Guo Su-Qing, Li Ying-Hua
Department of Hematology, Hengshui Harlson International Peace Hospital, Hengshui 053000, Hebei Province, China.
Department of Hematology, Hengshui Harlson International Peace Hospital, Hengshui 053000, Hebei Province, China. E-mail:
Zhongguo Shi Yan Xue Ye Xue Za Zhi. 2015 Aug;23(4):1199-202. doi: 10.7534/j.issn.1009-2137.2015.04.057.
Chronic myeloid leukemia (CML) is a myeloproliferative disorder, characterized by excessive proliferation of myeloid cells. CML patients in early phase [also known as chronic phase (CP)] usually respond to treatment with tyrosine kinase inhibitors (TKI), some patients respond initially to TKI, but later become resistant, then resulting in the transformation from CP to more advanced phase, which were subclassified as either accelerated phase or blastic phase. At present, the molecular mechanisms of CML have been not yet clear, and acute transformation has been not fully understood, studies have shown that genomic instability promotes the acute conversion of CML. This review discusses the molecular mechanisms leading to the transformation of CML, and some therapeutic approaches.
慢性髓性白血病(CML)是一种骨髓增殖性疾病,其特征为髓系细胞过度增殖。处于早期阶段[也称为慢性期(CP)]的CML患者通常对酪氨酸激酶抑制剂(TKI)治疗有反应,一些患者最初对TKI有反应,但后来会产生耐药性,进而导致从CP期转变为更晚期阶段,这些晚期阶段可细分为加速期或急变期。目前,CML的分子机制尚不清楚,急性转化也尚未完全了解,研究表明基因组不稳定促进了CML的急性转化。本综述讨论了导致CML转化的分子机制以及一些治疗方法。