Shah Neil P, Kasap Corynn, Weier Christopher, Balbas Minna, Nicoll John M, Bleickardt Eric, Nicaise Claude, Sawyers Charles L
Division of Hematology/Oncology, Department of Medicine, UCSF School of Medicine, San Francisco, CA 94143, USA.
Cancer Cell. 2008 Dec 9;14(6):485-93. doi: 10.1016/j.ccr.2008.11.001.
The BCR-ABL inhibitor dasatinib achieves clinical remissions in chronic myeloid leukemia (CML) patients using a dosing schedule that achieves potent but transient BCR-ABL inhibition. In vitro, transient potent BCR-ABL inhibition with either dasatinib or imatinib is cytotoxic to CML cell lines, as is transient potent EGFR inhibition with erlotinib in a lung cancer cell line. Cytotoxicity correlates with the magnitude as well as the duration of kinase inhibition. Moreover, cytotoxicity with transient potent target inhibition is equivalent to prolonged target inhibition and in both cases is associated with BIM activation and rescued by BCL-2 overexpression. In CML patients receiving dasatinib once daily, response correlates with the magnitude of BCR-ABL kinase inhibition, thereby demonstrating the potential clinical utility of intermittent potent kinase inhibitor therapy.
BCR-ABL抑制剂达沙替尼通过一种给药方案在慢性髓性白血病(CML)患者中实现了临床缓解,该方案可实现强效但短暂的BCR-ABL抑制。在体外,达沙替尼或伊马替尼的短暂强效BCR-ABL抑制对CML细胞系具有细胞毒性,就像厄洛替尼在肺癌细胞系中的短暂强效EGFR抑制一样。细胞毒性与激酶抑制的程度和持续时间相关。此外,短暂强效靶点抑制的细胞毒性等同于延长的靶点抑制,在这两种情况下都与BIM激活相关,并可通过BCL-2过表达得到挽救。在每天接受一次达沙替尼治疗的CML患者中,反应与BCR-ABL激酶抑制的程度相关,从而证明了间歇性强效激酶抑制剂治疗的潜在临床应用价值。