INSERM, U1015, 94805 Villejuif, France.
Immunity. 2013 Jul 25;39(1):74-88. doi: 10.1016/j.immuni.2013.06.014.
Conventional chemotherapeutics and targeted antineoplastic agents have been developed based on the simplistic notion that cancer constitutes a cell-autonomous genetic or epigenetic disease. However, it is becoming clear that many of the available anticancer drugs that have collectively saved millions of life-years mediate therapeutic effects by eliciting de novo or reactivating pre-existing tumor-specific immune responses. Here, we discuss the capacity of both conventional and targeted anticancer therapies to enhance the immunogenic properties of malignant cells and to stimulate immune effector cells, either directly or by subverting the immunosuppressive circuitries that preclude antitumor immune responses in cancer patients. Accumulating evidence indicates that the therapeutic efficacy of several antineoplastic agents relies on their capacity to influence the tumor-host interaction, tipping the balance toward the activation of an immune response specific for malignant cells. We surmise that the development of successful anticancer therapies will be improved and accelerated by the immunological characterization of candidate agents.
基于癌症是一种自主遗传或表观遗传疾病的简单概念，已经开发出了常规化疗药物和靶向抗肿瘤药物。然而，越来越明显的是，许多现有的抗癌药物通过引发新的或重新激活预先存在的肿瘤特异性免疫反应，共同挽救了数以百万计的生命年。在这里，我们讨论了常规和靶向抗癌疗法增强恶性细胞免疫原性和刺激免疫效应细胞的能力，无论是直接作用还是通过颠覆阻止癌症患者抗肿瘤免疫反应的免疫抑制回路。越来越多的证据表明，几种抗肿瘤药物的治疗效果依赖于它们影响肿瘤-宿主相互作用的能力，从而使免疫反应针对恶性细胞的激活达到平衡。我们推测，通过对候选药物进行免疫学特征分析，将改善和加速成功的抗癌疗法的发展。
