Chronic myelogenous leukaemia - new therapeutic principles

被引：33

作者：

O'Dwyer, ME ^{[1
]}

Druker, BJ ^{[1
]}

机构：

[1] Oregon Hlth & Sci Univ, Leukaemia Program, Portland, OR 97201 USA

来源：

JOURNAL OF INTERNAL MEDICINE | 2001年 / 250卷 / 01期

关键词：

BCR-ABL; chronic myelogenous leukaemia; signal transduction; STI571; therapy; tyrosine kinase inhibitor;

D O I：

10.1046/j.1365-2796.2001.00823.x

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

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), malting 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 encourageing and STI571 promises to be an important addition to the therapy of CML.

引用

页码：3 / 9

页数：7

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