SECONDARY ACUTE MYELOID-LEUKEMIA IN CHILDREN TREATED FOR ACUTE LYMPHOID LEUKEMIA
SECONDARY ACUTE MYELOID-LEUKEMIA IN CHILDREN TREATED FOR ACUTE LYMPHOID LEUKEMIA
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DOI：
10.1056/nejm198907203210302
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发表时间：
1989-07-20
影响因子：
158.5
通讯作者：
WILLIAMS, DL
中科院分区：
文献类型：
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作者：
PUI, CH;BEHM, FG;WILLIAMS, DL
我们研究了733例接受强化化疗的急性淋巴细胞白血病（ALL）患儿在初始缓解期发生急性髓细胞白血病（AmL）的风险。根据标准的形态学和细胞化学标准，13例患者在诊断为ALL后1.2至6年（中位数3.0）确定了这种并发症。在三年的随访中，第一次骨髓缓解期间继发性AML的累积风险为1.6%（95%置信区间为0.7%和3.5%）;在六年时，为4.7%（2%和10%）。与非T细胞免疫表型相比，T细胞免疫表型患者发生继发性AML的可能性要大得多（6年累积风险为19.1%[6%和47%]）。10例患者的连续细胞遗传学研究显示，9例患者的核型完全不同，提示诱导第二个肿瘤。在这些患者中的8例中，原始细胞具有11 w23染色体区域的异常，这与多能干细胞的恶性转化有关。没有证据表明5号或7号染色体的DNA丢失，这是在继发于烷化剂治疗、照射或两者的AML病例中常见的核型变化。我们的结论是，在接受强化治疗的ALL患者中，尤其是T细胞免疫表型的患者，AML的风险很大，并且11 q23染色体异常可能在这种并发症的发病机制中很重要。
We studied the risk of the development of acute myeloid leukemia (AmL) during initial remission in 733 consecutive children with acute lymphoid leukemia (ALL) who were treated with intensive chemotherapy. This complication was identified according to standard morphologic and cytochemical criteia in 13 patients 1.2 to 6 years (median 3.0) after the diagnosis of ALL. At three years of follow-up, the cumulative risk of secondary AML during the first bone marrow remission was 1.6 percent (95 percent confidence limits, 0.7 and 3.5 percent); at six years, it was 4.7 percent (2 and 10 percent). The development of secondary AML was much more likely among patients with a T-cell than a non-T cell immunophenotype (cumulative risk, 19.1 percent [6 and 47 percent] at six years). Sequential cytogenetic studies in 10 patients revealed entirely different karyotypes in 9, suggesting the induction of a second neoplasm. In eight of these patients, the blast cells had abnormalities of the 11w23 chromosomal region, which has been associated with malignant transformation of a pluripotential stem cell. There was no evidence of loss of DNA from chromosome 5 or 7, a karyotypic change commonly observed in cases of AML secondary to treatment with alkylating agents, irradiation, or both. We conclude that there is a substantial risk of AML in patients who receive intensive treatment for ALL, especially in those with a T-cell immunophenotype, and that 11q23 chromosomal abnormalities may be important in the pathogenesis of this complication.