医学
髓系白血病
伊马替尼
甲磺酸伊马替尼
肿瘤科
白血病
移植
费城染色体
内科学
癌症研究
免疫学
染色体易位
生物化学
基因
化学
作者
Martin Henkes,Heiko van der Kuip,Walter E. Aulitzky
出处
期刊:PubMed
日期:2008-02-01
卷期号:4 (1): 163-87
被引量:18
摘要
Treatment options for chronic myeloid leukemia (CML) have changed dramatically during the last decades. Interferon-alpha treatment and stem cell transplantation (SCT) clearly improved survival over conventional chemotherapy and offered the possibility of complete and durable responses. With the advent of the small molecule inhibitor imatinib mesylate (Glivec((R)), Gleevectrade mark) targeting the causative Bcr-Abl oncoprotein, the era of molecular cancer therapy began with remarkable success especially in chronic phase patients. Today, imatinib is the first-line treatment for CML. However, imatinib does not appear to be capable to eliminate all leukemia cells in the patients and pre-existing as well as acquired resistance to the drug has been increasingly recognized. To overcome these problems, several strategies involving dose escalation, combinations with other agents, and novel Bcr-Abl inhibitors have been developed.
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