Gustave Roussy; Villejuif, France ; Université Paris-Sud/Paris XI; Le Kremlin-Bicêtre, France ; INSERM, U848; Villejuif, France.
Oncoimmunology. 2013 Sep 1;2(9):e25595. doi: 10.4161/onci.25595. Epub 2013 Jul 3.
Radiotherapy has extensively been employed as a curative or palliative intervention against cancer throughout the last century, with a varying degree of success. For a long time, the antineoplastic activity of X- and γ-rays was entirely ascribed to their capacity of damaging macromolecules, in particular DNA, and hence triggering the (apoptotic) demise of malignant cells. However, accumulating evidence indicates that (at least part of) the clinical potential of radiotherapy stems from cancer cell-extrinsic mechanisms, including the normalization of tumor vasculature as well as short- and long-range bystander effects. Local bystander effects involve either the direct transmission of lethal signals between cells connected by gap junctions or the production of diffusible cytotoxic mediators, including reactive oxygen species, nitric oxide and cytokines. Conversely, long-range bystander effects, also known as out-of-field or abscopal effects, presumably reflect the elicitation of tumor-specific adaptive immune responses. Ionizing rays have indeed been shown to promote the immunogenic demise of malignant cells, a process that relies on the spatiotemporally defined emanation of specific damage-associated molecular patterns (DAMPs). Thus, irradiation reportedly improves the clinical efficacy of other treatment modalities such as surgery (both in neo-adjuvant and adjuvant settings) or chemotherapy. Moreover, at least under some circumstances, radiotherapy may potentiate anticancer immune responses as elicited by various immunotherapeutic agents, including (but presumably not limited to) immunomodulatory monoclonal antibodies, cancer-specific vaccines, dendritic cell-based interventions and Toll-like receptor agonists. Here, we review the rationale of using radiotherapy, alone or combined with immunomodulatory agents, as a means to elicit or boost anticancer immune responses, and present recent clinical trials investigating the therapeutic potential of this approach in cancer patients.
在过去的一个世纪里,放射疗法被广泛应用于癌症的治疗或姑息治疗,取得了不同程度的成功。长期以来,X 射线和γ射线的抗肿瘤活性完全归因于它们破坏大分子(特别是 DNA)的能力,从而引发(凋亡)恶性细胞死亡。然而,越来越多的证据表明(至少部分)放射治疗的临床潜力源于癌细胞外在机制,包括肿瘤血管正常化以及短程和长程旁观者效应。局部旁观者效应涉及通过间隙连接连接的细胞之间的致命信号的直接传递,或包括活性氧、一氧化氮和细胞因子在内的扩散细胞毒性介质的产生。相反,长程旁观者效应,也称为场外或远隔效应,可能反映了肿瘤特异性适应性免疫反应的激发。电离射线确实已被证明可促进恶性细胞的免疫原性死亡,这一过程依赖于特定损伤相关分子模式(DAMPs)的时空限定释放。因此,据报道,放射治疗可提高其他治疗方式(包括新辅助和辅助治疗中的手术)或化疗的临床疗效。此外,至少在某些情况下,放射治疗可能增强各种免疫治疗药物(包括但不限于免疫调节单克隆抗体、癌症特异性疫苗、基于树突状细胞的干预和 Toll 样受体激动剂)引发的抗癌免疫反应。在这里,我们回顾了单独或联合使用放射疗法作为引发或增强抗癌免疫反应的手段的基本原理,并介绍了最近的临床试验,这些试验研究了该方法在癌症患者中的治疗潜力。