近年来，一些研究揭示出，许多患有前列腺癌的男性存在DNA损伤修复基因反应和错配修复基因的遗传缺陷。其中一些修饰，尤其是被称为同源重组（HRR）基因的基因改变；PALB2、CHEK2、BRCA1、BRCA2、ATM，以及DNA错配修复（MMR）的基因；MLH1、MSH2、MSH6和PMS2与前列腺癌的风险增加和更严重的疾病类型有关。DNA损伤修复（DDR）在T和B细胞发育所需的抗原受体基因的构建和多样性中至关重要。但是，这种DDR不平衡会导致DNA复制和转录的压力、突变的积累，甚至细胞死亡，从而损害组织稳态。由于DDR异常的这些影响，肿瘤免疫可能受到影响，从而可能促进肿瘤的生长、炎症细胞因子的释放和异常免疫反应。同样地，具有改变的MMR基因的人可能会从免疫治疗中获益匪浅。因此，在这些治疗中，需要进行突变遗传学检测。错配修复基因（MMR）的缺陷也比以前认为的更普遍，尤其在转移性疾病、高Gleason分级和不同组织学类型的患者中。本综述总结了目前关于DDR机制（如HRR和MMR异常）在前列腺癌中的突变谱和临床意义的信息，并解释了由于这一认识而导致的患者管理的发展。版权所有© 2023 Bugoye, Torrorey-Sawe, Biegon, Dharsee, Mafumiko, Patel and Mining.

Over the past few years, a number of studies have revealed that a significant number of men with prostate cancer had genetic defects in the DNA damage repair gene response and mismatch repair genes. Certain of these modifications, notably gene alterations known as homologous recombination (HRR) genes; PALB2, CHEK2 BRCA1, BRCA2, ATM, and genes for DNA mismatch repair (MMR); MLH1, MSH2, MSH6, and PMS2 are connected to a higher risk of prostate cancer and more severe types of the disease. The DNA damage repair (DDR) is essential for constructing and diversifying the antigen receptor genes required for T and B cell development. But this DDR imbalance results in stress on DNA replication and transcription, accumulation of mutations, and even cell death, which compromises tissue homeostasis. Due to these impacts of DDR anomalies, tumor immunity may be impacted, which may encourage the growth of tumors, the release of inflammatory cytokines, and aberrant immune reactions. In a similar vein, people who have altered MMR gene may benefit greatly from immunotherapy. Therefore, for these treatments, mutational genetic testing is indicated. Mismatch repair gene (MMR) defects are also more prevalent than previously thought, especially in patients with metastatic disease, high Gleason scores, and diverse histologies. This review summarizes the current information on the mutation spectrum and clinical significance of DDR mechanisms, such as HRR and MMR abnormalities in prostate cancer, and explains how patient management is evolving as a result of this understanding.Copyright © 2023 Bugoye, Torrorey-Sawe, Biegon, Dharsee, Mafumiko, Patel and Mining.