Pedersen-Bjergaard J, Brøndum-Nielsen K, Karle H, Johansson B
Department of Hematology, Rigshospitalet, Copenhagen, Denmark.
Leukemia. 1997 Sep;11(9):1571-4. doi: 10.1038/sj.leu.2400769.
Therapy with DNA topoisomerase II inhibitors has been shown to result in an increased risk of acute myeloid leukemia (AML), often presenting balanced translocations to chromosome bands 11q23 and 21q22. Also other balanced aberrations, more rarely observed in therapy-related AML (t-AML), such as t(15;17) and inv(16) have been associated with these drugs. Recently we observed a case of chronic myeloid leukemia (CML) with t(9;22) after therapy of a germ cell tumor with etoposide, cisplatin and bleomycin. Based on this case and a review of chemotherapy-related leukemias with t(9;22) from the literature, we suggest a causal relationship between therapy with DNA topoisomerase II inhibitors and development of various types of leukemia carrying the Philadelphia chromosome.
DNA拓扑异构酶II抑制剂治疗已被证明会导致急性髓系白血病（AML）风险增加，常出现与11q23和21q22染色体带的平衡易位。在治疗相关AML（t-AML）中较少观察到的其他平衡畸变，如t(15;17)和inv(16)也与这些药物有关。最近，我们观察到1例在接受依托泊苷、顺铂和博来霉素治疗生殖细胞肿瘤后发生t(9;22)的慢性髓系白血病（CML）病例。基于该病例及文献中对化疗相关t(9;22)白血病的回顾，我们认为DNA拓扑异构酶II抑制剂治疗与携带费城染色体的各类白血病发生之间存在因果关系。
