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.

1957 年，Hillestad 等人。文献中首次将急性早幼粒细胞白血病 (APL) 定义为一种独特类型的急性髓细胞白血病 (AML)，具有“快速下坡过程”，以严重出血倾向为特征。APL 占新诊断的 AML 病例的 10-15%，由平衡易位t (15;17) (q22;q12-21) 引起，导致早幼粒细胞白血病 ( PML ) 基因与视黄酸受体α（RARA) 基因。PML-RARA 融合癌蛋白通过阻断正常的骨髓分化诱导白血病。在 1973 年在 APL 治疗中使用蒽环类药物之前，没有有效的治疗方法。在 1980 年代中期，使用全反式维甲酸 (ATRA) 单一疗法，反应率高，但反应持续时间短。后来，ATRA、化疗和三氧化二砷组合的发展将 APL 变成了一种高度可治愈的恶性肿瘤。在这篇综述中，我们总结了 APL 治疗的演变，重点关注导致当今可用的标准护理 APL 治疗的关键里程碑，并讨论治疗算法和管理技巧，以尽量减少诱导死亡率。