TKI treatment maintain molecular remission after discontinuation of TKIs. However, the factors responsible for successful treatment-free remission (TFR) remain unclear. This study reviews very recent TKI discontinuation studies, focusing on factors responsible for TFR in patients with CML-CP. Longer TKI treatment duration, time of deep molecular response, presence of withdrawal syndrome, deeper molecular response, lower Sokal score, interferon α treatment before TKI administration, and favorable natural killer or T-cell profiles may be associated with TFR. However, different study designs have generated inconsistent data. Further investigations are needed to identify factors that consistently favor achievement of TFR.

摘要

BCR-ABL1 酪氨酸激酶抑制剂(TKI)可改善慢性期(CP)慢性髓性白血病(CML)患者的长期生存。最近,CML-CP 患者的治疗目标已变为安全停用 TKI。几项临床试验表明,在 TKI 治疗期间获得持久深度分子缓解的患者中,约有一半在停用 TKI 后仍保持分子缓解。然而,导致成功无治疗缓解(TFR)的因素仍不清楚。本研究复习了最近的 TKI 停药研究,重点探讨了 CP-CML 患者 TFR 的相关因素。更长的 TKI 治疗持续时间、深度分子反应时间、停药综合征的存在、更深的分子反应、更低的 Sokal 评分、TKI 治疗前的干扰素α治疗以及有利的自然杀伤细胞或 T 细胞表型可能与 TFR 相关。然而,不同的研究设计产生了不一致的数据。需要进一步的研究来确定一致有利于实现 TFR 的因素。

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