Poor prognosis of children with pre-B acute lymphoblastic leukemia is associated with the t(1;19)(q23;p13): a Pediatric Oncology Group study.
Poor prognosis of children with pre-B acute lymphoblastic leukemia is associated with the t(1;19)(q23;p13): a Pediatric Oncology Group study.
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DOI：
10.1182/blood.v76.1.117.117
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发表时间：
1990
期刊：
影响因子：
20.3
通讯作者：
W. Crist;A. Carroll;J. Shuster;F. Behm;M. Whitehead;T. Vietti;A. Look;D. Mahoney;A. Ragab;D. Pullen
中科院分区：
文献类型：
--
作者：
W. Crist;A. Carroll;J. Shuster;F. Behm;M. Whitehead;T. Vietti;A. Look;D. Mahoney;A. Ragab;D. Pullen
染色体易位，特别是t(1;19) （q23;p13）在b前和早期b前急性淋巴细胞白血病（ALL）患儿中的预后意义进行了评估。患者在1986年2月至1989年5月期间接受儿科肿瘤组（POG）基于风险的方案治疗。46%（285例中有130例）和56%（679例中有380例）的早期b前病变患者检测到异常克隆。与其他核型异常相比，任何类型的易位与更差的治疗结果相关：在b前组中，66人中有15人治疗失败，64人中有3人治疗失败（P = 0.001），在早期b前组中，141人中有37人失败，239人中有23人失败（P < 0.001）。t(1;19) （q23;p13）在伴有克隆异常的b前ALL患者中出现的频率明显高于早期b前ALL患者（130∶29∶380∶5,P < 0.001）。在285例骨髓细胞遗传学研究的b前患者中，t（1;19）患者的治疗效果明显差于其他所有患者（29例中有11例治疗失败，256例中有27例治疗失败，P < 0.001）。这种差异是显著的(P小于。001)在调整白细胞计数、年龄和其他相关特征后。t（1;19）患者的预后也比b前其他易位患者差(37例中有4例失败，P <。01)或任何其他核型异常（101例中有7例失败，P < 0.001）。我们得出结论，染色体易位导致非t细胞、非b细胞儿童ALL预后较差，而t（1;19）是导致前b亚群预后差的主要原因。
The prognostic significance of chromosomal translocations, particularly t(1;19) (q23;p13), was evaluated in children with pre-B and early pre-B acute lymphoblastic leukemia (ALL). Patients were treated on a risk-based protocol of the Pediatric Oncology Group (POG) between February 1986 and May 1989. An abnormal clone was detected in 46% (130 of 285) of pre-B cases and 56% (380 of 679) of early pre-B cases. Translocation of any type was associated with a worse treatment outcome than other karyotypic abnormalities: 15 of 66 versus 3 of 64 failed therapy in the pre-B group (P = .001), and 37 of 141 versus 23 of 239 failed in the early pre-B group (P less than .001). The t(1;19) (q23;p13) occurred significantly more often in cases of pre-B ALL with a clonal abnormality than in early pre-B ALL cases (29 of 130 v 5 of 380, P less than .001). Among the 285 pre-B cases in which bone marrow was studied cytogenetically, those with t(1;19) had a significantly worse treatment outcome than all others (11 of 29 v 27 of 256 have failed therapy, P less than .001). This difference is significant (P less than .001) after adjustment for leukocyte count, age, and other relevant features. Cases with the t(1;19) also had a worse prognosis than pre-B patients with other translocations (4 of 37 have failed, P less than .01) or with any other karyotypic abnormality (7 of 101 have failed, P less than .001). We conclude that chromosomal translocations confer a worse prognosis for non-T, non-B-cell childhood ALL, and that the t(1;19) is largely responsible for the poor prognosis of the pre-B subgroup.