Druker B J, Tamura S, Buchdunger E, Ohno S, Segal G M, Fanning S, Zimmermann J, Lydon N B
Division of Hematology and Medical Oncology, Oregon Health Sciences University, Portland, USA.
Nat Med. 1996 May;2(5):561-6. doi: 10.1038/nm0596-561.
The bcr-abl oncogene, present in 95% of patients with chronic myelogenous leukemia (CML), has been implicated as the cause of this disease. A compound, designed to inhibit the Abl protein tyrosine kinase, was evaluated for its effects on cells containing the Bcr-Abl fusion protein. Cellular proliferation and tumor formation by Bcr-Abl-expressing cells were specifically inhibited by this compound. In colony-forming assays of peripheral blood or bone marrow from patients with CML, there was a 92-98% decrease in the number of bcr-abl colonies formed but no inhibition of normal colony formation. This compound may be useful in the treatment of bcr-abl-positive leukemias.
bcr-abl癌基因存在于95%的慢性粒细胞白血病（CML）患者中，被认为是这种疾病的病因。一种设计用于抑制Abl蛋白酪氨酸激酶的化合物，对含有Bcr-Abl融合蛋白的细胞的作用进行了评估。该化合物特异性抑制了表达Bcr-Abl的细胞的细胞增殖和肿瘤形成。在CML患者外周血或骨髓的集落形成试验中，形成的bcr-abl集落数量减少了92%-98%，但对正常集落形成没有抑制作用。这种化合物可能对治疗bcr-abl阳性白血病有用。
