O'Dwyer M E, Druker B J
Leukaemia Program, Oregon Health Sciences University, Portland, OR, USA.
J Intern Med. 2001 Jul;250(1):3-9. doi: 10.1046/j.1365-2796.2001.00823.x.
The deregulated tyrosine kinase activity of the BCR-ABL fusion protein is the cause of malignant transformation in almost all cases of chronic myelogenous leukaemia (CML), making BCR-ABL an ideal target for pharmacological inhibition. Signal transduction inhibitor (STI571) (formerly CGP57 148B), is an ABL specific, tyrosine kinase inhibitor. In preclinical studies, it has been shown to selectively kill BCR-ABL expressing cells, both in-vitro and in vivo. The results of clinical studies to date are highly encouraging and STI571 promises to be an important addition to the therapy of CML.
在几乎所有慢性粒细胞白血病（CML）病例中，BCR-ABL融合蛋白酪氨酸激酶活性失调是恶性转化的原因，这使得BCR-ABL成为药物抑制的理想靶点。信号转导抑制剂（STI571）（原名CGP57 148B）是一种ABL特异性酪氨酸激酶抑制剂。临床前研究表明，它在体外和体内均能选择性杀死表达BCR-ABL的细胞。迄今为止的临床研究结果非常令人鼓舞，STI571有望成为CML治疗的重要补充药物。
