Ohshima A, Miura I, Chubachi A, Hashimoto K, Nimura T, Utsumi S, Takahashi N, Hayashi Y, Seto M, Ueda R, Miura A B
Third Department of Internal Medicine, Akita University School of Medicine, Japan.
Am J Hematol. 1996 Dec;53(4):264-6. doi: 10.1002/(SICI)1096-8652(199612)53:4<264::AID-AJH12>3.0.CO;2-C.
We report on 2 patients with acute leukemia who had an 11q23 chromosomal aberration as an additional change after treatment with etoposide and mitoxantrone, agents that affect topoisomerase II (Topo II). One patient with Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukemia (L2) received chemotherapy, including 1,000 mg of etoposide and 75 mg of mitoxantrone. She relapsed 10 months later. Analysis at time of relapse showed a chromosomal aberration of del(11)(q23) as an additional cytogenetic change. The other patient was diagnosed with acute monoblastic leukemia (M5a) and received two autologous peripheral blood stem-cell transplantations. Her cumulative doses of etoposide and mitoxantrone were 6,000 mg and 42 mg, respectively. She also relapsed, and analysis at that time revealed del(11)(q23) as an additional chromosomal aberration. The mixed lineage leukemia/myeloid-lymphoid leukemia (MLL) gene was not rearranged in either case, making these cases distinct from previously described therapy-related leukemias caused by Topo II inhibitors. Based on these two cases, it may be that Topo II inhibitors can cause clonal evolution affecting chromosome band 11q23.
我们报告了2例急性白血病患者,他们在接受依托泊苷和米托蒽醌治疗后出现11q23染色体畸变作为额外的改变,这两种药物会影响拓扑异构酶II(Topo II)。1例费城染色体阳性(Ph+)急性淋巴细胞白血病(L2)患者接受了化疗,包括1000mg依托泊苷和75mg米托蒽醌。10个月后她复发了。复发时的分析显示,del(11)(q23)染色体畸变作为额外的细胞遗传学改变。另1例患者被诊断为急性单核细胞白血病(M5a),并接受了两次自体外周血干细胞移植。她的依托泊苷和米托蒽醌累积剂量分别为6000mg和42mg。她也复发了,当时的分析显示del(11)(q23)作为额外的染色体畸变。在这两例中,混合谱系白血病/髓系-淋巴系白血病(MLL)基因均未重排,这使得这些病例与先前描述的由Topo II抑制剂引起的治疗相关白血病不同。基于这两例病例,可能是Topo II抑制剂可导致影响染色体带11q23的克隆进化。