一系列已发表的基于细胞和小动物的研究表明，癌细胞或实验性癌组织多次暴露于非电离和非热的电磁 (EM) 波平台。总体效果似乎是抑制性的，在实验模型中诱导癌细胞应激或死亡以及抑制肿瘤生长。已经测试了各种物理输入变量，包括离散频率、振幅和暴露时间，但在研究中得出方法论原理和机制结论具有挑战性。然而，诸如肿瘤细胞毒性、细胞凋亡、肿瘤膜电穿孔和渗漏以及活性氧生成等输出是令人感兴趣的。早期的人类 EM 平台采用外部施加的脉冲电场或使用介入肿瘤接触来诱导肿瘤细胞电穿孔，同时保留基质、血管和免疫。直接或外部暴露于非热电磁波或脉冲磁场也可能产生电动势，以与独特的肿瘤细胞特性（包括肿瘤糖萼）相结合，从而诱导癌膜破坏和应激，从而提供增强肿瘤抗原释放的新途径、肿瘤驻留免疫细胞的交叉呈递和抗肿瘤免疫。与现有的检查点抑制剂策略相结合以增强癌症的免疫治疗效果也可能成为一种广泛有效的策略，但在这一领域几乎没有被考虑或测试过。与癌症中使用化学/放射和/或靶向治疗不同，EM 平台可以允许肿瘤相关免疫细胞（包括初始和致敏的抗肿瘤 T 细胞）存活。此外，EM诱导的癌细胞应激和细胞凋亡可能增强内源性肿瘤抗原特异性抗肿瘤免疫。检验这些组合 EM 平台方法中的一些的临床研究还处于起步阶段，在了解 EM 平台如何与免疫疗法整合方面加大研究力度（包括基础、临床和转化工作）对于推动癌症的进展至关重要这一充满希望的组合下的成果。版权所有 © 2024 Fuster。

An array of published cell-based and small animal studies have demonstrated a variety of exposures of cancer cells or experimental carcinomas to electromagnetic (EM) wave platforms that are non-ionizing and non-thermal. Overall effects appear to be inhibitory, inducing cancer cell stress or death as well as inhibition in tumor growth in experimental models. A variety of physical input variables, including discrete frequencies, amplitudes, and exposure times, have been tested, but drawing methodologic rationale and mechanistic conclusions across studies is challenging. Nevertheless, outputs such as tumor cytotoxicity, apoptosis, tumor membrane electroporation and leak, and reactive oxygen species generation are intriguing. Early EM platforms in humans employ pulsed electric fields applied either externally or using interventional tumor contact to induce tumor cell electroporation with stromal, vascular, and immunologic sparing. It is also possible that direct or external exposures to non-thermal EM waves or pulsed magnetic fields may generate electromotive forces to engage with unique tumor cell properties, including tumor glycocalyx to induce carcinoma membrane disruption and stress, providing novel avenues to augment tumor antigen release, cross-presentation by tumor-resident immune cells, and anti-tumor immunity. Integration with existing checkpoint inhibitor strategies to boost immunotherapeutic effects in carcinomas may also emerge as a broadly effective strategy, but little has been considered or tested in this area. Unlike the use of chemo/radiation and/or targeted therapies in cancer, EM platforms may allow for the survival of tumor-associated immunologic cells, including naïve and sensitized anti-tumor T cells. Moreover, EM-induced cancer cell stress and apoptosis may potentiate endogenous tumor antigen-specific anti-tumor immunity. Clinical studies examining a few of these combined EM-platform approaches are in their infancy, and a greater thrust in research (including basic, clinical, and translational work) in understanding how EM platforms may integrate with immunotherapy will be critical in driving advances in cancer outcomes under this promising combination.Copyright © 2024 Fuster.