George Binsah, Yohannan Binoy, Mohlere Virginia, Gonzalez Anneliese
Department of Hematology/Oncology, McGovern Medical School, The University of Texas Health Sciences Center at Houston, 6410 Fannin, Suite 830 Houston, TX 77030, USA.
Int J Hematol Oncol. 2023 Feb 14;12(1):IJH43. doi: 10.2217/ijh-2022-0004. eCollection 2023 Feb.
Therapy-related acute myeloid leukemia (t-AML) usually stems from exposure of the bone marrow to cytotoxic chemotherapy and/or radiation therapy. t-AML is usually associated with poor overall survival, but occasionally t-AML can involve favorable-risk cytogenetics, including core binding factor AML (CBF-AML), which shows a recurrent chromosomal rearrangement with t(8;21) (q22;22) and 'inv(16) (p13.1;q22)/t(16;16)(p13.1;q22)', leading to '' fusion genes, respectively. Therapy-related CBF-AML (t-CBF-AML) accounts for 5-15% of CBF-AML cases and tends to have better outcomes than t-AML with unfavorable cytogenetics. Although CBF-AML is sensitive to high-dose cytarabine, t-CBF-AML has worse overall survival than CBF- AML. The objective of this review is to discuss the available data on the pathogenesis, mutations, and therapeutic options in patients with t-CBF-AML.
治疗相关的急性髓系白血病(t-AML)通常源于骨髓暴露于细胞毒性化疗和/或放射治疗。t-AML通常与总体生存率低相关,但偶尔t-AML可涉及有利风险的细胞遗传学,包括核心结合因子AML(CBF-AML),其显示出与t(8;21)(q22;22)和“inv(16)(p13.1;q22)/t(16;16)(p13.1;q22)”的复发性染色体重排,分别导致“ ”融合基因。治疗相关的CBF-AML(t-CBF-AML)占CBF-AML病例的5-15%,并且与细胞遗传学不良的t-AML相比往往有更好的结果。虽然CBF-AML对高剂量阿糖胞苷敏感,但t-CBF-AML的总体生存率比CBF-AML更差。本综述的目的是讨论t-CBF-AML患者发病机制、突变和治疗选择的现有数据。