酪氨酸激酶抑制剂时代慢性髓性白血病的分子生物学变化
Changes in molecular biology of chronic myeloid leukemia in tyrosine kinase inhibitor era.
作者信息
Comert Melda, Baran Yusuf, Saydam Guray
机构信息
Department of Hematology, Medical School, Ege University Izmir, Turkey.
出版信息
Am J Blood Res. 2013 Aug 19;3(3):191-200. eCollection 2013.
Abstract
Chronic myeloid leukemia (CML) is a clonal myeloproliferative disease characterized by a reciprocal translocation between long arms of chromosomes 9 and 22 t(9;22) that generates the BCR-ABL fusion gene. If left untreated, newly diagnosed chronic phase CML patients finally progress to accelerated and blastic phase. After the introduction of tyrosine kinase inhibitors (TKIs), treatment strategies of CML changed dramatically. However, the development of resistance to TKIs started to create problems over time. In this review, the current information about CML biology before and after imatinib mesylate treatment is summarized.
摘要
慢性髓性白血病（CML）是一种克隆性骨髓增殖性疾病，其特征是9号和22号染色体长臂之间发生相互易位t(9;22)，产生BCR-ABL融合基因。如果不进行治疗，新诊断的慢性期CML患者最终会进展为加速期和急变期。在引入酪氨酸激酶抑制剂（TKIs）后，CML的治疗策略发生了巨大变化。然而，随着时间的推移，对TKIs产生耐药性的问题开始出现。在这篇综述中，总结了关于甲磺酸伊马替尼治疗前后CML生物学的当前信息。
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