慢性粒细胞白血病是起源于多能造血干细胞的恶性血液病。病程分为慢性期、加速期及急变期。患者中可发现BCR/ABL1融合蛋白。BCR/ABL1介导的染色体畸变被认为是CML的驱动突变。目前CML急变的机制仍然不清楚，因此临床上无法将其阻断在缓解率较高的慢性期，而且也没有一个既安全，同时又对所有BCR/ABL1融合突变蛋白有效的药物。目前尚未有可供药物筛选的斑马鱼CML模型，因此我们构建了能稳定遗传的人源性BCR/ABL1 P210斑马鱼并对其进行研究，发现其具有：1.幼鱼时期原始造血各谱系标记基因不受影响；2.定向造血髓系增多，而红系，淋系减少；3.部分转基因鱼成年时期出现消瘦、贫血、出血、脾肿大等类似人类CML/AML1表型。我们初步认为该斑马鱼可模拟人类CML甚至急变成AML，但其与人类CML的病理、疾病进程的相似性、疾病调控网络以及进展为ALL/AML的关键因素等科学问题仍需解决。

Chronic myeloid leukemia is a hematopoietic malignancy originated from pluripotent hematopoietic stem cells, The course of which is divided into chronic phase, accelerate phase and blast crisis. BCR/ABL fusion protein can be found in patients. BCR/ABL mediated chromosome aberration is considered to be the driver mutation of CML. The mechanism of how to transforming to blast crisis is still not clear, so it is unable to intervene the disease progress in cronic phase whose remission rate is much lower. And there is no any drug that is effective to all mutations of BCR/ABL fusion protein and is really safe. Since there is no zebrafish CML model for drug screening, we established a humanized BCR/ABL P210 transgenic zebrafish and found: 1.Primitive hematopoietic was not affected; 2.Definitive myeloid population was increased, while erythroid and lymphoid population were decreased; 3. A part of adulthood BCR/ABL transgenic zebrafish showed emaciation, anemia, bleeding and splenomegaly that similar to the phenotypes of human CML/AML. We tentatively speculate that this transgenic zebrafish can mimic human CML even include the progress to AML. However, more scientific problems, such as the similarity of pathology and disease process to ALL/AML with human CML, control network and the key factors of disease progression are still needed to be solved.