Fu Rongfeng, Dong Huan, Gu Wenjing, Meng Ke, Sun Ting, Liu Xiaofan, Qu Xinmiao, Chen Jia, Xue Feng, Liu Wei, Chen Yunfei, Ju Mankai, Dai Xinyue, Chi Ying, Wang Wentian, Pei Xiaolei, Zhu Xiaofan, Yang Renchi, Li Huiyuan, Zhang Lei
State Key Laboratory of Experimental Hematology, National Clinical Research Center for Blood Diseases, Haihe Laboratory of Cell Ecosystem, Tianjin Key Laboratory of Gene Therapy for Blood Diseases, CAMS Key Laboratory of Gene Therapy for Blood Diseases, Institute of Hematology & Blood Diseases Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Tianjin, 300020, China.
Tianjin Institutes of Health Science, Tianjin, 301600, China.
Leukemia. 2025 Jan;39(1):155-165. doi: 10.1038/s41375-024-02432-2. Epub 2024 Oct 8.
The paucity of essential thrombocythemia (ET) and prefibrotic primary myelofibrosis (pre-PMF) in individuals younger than 18 years highlights several unresolved issues in diagnosis, clinical outcomes, and treatment strategies. To address these knowledge gaps, we analyzed a large bidirectional cohort consisting of childhood and adolescent ET (CAA-ET, n = 156) and pre-PMF (CAA-preMF, n = 13), as well as adult ET (n = 349). We introduced immunophenotypic abnormalities as novel clonal markers in CAA-ET and CAA-preMF, establishing a comprehensive method for clonal marker detection that integrated driver and non-driver mutations, positive endogenous erythroid colony formation, immunophenotypic abnormalities, and chromosomal aberrations. Next-generation sequencing revealed distinct mutational profiles between CAA-ET and adult ET, along with different age-related trends in the distribution of driver mutations. Venous thrombosis was more prevalent in CAA-ET, with JAK2 V617F emerging as a potential risk factor (P = 0.018). Immunophenotypic abnormalities were identified as risk factors for disease progression (P = 0.027). Significant differences between expected and actual treatment practices were identified. Compared to CAA-ET, CAA-preMF demonstrated poorer progression-free survival (P < 0.001) and faster disease progression (P = 0.019). This study provides a critical foundation for refining diagnostic, prognostic, and therapeutic approaches for CAA-ET and CAA-preMF.
18岁以下个体中原发性血小板增多症(ET)和纤维化前期原发性骨髓纤维化(pre-PMF)病例稀少,这凸显了诊断、临床结局及治疗策略方面的几个未解决问题。为填补这些知识空白,我们分析了一个大型双向队列,其中包括儿童及青少年ET(儿童及青少年ET,n = 156)和pre-PMF(儿童及青少年pre-PMF,n = 13),以及成人ET(n = 349)。我们引入免疫表型异常作为儿童及青少年ET和儿童及青少年pre-PMF中的新型克隆标志物,建立了一种综合的克隆标志物检测方法,该方法整合了驱动和非驱动突变、内源性红系集落形成阳性、免疫表型异常及染色体畸变。二代测序揭示了儿童及青少年ET与成人ET之间不同的突变谱,以及驱动突变分布中与年龄相关的不同趋势。静脉血栓形成在儿童及青少年ET中更为普遍,JAK2 V617F成为一个潜在危险因素(P = 0.018)。免疫表型异常被确定为疾病进展的危险因素(P = 0.027)。研究发现预期治疗实践与实际治疗实践之间存在显著差异。与儿童及青少年ET相比,儿童及青少年pre-PMF的无进展生存期更短(P < 0.001),疾病进展更快(P = 0.019)。本研究为完善儿童及青少年ET和儿童及青少年pre-PMF的诊断、预后及治疗方法提供了关键基础。