Shu Ling-Ling, Jiang Qian-Li, Meng Fan-Yi, Yang Mo
Department of Hematology, Southern Medical University, Guangdong Province, China.
Zhongguo Shi Yan Xue Ye Xue Za Zhi. 2011 Oct;19(5):1314-8.
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.
甲磺酸伊马替尼已普遍用于治疗慢性髓性白血病(CML)患者。然而,大量接受伊马替尼治疗的CML患者出现了血小板减少症。血小板衍生生长因子(PDGF)/血小板衍生生长因子受体(PDGFR)在血小板生成的调节中起重要作用。有人提出,伊马替尼可能会阻断PDGF/PDGFR和PI3-K/Akt途径,进而诱导巨核细胞凋亡并导致这些患者出现血小板减少症。在这篇综述中,讨论了伊马替尼在治疗CML患者时导致血小板减少症的潜在分子机制,包括伊马替尼与血小板减少症、PDGF/PDGFR与血小板生成、伊马替尼在治疗CML患者时导致血小板减少症的潜在机制等。