慢性淋巴细胞白血病细胞对氟达拉滨耐药机制研究进展  

Research Advance on Fludarabine Resistance Mechanisms in Chronic Lymphocytic Leukemia Cells——Review

作　　者：姚琳[1] 徐卫[1] 李建勇[1] 

机构地区：[1]南京医科大学第一附属医院,江苏省人民医院血液科,江苏南京210029

出　　处：《中国实验血液学杂志》2010年第3期821-824,共4页Journal of Experimental Hematology

基　　金：国家自然基金资助项目(编号30871104;30971296;30971295);江苏省医学领军人才基金资助项目(编号LJ200623);江苏省医学重点人才基金资助项目(编号RC2007042);江苏省自然基金基助项目(编号BK2007249);江苏省"青蓝工程"中青年学术带头人培养对象项目;江苏省"六大人才高峰"资助项目

摘　　要：嘌呤核苷类似物氟达拉滨(Flu)是慢性淋巴细胞白血病(CLL)的一线治疗药物,可诱导CLL细胞凋亡。然而,CLL仍然不可治愈,其治疗失败的主要原因是CLL细胞对氟达拉滨产生耐药性。为了更科学地指导临床用药,本文就氟达拉滨的代谢、作用机制、CLL细胞对氟达拉滨的抵抗机制及逆转策略作一综述,着重介绍诱导临床耐药过程中的核苷转运体、p53诱导凋亡途径以及使Flu活化或失活的酶类的最新研究进展。Fludarabine （Flu）, a purine nucleoside analogue, is the firstline drug for patients with chronic lymphocytic leukemia （CLL）, and can induce apoptosis of malignant cells in CLL patients. However, CLL remains an incurable disease. Fludarabine-resistance is one of the predominant reasons for treatment failure. In this paper, the metabolism, action and drug-resistance mechanisms of Fludarabine in CLL as well as possible reversible strategies are reviewed, with particular emphasis on recent advances in the characterization of nucleoside transporters and p53-mediated apoptosis and on the potential role of activating or inactivating enzymes in the induction of clinical resistance to Flu.

关 键 词：慢性淋巴细胞胞白血病 氟达拉滨 耐药 

分 类 号：R733.72[医药卫生—肿瘤] R979.1[医药卫生—临床医学]