Gaut Daria, Sasine Joshua, Schiller Gary
Department of Medicine, David Geffen School of Medicine, University of California Los Angeles, LA, California, USA.
Division of Hematology/Oncology, Department of Medicine, David Geffen School of Medicine, University of California Los Angeles, LA, California, USA.
Leuk Res Rep. 2018 Apr 16;9:65-71. doi: 10.1016/j.lrr.2018.04.005. eCollection 2018.
Although rare, secondary clonal hematologic neoplasia may occur after successful therapy for acute promyelocytic leukemia (APL). These secondary clonal events may be considered therapy-related, but may also be due to an underlying background of clonal hematopoiesis from which both malignancies may develop. In this manuscript, we describe two patients with secondary clones after APL therapy characterized in one patient by deletion of chromosome 11q23 and, in the other, by monosomy of chromosome 7, and also provide a review of all secondary clonal disorders described after APL therapy. We suggest that since most reports identify karyotypic abnormalities not typically associated with chemotherapy, there may be another mechanism underlying secondary clonal development after complete response to initial APL therapy.
尽管罕见，但急性早幼粒细胞白血病（APL）成功治疗后可能会发生继发性克隆性血液系统肿瘤。这些继发性克隆事件可能被认为与治疗相关，但也可能是由于潜在的克隆性造血背景所致，两种恶性肿瘤都可能由此发展而来。在本手稿中，我们描述了两名APL治疗后出现继发性克隆的患者，其中一名患者的特征是11q23染色体缺失，另一名患者的特征是7号染色体单体性，并且还对APL治疗后描述的所有继发性克隆性疾病进行了综述。我们认为，由于大多数报告都发现了通常与化疗无关的核型异常，因此在对初始APL治疗完全缓解后，继发性克隆发展可能存在另一种潜在机制。
