Infant leukemia, topoisomerase II inhibitors, and the MLL gene.
Infant leukemia, topoisomerase II inhibitors, and the MLL gene.
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婴儿白血病、拓扑异构酶 II 抑制剂和 MLL 基因。
DOI：
10.1093/jnci/86.22.1678
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发表时间：
1994
期刊：
影响因子：
--
通讯作者：
Robison,LL
中科院分区：
文献类型：
--
作者：
Ross,JA;Potter,JD;Robison,LL
接受不同形式化疗的患者发生继发性白血病的情况并不少见。大多数化疗或放疗后的白血病病例属于急性髓系白血病 (AML) 类型 (1)。这些患者通常会经历骨髓增生异常阶段，据报道，原发性癌症的最初诊断与继发性 AML 的诊断之间有约 6 年的潜伏期。由此产生的 AML 通常表现出 5 号和/或 7 号染色体的部分或完全缺失 (2)。通常，这些病例是在使用烷化剂治疗并进行或不进行放射治疗后发生的 (3)。最近，一项涉及染色体带 11q23 异常的细胞遗传学发现伴随着一部分继发性 AML 病例（特别是单核细胞 [AML-M5] 和骨髓单核细胞 [AML-M4] 形式）；这些病例绝大多数是在使用表鬼臼毒素的治疗方案后发生的 (4, 5)。
Secondary leukemias occurring in patients treated with different forms of chemotherapy are not uncommon. The majority of leukemia cases following either chemotherapy or radiation treatment are of the acute myeloid leukemia (AML) type (1). These patients often follow a myelodysplastic phase, with a reported latent period of about 6 years between the original diagnosis of the primary cancer and that of the secondary AML. The resulting AML usually exhibits partial or complete dele-tions of chromosomes 5 and/or 7 (2). Typically, these cases developed after treatment with an alkylating agent with or without radiotherapy (3). Recently, a cytogenetic finding involving abnormalities at chromosome band 11q23 has accompanied a subset of secondary AML cases (particularly monoblastic [AML-M5] and myelomonoblastic [AML-M4] forms); the vast majority of these cases developed after treat-ment regimens involving the epipodophyllotoxins (4, 5).