DNA 损伤可能导致错误的改变和突变，进而导致多种疾病，包括衰老、严重炎症，最重要的是癌症。由于持续暴露于外源性和内源性 DNA 损伤剂等高风险因素，细胞可能会遭受 DNA 损伤，从而损害基因组的稳定性和完整性。 DNA 结构的这些扰动可能是由基因组中的几种突变引起的。因此，DNA损伤修复/反应（DDR）通过诱导DNA修复、细胞周期停滞、细胞凋亡等过程来检测并纠正这些潜在的致瘤问题。此外，DDR可以激活与免疫系统相关的信号通路，作为针对癌症的保护机制。基因组损伤。这些保护机制被点燃并通过分子网络传播，包括 DNA 损伤传感器、传感器、激酶和下游效应器。在这篇综述中，我们将讨论先天免疫系统和 DDR 之间的分子串扰，以及它们对癌症病理生理学的潜在影响。版权所有 © 2024 Elsevier GmbH。版权所有。

DNA damage can lead to erroneous alterations and mutations which in turn can result into wide range of disease condition including aging, severe inflammation, and, most importantly, cancer. Due to the constant exposure to high-risk factors such as exogenous and endogenous DNA-damaging agents, cells may experience DNA damage impairing stability and integrity of the genome. These perturbations in DNA structure can arise from several mutations in the genome. Therefore, DNA Damage Repair/Response (DDR) detects and then corrects these potentially tumorigenic problems by inducing processes such as DNA repair, cell cycle arrest, apoptosis, etc. Additionally, DDR can activate signaling pathways related to immune system as a protective mechanism against genome damage. These protective machineries are ignited and spread through a network of molecules including DNA damage sensors, transducers, kinases and downstream effectors. In this review, we are going to discuss the molecular crosstalk between innate immune system and DDR, as well as their potential effects on cancer pathophysiology.Copyright © 2024 Elsevier GmbH. All rights reserved.