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三氧化二砷治疗急性早幼粒细胞白血病 (APL)近年来成为血液学界研究热点 ,临床研究表明三氧化二砷治疗APL有效率达 80 %以上 ,特别是对维甲酸耐药、难治性的APL病例特别有效。有研究认为三氧化二砷治疗APL可能是通过PML -RARα蛋白的降解、促进细胞凋亡达到治疗目的。由于三氧化二砷的治疗作用机制仍未十分明了 ,拟以亲和毛细管电泳和单细胞、单分子检测芯片为平台 ,分别从细胞外到细胞内 ,多细胞到单细胞 ,多分子到单分子入手 ,在不同层次上逐步深入地研究PML -RARα蛋白和三氧化二砷的相互作用 ,以期更为深入地了解相应的细胞分化和凋亡过程 ,更为清晰地阐明三氧化二砷对APL的治疗的药理机制
Arsenic trioxide in the treatment of acute promyelocytic leukemia (APL) has become a hot spot in the field of hematology in recent years. Clinical studies have shown that the effective rate of arsenic trioxide in treating APL is more than 80%, especially for APR patients with refractory retinoid acid. Some studies suggest that arsenic trioxide treatment of APL may be through the degradation of PML -RARα protein to promote apoptosis for therapeutic purposes. As the mechanism of action of arsenic trioxide is still not yet clear, it is proposed to use affinity capillary electrophoresis and single-cell, single-molecule detection chip as a platform, starting from the extracellular to intracellular, multicellular to unicellular, multimolecule to single molecule, respectively At different levels, the interaction between PML-RARα protein and arsenic trioxide has been studied step by step. With a view to understanding the process of cell differentiation and apoptosis more deeply, the pharmacological mechanism of arsenic trioxide on the treatment of APL is clarified more clearly