...
首页> 外文期刊>Leukemia and lymphoma >Therapy-related myelodysplastic syndrome/acute myeloid leukemia following fludarabine therapy for non-Hodgkin lymphoma and chronic lymphocytic leukemia in Thai patients.
【24h】

Therapy-related myelodysplastic syndrome/acute myeloid leukemia following fludarabine therapy for non-Hodgkin lymphoma and chronic lymphocytic leukemia in Thai patients.

机译:氟达拉滨治疗泰国患者后非霍奇金淋巴瘤和慢性淋巴细胞性白血病的治疗相关的骨髓增生异常综合症/急性髓细胞性白血病。

获取原文
获取原文并翻译 | 示例
   

获取外文期刊封面封底 >>

       

摘要

Therapy related myelodysplastic syndrome (t-MDS) and secondary acute myeloid leukemia (AML) are seriously late complications of the use of alkylating agents, topoisomerase II inhibitors, and other chemotherapies. Deoxyribonucleic acid (DNA) damage that leads to chromosomal deletions or balanced translocations partly cause t-MDS. Deletions of chromosomes 5 and 7 are also commonly found in alkylator-associated MDS/AML. Over the last half decade, fludarabine has been widely used as frontline therapy for indolent B-cell lymphomas and chronic lymphocytic leukemia (CLL). The incidence of t-MDS/AML following fludarabine-based therapies is 0.5%, 3.5%, 9%, and 2% of patients receiving treatment with fludarabine alone, fludarabine plus chlorambucil, fludarabine combined with cyclopho-sphamide, and the combination of rituximab, fludarabine, and cyclophosphamide, respectively [1,2]. Nevertheless, the risk factor for fludarabine-induced t-MDS/AML has not been established. We therefore performed a retrospective study to analyze the predicting factors for t-MDS/AML in patients with B-cell lymphomas and CLL treated with fludarabine-based therapy.
机译:与治疗有关的骨髓增生异常综合症(t-MDS)和继发性急性髓细胞性白血病(AML)是使用烷基化剂,拓扑异构酶II抑制剂和其他化学疗法的严重晚期并发症。导致染色体缺失或平衡易位的脱氧核糖核酸(DNA)损伤部分导致t-MDS。在与烷基化剂相关的MDS / AML中通常还发现了5号和7号染色体的缺失。在过去的五年中,氟达拉滨已被广泛用作惰性B细胞淋巴瘤和慢性淋巴细胞性白血病(CLL)的一线治疗方法。以氟达拉滨为基础的治疗后,分别接受氟达拉滨,氟达拉滨联合苯丁酸氮芥,氟达拉滨联合环磷酰胺和利妥昔单抗联合治疗的患者中,t-MDS / AML的发生率分别为0.5%,3.5%,9%和2% ,氟达拉滨和环磷酰胺[1,2]。然而,氟达拉滨诱导的t-MDS / AML的危险因素尚未确定。因此,我们进行了一项回顾性研究,以分析基于氟达拉滨治疗的B细胞淋巴瘤和CLL患者t-MDS / AML的预测因素。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号