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Clinical features and prognosis of core binding factor acute myeloid leukemia in children
LIU Chao, CHEN Xiao-Yan, YI Mei-Hui, WU Wen-Qi, RUAN Min, ZHU Xiao-Fan
Chinese Journal of Contemporary Pediatrics ›› 2020, Vol. 22 ›› Issue (7) : 739-743.
PDF(1496 KB)
PDF(1496 KB)
Clinical features and prognosis of core binding factor acute myeloid leukemia in children
Objective To study the clinical features and prognosis of core binding factor acute myeloid leukemia (CBF-AML) in children. Methods A retrospective analysis was performed from the chart review data of children who were newly diagnosed with CBF-AML in the Institute of Hematology & Blood Diseases Hospital, Chinese Academy of Medical Sciences, from August 2009 to November 2015. According to the type of fusion gene, the children were divided into CBFB-MYH11 and AML1-ETO groups. Clinical features and prognosis were analyzed and compared between the two groups. Results A total of 91 children with CBF-AML were enrolled in this study, among whom there were 74 (81%) in the AML1-ETO group and 17 (19%) in the CBFB-MYH11 group. Additional chromosomal abnormalities were observed in 38 children (42%), and deletion of sex chromosome was the most common abnormality and was observed in 28 children (31%). After the first course of induction treatment, the complete remission rate was 97% (88/91), the recurrence rate was 29% (26/91), the 5-year event-free survival (EFS) rate was 65%±6%, and the 5-year overall survival (OS) rate was 75%±5%. There were no significant differences between the AML1-ETO and CBFB-MYH11 groups in 5-year EFS rate (62%±7% vs 77%±11%, P > 0.05) or 5-year OS rate (72%±6% vs 88%±9%, P > 0.05). Conclusions AML1-ETO is the main type of fusion gene in children with CBF-AML, and deletion of sex chromosome is the most common type of additional chromosomal abnormalities. Children with CBF-AML often have a good prognosis, and the children with AML1-ETO have a similar prognosis to those with CBFB-MYH11.
Acute myeloid leukemia / Core binding factor / Clinical feature / Prognosis / Child
[1] Pui CH, Carroll WL, Meshinchi S, et al. Biology, risk stratification, and therapy of pediatric acute leukemias:an update[J]. J Clin Oncol, 2011, 29(5):551-565.
[2] Badr P, Elsayed GM, Eldin DN, et al. Detection of KIT mutations in core binding factor acute myeloid leukemia[J]. Leuk Res Rep, 2018, 10:20-25.
[3] Faber ZJ, Chen X, Gedman AL, et al. The genomic landscape of core-binding factor acute myeloid leukemias[J]. Nat Genet, 2016, 48(12):1551-1556.
[4] 陈晓燕, 刘超, 吴文齐, 等. 儿童非核心结合因子急性髓系白血病的疗效及预后因素分析[J]. 中国当代儿科杂志, 2020, 22(5):466-472.
[5] 沈悌, 赵永强. 血液病诊断及疗效标准[M]. 第4版. 北京:科学出版社, 2018:91-94.
[6] 车琳, 许云云, 庞丽, 等. 核因子阳性儿童急性髓细胞性白血病临床特征及预后因素分析[J]. 中华实用儿科临床杂志, 2014, 29(3):207-211.
[7] Chen X, Dou H, Wang X, et al. KIT mutations correlate with adverse survival in children with core-binding factor acute myeloid leukemia[J]. Leuk Lymphoma, 2018, 59(4):829-836.
[8] Zwaan CM, Kolb EA, Reinhardt D, et al. Collaborative efforts driving progress in pediatric acute myeloid leukemia[J]. J Clin Oncol, 2015, 33(27):2949-2962.
[9] Klein K, Kaspers G, Harrison CJ, et al. Clinical impact of additional cytogenetic aberrations, cKIT and RAS mutations, and treatment elements in pediatric t(8;21)-AML:results from an international retrospective study by the International Berlin-Frankfurt-Münster Study Group[J]. J Clin Oncol, 2015, 33(36):4247-4258.
[10] Kolb EA, Meshinchi S. Acute myeloid leukemia in children and adolescents:identification of new molecular targets brings promise of new therapies[J]. Hematology Am Soc Hematol Educ Program, 2015, 2015:507-513.
[11] 吴珺, 陆爱东, 张乐萍, 等. 儿童核心结合因子相关性急性髓系白血病疗效及预后因素分析[J]. 中华血液学杂志, 2019, 40(1):52-57.
[12] 阮敏, 戚本泉, 刘芳, 等. 儿童急性髓系白血病82例长期随访研究[J]. 中华儿科杂志, 2018, 56(10):730-734.
[13] Marcucci G, Mrózek K, Ruppert AS, et al. Prognostic factors and outcome of core binding factor acute myeloid leukemia patients with t(8;21) differ from those of patients with inv(16):a Cancer and Leukemia Group B study[J]. J Clin Oncol, 2005, 23(24):5705-5717.
[14] Rubnitz JE, Inaba H, Dahl G, et al. Minimal residual disease-directed therapy for childhood acute myeloid leukaemia:results of the AML02 multicentre trial[J]. Lancet Oncol, 2010, 11(6):543-552.
[15] Tsukimoto I, Tawa A, Horibe K, et al. Risk-stratified therapy and the intensive use of cytarabine improves the outcome in childhood acute myeloid leukemia:the AML99 trial from the Japanese Childhood AML Cooperative Study Group[J]. J Clin Oncol, 2009, 27(24):4007-4013.
[16] Ishikawa Y, Kawashima N, Atsuta Y, et al. Prospective evaluation of prognostic impact of KIT mutations on acute myeloid leukemia with RUNX1-RUNX1T1 and CBFB-MYH11[J]. Blood Adv, 2020, 4(1):66-75.
[17] Paschka P, Schlenk RF, Weber D, et al. Adding dasatinib to intensive treatment in core-binding factor acute myeloid leukemia-results of the AMLSG 11-08 trial[J]. Leukemia, 2018, 32(7):1621-1630.
[18] Duployez N, Marceau-Renaut A, Boissel N, et al. Comprehensive mutational profiling of core binding factor acute myeloid leukemia[J]. Blood, 2016, 127(20):2451-2459.
[19] Creutzig U, Zimmermann M, Bourquin JP, et al. Second induction with high-dose cytarabine and mitoxantrone:different impact on pediatric AML patients with t(8;21) and with inv(16)[J]. Blood, 2011, 118(20):5409-5415.
[20] 贾月萍, 左英熹, 陆爱东, 等. 儿童急性髓系白血病M2型性染色体缺失的预后意义[J]. 中国当代儿科杂志, 2015, 17(2):168-171.
[21] 姚新原, 赵利师, 安曦洲, 等. 附加染色体异常的t(8;21)阳性儿童急性髓细胞白血病临床分析[J]. 现代医药卫生, 2018, 34(17):2613-2615, 2618.
