Radiotherapy is one of the most common modalities for the treatment of cancer. One of the most promising effects of radiotherapy is immunologic cell death and the release of danger alarms, which are known as damage-associated molecular patterns (DAMPs). DAMPs are able to trigger cancer cells and other cells within tumor microenvironment (TME), either for suppression or promotion of tumor growth. Heat shock proteins (HSPs) including HSP70 and HSP90, high mobility group box 1 (HMGB1), and adenosine triphosphate (ATP) and its metabolites such as adenosine are the most common danger alarms that are released after radiotherapy-induced immunologic cell death. Some DAMPs including adenosine is able to interact with both cancer cells as well as other cells in TME to promote tumor growth and resistance to radiotherapy. However, others are able to trigger anti-tumor immunity or both tumor suppressive and immunosuppressive mechanisms depending on affected cells. In this review, we explain the mechanisms behind the release of radiation-induced DAMPs, and its consequences on cells within tumor. Targeting of these mechanisms may be in favor of tumor control in combination with radiotherapy and radioimmunotherapy.

放射疗法是治疗癌症的最常见方式之一。放射疗法最有希望的作用之一是免疫细胞死亡和释放危险警报，这被称为损害相关分子模式（DAMP）。DAMPs能够触发肿瘤微环境（TME）内的癌细胞和其他细胞，从而抑制或促进肿瘤的生长。热休克蛋白（HSP）包括HSP70和HSP90，高迁移率族框1（HMGB1）和三磷酸腺苷（ATP）及其代谢产物如腺苷是放疗引起的免疫细胞死亡后释放的最常见危险警报。包括腺苷在内的某些DAMP能够与TME中的癌细胞以及其他细胞相互作用，从而促进肿瘤生长和对放射疗法的抵抗力。然而，其他的能够触发抗肿瘤免疫力或肿瘤抑制和免疫抑制机制，具体取决于受影响的细胞。在这篇综述中，我们解释了辐射诱导的DAMPs释放的机制及其对肿瘤细胞的影响。这些机制的目标可能与放疗和放射免疫疗法相结合有利于控制肿瘤。