Tianjin Medical University.
Department of Pediatric, Maternal and Child Health Hospital of Tangshan, Tangshan.
J Pediatr Hematol Oncol. 2023 Aug 1;45(6):e739-e745. doi: 10.1097/MPH.0000000000002632. Epub 2023 Feb 20.
Polo-like kinase 1 (PLK1) modulates leukemia cell apoptosis, proliferation, and cell cycle arrest in the progression of acute lymphoblastic leukemia (ALL). This study intended to investigate the dysregulation of PLK1 and its association with induction therapy response and prognosis in pediatric ALL patients.
Bone marrow mononuclear cell samples were collected from 90 pediatric ALL patients at baseline and on the 15th day of induction therapy (D15), as well as from 20 controls after enrollment, for the detection of PLK1 by reverse transcription-quantitative polymerase chain reaction.
PLK1 was increased in pediatric ALL patients compared with controls ( P <0.001). In pediatric ALL patients, PLK1 decreased from baseline to D15 ( P <0.001). Lower PLK1 at baseline was associated with a good prednisone response ( P =0.002), while decreased PLK1 at D15 was related to good prednisone response ( P =0.001), better bone marrow response ( P =0.025), and favorable risk stratification ( P =0.014). In addition, reduced PLK1 at baseline was linked with better event-free survival (EFS) ( P =0.046), and decreased PLK1 at D15 was related to prolonged EFS ( P =0.027) and overall survival (OS) ( P =0.047). Moreover, PLK1 decline ≥25% was linked to favorable EFS ( P =0.015) and OS ( P =0.008). Further multivariate Cox proportional regression analysis revealed that PLK1 decline ≥25% was independently linked with prolonged EFS (hazard ratio (HR)=0.324, P =0.024) and OS (HR=0.211, P =0.019).
The reduction of PLK1 after induction therapy reflects a good treatment response and correlates with a favorable survival profile in pediatric ALL patients.
丝氨酸/苏氨酸激酶 Polo-like 激酶 1(PLK1)在急性淋巴细胞白血病(ALL)的进展中调节白血病细胞凋亡、增殖和细胞周期停滞。本研究旨在探讨 PLK1 的失调及其与儿科 ALL 患者诱导治疗反应和预后的关系。
基线时和诱导治疗第 15 天(D15)采集 90 例儿科 ALL 患者和 20 例对照者的骨髓单个核细胞样本,通过逆转录定量聚合酶链反应检测 PLK1。
与对照组相比,儿科 ALL 患者的 PLK1 升高(P<0.001)。儿科 ALL 患者的 PLK1 从基线到 D15 下降(P<0.001)。基线时较低的 PLK1 与泼尼松良好反应相关(P=0.002),而 D15 时 PLK1 的降低与泼尼松良好反应相关(P=0.001)、骨髓反应更好(P=0.025)和风险分层有利(P=0.014)相关。此外,基线时 PLK1 的降低与更好的无事件生存(EFS)相关(P=0.046),D15 时 PLK1 的降低与 EFS 延长(P=0.027)和总生存(OS)延长(P=0.047)相关。此外,PLK1 下降≥25%与有利的 EFS(P=0.015)和 OS(P=0.008)相关。进一步的多变量 Cox 比例风险回归分析显示,PLK1 下降≥25%与 EFS 延长(风险比(HR)=0.324,P=0.024)和 OS 延长(HR=0.211,P=0.019)独立相关。
诱导治疗后 PLK1 的减少反映了良好的治疗反应,并与儿科 ALL 患者良好的生存预后相关。