The DNA double-strand break (DSB) is the most cytotoxic lesion and compromises genome stability. In an attempt to efficiently repair DSBs, cells activate ATM kinase, which orchestrates the DNA damage response (DDR) by activating cell cycle checkpoints and initiating DSB repair pathways. In physiological B cell development, however, programmed DSBs are generated as intermediates for effective immune responses and the maintenance of genomic integrity. Disturbances of these pathways are at the heart of B cell lymphomagenesis. Here, we review the role of DNA repair and cell cycle control on B cell development and lymphomagenesis. In addition, we highlight the intricate relationship between the DDR and the tumor microenvironment (TME). Lastly, we provide a clinical perspective by highlighting treatment possibilities of defective DDR signaling and the TME in mantle cell lymphoma, which serves as a blueprint for B cell lymphomas.

中文翻译：

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针对B细胞淋巴瘤的DNA修复，细胞周期和肿瘤微环境

DNA双链断裂（DSB）是最具细胞毒性的病变，会损害基因组稳定性。为了有效修复DSB，细胞激活了ATM激酶，该激酶通过激活细胞周期检查点和启动DSB修复途径来协调DNA损伤反应（DDR）。但是，在生理性B细胞发育中，程序化DSB会作为中间体产生，以实现有效的免疫反应和维持基因组完整性。这些途径的障碍是B细胞淋巴瘤发生的核心。在这里，我们综述了DNA修复和细胞周期控制在B细胞发育和淋巴瘤发生中的作用。此外，我们强调了DDR与肿瘤微环境（TME）之间的复杂关系。最后，