Chronic myeloid leukemia (CML) is a myeloproliferative disorder characterized by the BCR-ABL oncoprotein, known to drive leukemogenesis by orchestrating multiple signaling pathways ultimately involved in cell survival. Despite successful response rates of CML patients to tyrosine kinase inhibitors (TKIs), resistance eventually arises due to BCR-ABL-dependent and independent mechanisms. Survivin is an inhibitor of apoptosis protein acting in the interface between apoptosis deregulation and cell cycle progression. In CML, high levels of survivin have been associated with late stages of disease and therapy resistance. In this review, we provide an overview of important aspects concerning survivin subcellular localization and expression pattern in CML patients and cell lines. Moreover, we highlight the relevance of molecular networks involving survivin for disease progression and treatment resistance. Finally, we discuss the mechanisms accounting for survivin overexpression, as well as novel therapeutic interventions that have been designed to counteract survivin-associated malignancy in CML.

慢性粒细胞白血病（CML）是一种以BCR-ABL癌蛋白为特征的骨髓增生性疾病，已知可通过编排最终参与细胞存活的多种信号通路来驱动白血病的发生。尽管CML患者对酪氨酸激酶抑制剂（TKIs）的反应成功率很高，但由于BCR-ABL依赖性和独立机制，最终产生了耐药性。Survivin是凋亡蛋白的抑制剂，作用于凋亡失调与细胞周期进程之间的界面。在CML中，高水平的生存素与疾病晚期和治疗耐药性有关。在这篇综述中，我们提供了有关CML患者和细胞系中survivin亚细胞定位和表达模式的重要方面的概述。此外，我们强调了涉及survivin的分子网络与疾病进展和治疗耐药性的相关性。最后，我们讨论了survivin过表达的机制，以及旨在抵消CML中与survivin相关的恶性肿瘤的新型治疗性干预措施。