文章：

血清BCMA水平可预测MGUS和冒烟型骨髓瘤患者的预后

Acute promyelocytic leukemia current treatment algorithms

原文发布日期：2021-06-30

DOI: 10.1038/s41408-021-00514-3

类型: Review Article

开放获取: 是

英文摘要：

In 1957, Hillestad et al. defined acute promyelocytic leukemia (APL) for the first time in the literature as a distinct type of acute myeloid leukemia (AML) with a “rapid downhill course” characterized with a severe bleeding tendency. APL, accounting for 10–15% of the newly diagnosed AML cases, results from a balanced translocation, t(15;17) (q22;q12-21), which leads to the fusion of the promyelocytic leukemia (PML) gene with the retinoic acid receptor alpha (RARA) gene. The PML–RARA fusion oncoprotein induces leukemia by blocking normal myeloid differentiation. Before using anthracyclines in APL therapy in 1973, no effective treatment was available. In the mid-1980s, all-trans retinoic acid (ATRA) monotherapy was used with high response rates, but response durations were short. Later, the development of ATRA, chemotherapy, and arsenic trioxide combinations turned APL into a highly curable malignancy. In this review, we summarize the evolution of APL therapy, focusing on key milestones that led to the standard-of-care APL therapy available today and discuss treatment algorithms and management tips to minimize induction mortality.
 

摘要翻译： 

1957年，Hillestad等人首次在文献中将急性早幼粒细胞白血病（APL）定义为一种独特的急性髓系白血病（AML）亚型，其特点是“病情急剧恶化”并伴有严重出血倾向。APL占新诊断AML病例的10-15%，由t(15;17)(q22;q12-21)平衡易位导致早幼粒细胞白血病（PML）基因与维甲酸受体α（RARA）基因融合而形成。PML-RARA融合癌蛋白通过阻断正常髓系分化诱发白血病。在1973年将蒽环类药物应用于APL治疗前，该疾病缺乏有效疗法。20世纪80年代中期，全反式维甲酸（ATRA）单药治疗虽获得高缓解率，但缓解持续时间短暂。后来，ATRA联合化疗及三氧化二砷治疗方案的发展使APL转变为高度可治愈的恶性肿瘤。本文综述将梳理APL治疗的演进历程，重点阐述促成当代标准治疗方案的关键里程碑事件，并探讨旨在降低诱导期死亡率的治疗策略与管理要点。

原文链接：

Acute promyelocytic leukemia current treatment algorithms