Letai Anthony
Department of Medical Oncology, Dana-Farber Cancer Institute, 44 Binney Street, Dana 530B, Boston, Massachusetts 02115, USA.
Cancer Cell. 2006 Nov;10(5):343-5. doi: 10.1016/j.ccr.2006.10.014.
In this issue of Cancer Cell, two groups present data on the function of an antagonist of BCL-2, ABT-737. Both groups find that expression of MCL-1, an antiapoptotic protein related to BCL-2, is a key determinant of resistance to ABT-737. Lowering MCL-1 levels is an effective adjunct to BCL-2 antagonism, and both groups suggest ways that this might be accomplished practically in a clinical setting. The mechanism by which ABT-737 selectively kills cancer cells is discussed below in the context of these and prior reports of ABT-737's function. Antagonism of BCL-2 is an exciting anticancer strategy that may soon become a clinical reality.
在本期《癌细胞》杂志中，两个研究小组展示了关于BCL-2拮抗剂ABT-737功能的数据。两个小组均发现，与BCL-2相关的抗凋亡蛋白MCL-1的表达是对ABT-737耐药的关键决定因素。降低MCL-1水平是BCL-2拮抗作用的有效辅助手段，两个小组都提出了在临床环境中实际实现这一目标的方法。下文将结合这些以及之前关于ABT-737功能的报道，讨论ABT-737选择性杀死癌细胞的机制。BCL-2拮抗作用是一种令人兴奋的抗癌策略，可能很快成为临床现实。
