Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts.
Clin Cancer Res. 2015 Nov 15;21(22):5015-20. doi: 10.1158/1078-0432.CCR-15-1204.
In our current age of targeted therapies, there is understandably considerable attention paid to the specific molecular targets of pharmaceutical intervention. For a targeted drug to work, it must bind to a target selectively and impair its function. Monitoring biomarkers of the impaired target function can provide vital in vivo pharmacodynamic information. Moreover, genetic changes to the target are often the source of resistance to targeted agents. However, for the treatment of cancer, it is necessary that the therapy not only provide efficient binding and inhibition of the target, but also that this intervention reliably kills the cancer cell. In this CCR Focus section, four articles make the connection between therapies that target T-cell activation, autophagy, IAP proteins, and BCL-2 and the commitment of cancer cells to cell death. Before addressing those exciting classes of targeted therapies, however, an overview is provided to discuss cell death induced by what is arguably still the most successful set of drugs in the history of medical oncology, conventional chemotherapy. See all articles in this CCR Focus section, "Cell Death and Cancer Therapy."
在我们这个靶向治疗的时代，人们自然而然地将大量注意力集中在药物干预的特定分子靶点上。为了使靶向药物发挥作用，它必须选择性地与靶点结合并破坏其功能。监测靶点功能受损的生物标志物可以提供重要的体内药效学信息。此外，靶点的遗传变化往往是靶向药物产生耐药性的根源。然而，对于癌症的治疗，不仅需要治疗方法能有效地与靶点结合并抑制其功能，还需要该干预措施能可靠地杀死癌细胞。在本期 CCR 焦点特刊中，有四篇文章将靶向 T 细胞激活、自噬、IAP 蛋白和 BCL-2 的治疗方法与癌细胞走向死亡的过程联系起来。然而，在探讨这些激动人心的靶向治疗方法之前，我们首先提供了一个概述，讨论了可能仍然是肿瘤学史上最成功的一组药物——传统化疗所诱导的细胞死亡。查看本期 CCR 焦点特刊中所有题为“细胞死亡与癌症治疗”的文章。
