慢性粒细胞性白血病（CML）的发病率约占成人白血病的15％～20％。近10近来,对CML致病的分子基础的研究及其早期治疗有较大进展,但对晚期病人的治疗仍显得束手无策。超过90％的CML病人白细胞内存在着一种philadclphia（Ph）染色体,是由1个22号染色体与1个9号染色体的长臂相互融合而成,即（9;22）（q34;q21）移位。这种Ph染色体携带着BCR-ABL融合基因,通过酪氨酸激酶催化,表达为一种磷蛋白（P210）,P210~（BCR-ABL）在 The incidence of chronic myeloid leukemia (CML) accounts for about 15% to 20% of adult leukemia. Nearly 10 recently, the research on the molecular basis of CML’s pathogenesis and its early treatment have made great progress, but the treatment of advanced patients still seems helpless. In more than 90% of CML patients, there is a philadclphia (Ph) chromosome in leukocytes, which is formed by the fusion of a chromosome 22 and the long arm of chromosome 9 (9; 22) (q34; q21). Shift. This Ph chromosome carries the BCR-ABL fusion gene, which is catalyzed by tyrosine kinase and expressed as a phosphoprotein (P210), P210~(BCR-ABL) in