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慢性髓细胞白血病(chronic myeloid leukemia,CML)是一种发生在造血干细胞水平的髓系恶性克隆性白血病,以因9号、22号染色体易位t(9;22)(q34;q11)而形成的费城(Ph)染色体及由此产生的BCR-ABL融合基因为特征~([1-2])。BCR-ABL融合基因及其表达产物P210被认为在CML的发病机制中起关键作用,其主要机制在于引起异常的下游信号通路,从而影响细胞的黏附、
Chronic myeloid leukemia (CML) is a myeloid malignant myeloid leukemia that occurs at the level of hematopoietic stem cells and is formed by chromosomal translocation 9 (9), 22 (q34; q11) on chromosome 9 Philadelphia Ph chromosome and the resultant BCR-ABL fusion gene ~ ([1-2]). BCR-ABL fusion gene and its expression product P210 is considered to play a key role in the pathogenesis of CML, the main mechanism is to cause abnormal downstream signaling pathway, thus affecting cell adhesion,