摘要
甲磺酸伊马替尼(imatinib mesylate)是目前治疗慢性髓系白血病(CML)的常用药物。临床数据显示,很多白血病患者在服用伊马替尼后血小板均有不同程度的减少。PDGF/PDGFR在血小板造血中发挥着重要作用,提示伊马替尼可能正是通过阻滞PDGF/PDGFR通路,阻断受体的PI3-K/Akt信号通路,减弱其抑制caspase-3活化的作用,促进巨核细胞的凋亡,从而导致血小板减少。本文从PDGF/PDGFR信号通路方面探究伊马替尼治疗CML引致血小板减少的可能机制,讨论的问题包括伊马替尼与血小板减少,PDGF/PDGFR与血小板生成,伊马替尼治疗引致血小板减少的可能机制等。
Imatinib mesylate has been commonly used in the treatment of patients with chronic myeloid leukemia（CML）.However,a significant number of CML patients treated with imatinib developed thrombocytopenia.Platelet-derived growth factor（PDGF）/platelet-derived growth factor receptor（PDGFR） plays a significant role in the regulation of thrombopoiesis.It is suggested that imatinib may block the PDGF/PDGFR and PI3-K/Akt pathway,then inducing the apoptosis of megakaryocytes and developing thrombocytopenia in these patients.In this review,the potential molecular mechanism of imatinib-induced thrombocytopenia in the treatment of CML patients is discussed,including imatinib and thrombocytopenia,PDGF/PDGFR and thrombopoiesis,potential mechanism of imatinib-induced thrombocytopenia in treatment of patients with CML and so on.
出处
《中国实验血液学杂志》
CAS
CSCD
2011年第5期1314-1318,共5页
Journal of Experimental Hematology
